




^ v #I ^ # \^ ^^^v ~v* T ^\</ °°^ * 




» / 1 



0* *o 








** v % 








^ 



^ 1* 




V« 6 .\S&X ^ j 20fe\ /\S&X ^4Sfe-i 

♦;**.X y.oa*.^ ^>:^:.V y.itfk.^ ^1 




'^^* 









♦ v ^ 







4>*. titer X <-°* 



o ■ • 








• / t 





» • o. 










^rf 1 




r oV 







Q. 




kPv^ 















^a ^ 












,V + 




***** ' 



o * • 





^ 











•. v/ 



«*' 



^^Ur"°o A^\ /.gi>o A A^kV ^° 



>°% 



A TEXT-BOOK 



OF THE 



PRACTICE OF MEDICINE 



FOR STUDENTS AND PRACTITIONERS 



BY 



/a 



HOB ART AMORY pARE, B.Sc, M.D. 



PROFESSOR OF THERAPEUTICS, MATERIA MEDICA, AND DIAGNOSIS IN THE JEFFERSON MEDICAL COLLEGE OF PHILADELPHIA: 

PHYSICIAN TO THE JEFFERSON MEDICAL COLLEGE HOSPITAL; ONE TIME CLINICAL PROFESSOR OF DISEASES OF 

CHILDREN IN THE UNIVERSITY OF PENNSYLVANIA; AUTHOR OF "a TEXT-BOOK OF PRACTICAL 

THERAPEUTICS," AND "DIAGNOSIS IN THE OFFICE AND AT THE BEDSIDE" 



THIRD EDITION, REVISED AND ENLARGED 



ILLUSTRATED WITH 142 ENGRAVINGS AND 16 PLATES IN 
COLORS AND MONOCHROME 




LEA & FEBIGER 
PHILADELPHIA AND NEW YORK 

1915 



**P 






< 



Entered according to the Act of Congress,, in the year 1915, by 

LEA & FEBIGER, 

in the Office of the Librarian of Congress. All rights reserved. 



FEB 19 1915 



PREFACE TO THIRD EDITION 



The preparation of a third edition of a book on the Practice of Medicine is a task 
almost equal to the preparation of the text of. a first edition, particularly if so long 
a period as eight years has elapsed since the second edition appeared. Only those 
who keep themselves thoroughly abreast of all departments of medical endeavor 
can estimate what the changes have been in our conception of almost every dis- 
ease as to etiology, pathology, and symptomatology, not to speak of treatment. 
Furthermore, only those who keep themselves thoroughly well informed can be as 
optimistic in regard to our struggle with disease as the nature of the advances 
justify. Every year sees an increasing army of investigators in physiology, 
pathology, bacteriology, protozoology, and therapeutics, meeting with occasional 
reverses, but as a whole moving onward to clearer ideas concerning some of the 
problems which but a short time ago seemed quite beyond hope of elucidation. 

The text of the present edition has been most carefully revised, and on almost 
every page corrections and additions have been made, based upon a careful study 
of the contributions of others and the writer's increasing experience in hospital 
and private practice. An endeavor has been made to place the necessary facts 
in a concise form and to prepare the text so that it is easily read, rather than to 
resort to short, dogmatic sentences, which do not hold the attention because they 
do not lead the reader forward step by step. 

My cordial thanks are due to Dr. Aller G. Ellis, Associate Professor of Pathology, 
for his careful reading and revision of the sections dealing with etiology and 
pathology, and to Dr. G. E. Price, Associate Professor of Nervous and Mental 
Diseases in the Jefferson Medical College, for similar services in connection with 
those parts of the volume dealing w T ith Diseases of the Nervous System. 

H. A. H. 

Philadelphia, 1915. 



(v) 



CONTENTS 



DISEASES DUE TO A SPECIFIC INFECTION. 

Typhoid Fever 17 

Paratyphoid Fever 53 

Typhus Fever 54 

Variola 60 

Vaccinia and Vaccination 74 

Varicella 77 

Scarlet Fever 79 

Measles ' 92 

Rubella 98 

Mumps 99 

Whooping-cough 101 

Influenza 106 

Acute Poliomyeloencephalitis Ill 

Dengue • . 117 

Meningococcic Meningitis 120 

Croupous Pneumonia 128 

Diphtheria . .• * . 151 

Gonorrheal Infection 165 

Erysipelas 168 

Septicemia and Pyemia 171 

Acute Rheumatic Fever 174 

Cholera 181 

Yellow Fever ' 187 

Plague (Bubonic Plague) 194 

Climatic Bubo 200 

Dysentery 200 

Epidemic Gangrenous Proctitis 213 

Hill Diarrhea : 214 

Malta Fever 215 

Phlebotomous Fever 218 

Anthrax 219 

Hydrophobia 222 

Tetanus 227 

Glanders 231 

Actinomycosis 233 

Mycetoma (Madura Foot, Fungus Foot of India) 234 

Frambesia (Frambesia Tropica. Yaws) 235 

Tuberculosis 237 

Acute Miliary Tuberculosis 243 

Glandular Tuberculosis 245 

Tuberculosis of the Serous Membranes 247 

Pulmonary Tuberculosis 255 

Tuberculosis of the Alimentary Canal 278 

Tuberculosis of the Liver 281 

Tuberculosis of the Genito-urinary System 281 

Tuberculosis of the Fallopian Tubes, Ovaries and Uterus 285 

Tuberculosis of the Heart 285 

(vii) 



viii CONTENTS 

Tuberculosis : 

Tuberculosis of the Thyroid Gland 286 

Tuberculosis of the Brain and Cord 286 

Hodgkin's Disease 286 

Leprosy 289 

Febricula 295 

Milk Sickness 295 

Weil's Disease 296 

Glandular Fever 296 

Mountain Fever 297 

Spotted or Tick Fever 299 

Foot-and-Mouth Disease 299 

Miliary Fever 299 

Verruga (Verruga Peruviana) 300 

Gangosa 302 

Syphilis 302 

Hereditary Syphilis 312 

Malarial Infection ' 316 

Latent Malarial Infection and Relapse 328 

Relapsing Fever 329 

Psorospermiasis 331 

Trypanosomiasis 331 

Human Trypanosomiasis (Trypanosoma Fever) 333 

African Lethargy (Sleeping Sickness) 333 

Kala-azar 335 

Tropical Sore 336 

Nematodes 336 

Ascariasis 336 

Oxyuris Vermicularis 337 

Trichina Spiralis 337 

Uncinariasis (Ankylostomiasis) 338 

Filariasis (Filaria Sanguinis Hominis) 343 

Guinea-worm Disease (Dracontiasis) 346 

Strongyloides Intestinalis 348 

Tricocephalus Dispar 349 

Cestodes or Tapeworm 350 

Trematodes 353 

Bilharzia Disease 353 

Distomatosis of the Lung 355 

Distomatosis of the Liver . 356 

Parasitic Infusoria 357 

Chigger (Sand Flea) 357 

Myiasis 357 

Infection by Larva? of the Diptera 357 

Intestinal Myiasis 358 

Dermatobia Cyaniventris 358 

Tumbu-fly Disease 358 



DISEASES OF THE RESPIRATORY SYSTEM . 

Diseases of the Nose 359 

Acute Coryza 359 

Chronic Nasal Catarrh 360 

Atrophic Nasal Catarrh 361 

Hay Fever 362 

Epistaxis 364 

Diseases of the Larynx 364 

Acute Catarrhal Laryngitis 364 



CONTENTS ix 

Diseases of the Larynx: 

Chronic Catarrhal Laryngitis ■ 366 

Edematous Laryngitis 366 

Spasmodic Laryngitis 368 

Tuberculous Laryngitis 368 

Syphilitic Laryngitis 370 

Diseases of the Bronchi 370 

Acute Catarrhal Bronchitis 370 

Chronic Catarrhal Bronchitis 374 

Bronchiectasis 375 

Fibrinous Bronchitis 379 

Bronchial Asthma 381 

Diseases of the Lungs 386 

Bronchopneumonia 386 

Metastatic Pneumonia 396 

Pneumonoconiosis 398 

Emphysema of the Lungs 400 

Compensatory or Acute Emphysema 404 

Small-lunged Emphysema 405 

Interstitial Emphysema 405 

Gangrene of the Lung 405 

Pulmonary Abscess 407 

Congestion of the Lungs 409 

Tumors in the Lungs 412 

Diseases of the Pleura 413 

Pleuritis 413 

Dry Pleurisy 414 

Pleurisy with Effusion 417 

Purulent Pleural Effusion or Empyema 423 

Chronic Pleurisy 427 

Hydrothorax 428 

Pneumothorax, Hydropneumothorax, Pyopneumothorax 429 

Diseases of the Mediastinum 431 



DISEASES OF THE CIRCULATORY SYSTEM. 

Diseases of the Pericardium 435 

Pericarditis 435 

Acute Pericarditis 435 

Chronic Pericarditis 440 

Hydropericardium 442 

Hemopericardium 443 

Pneumopericardium . 443 

Pyopericardium 444 

Diseases of the Heart 444 

Hypertrophy and Dilatation of the Heart 444 

Diseases of the Myocardium 448 

Degenerative Changes 448 

Stokes-Adams Disease 450 

Myocarditis 450 

Cardiac Aneurysm 453 

Wounds of the Heart 454 

Endocarditis 454 

Acute Endocarditis 455 

Ulcerative Endocarditis 458 

Chronic Endocarditis 460 

Chronic Valvular Disease as a Result of Chronic Endocarditis 461 

Mitral Regurgitation 464 



x CONTENTS 

Diseases of the Heart: 

Chronic Valvular Disease as a Result of Chronic Endocarditis: 

Mitral Stenosis • . 469 

Aortic Stenosis 474 

Aortic Regurgitation 476 

Tricuspid Regurgitation 480 

Tricuspid Stenosis 482 

• Disease of the Pulmonary Valves 482 

Disorders of Cardiac Action not due to Valvular Lesions 487 

Neuroses of the Heart 487 

Palpitation . . ■ 487 

Tachycardia 487 

Bradycardia 488 

Arrhythmia 488 

Angina Pectoris 491 

Congenital Cardiac Defects 494 

Diseases of the Arteries 495 

Aortitis 495 

Arteriosclerosis 496 

Aneurysm 500 

Aneurysm of Thoracic Aorta 501 

Aneurysm of the Abdominal Aorta 507 

DISEASES OF THE DIGESTIVE TRACT. 

Diseases of the Mouth 509 

Stomatitis 509 

Catarrhal Stomatitis 509 

Aphthous Stomatitis 509 

Ulcerative Stomatitis 510 

Thrush 511 

Gangrenous Stomatitis, Cancrum Oris or Noma 511 

Eczema of the Tongue 512 

Leukoplakia Buccalis 513 

Mucous Patches. 513 

Diseases of the Salivary Glands 513 

Functional Disorders of the Salivary Glands 513 

Ptyalism .513 

Dry Mouth 514 

Inflammation of the Salivary Glands 514 

Mickulicz's Disease 514 

Diseases of the Pharynx 515 

Acute Pharyngitis 515 

Ulcerative or Phlegmonous Pharyngitis 516 

Croupous Pharyngitis 517 

Chronic Pharyngitis 517 

Follicular Pharyngitis 517 

Epidemic Sore Throat 518 

Diseases of the Tonsils 518 

Acute Tonsillitis 518 

Ludwig's Angina 520 

Vincent's Angina 521 

Chronic Hypertrophic Tonsillitis 521 

Diseases of the Esophagus ...."... 522 

Esophagitis 522 

Organic Stricture of the Esophagus 523 

Dilatation of the Esophagus 523 

Spasm of the Esophagus 524 

Cancer of the Esophagus 525 



CONTENTS xi 

Diseases of the Stomach 525 

Acute Gastric Catarrh 525 

Phlegmonous Gastritis 526 

Diphtheritic Gastritis 527 

Mycotic Gastritis 528 

Chronic Gastritis 528 

Gastric Dilatation 531 

Acute Gastrectasis 535 

Gastric Ulcer 536 

Cancer of the Stomach 545 

Hypertrophic Stenosis of the Pylorus 552 

Hour-glass Stomach 555 

Gastric Neuroses 556 

Cardiospasm 556 

Pylorospasm 557 

Gastric Hyperperistalsis 557 

Merycismus 557 

Nervous Eructation 558 

Hyperesthesia 558 

Gastralgia 558 

Bulimia 559 

Anorexia Nervosa 559 

Nervous Disorders of Secretion • 559 

Hemorrhage from the Stomach 559 

Cyclic Vomiting 560 

Diseases of the Intestines 561 

Duodenal Ulcer 561 

Diarrhea " . 565 

Serous Diarrhea . . 565 

Catarrhal Enteritis 566 

Ileocolitis of Childhood 566 

Cholera Infantum 569 

Appendicitis 572 

Intestinal Obstruction 579 

Congenital Malformation 579 

Intussusception 579 

Internal Strangulation 581 

Volvulus 581 

Obstruction from Foreign Bodies 582 

Enteroptosis '• 582 

Colitis • ... 586 

Acute Colitis 586 

Mucous Colitis 586 

Folliculus and Croupous Colitis 587 

Pseudomembranous Colitis 588 

Sprue (Psilosis) 588 

Dilatation of the Colon 591 

Membranous Pericolitis ■ 592 

Adhesions, Displacements, and Redundancy of Colon 592 

DISEASES OF THE PERITONEUM. 

Acute Peritonitis 592 

Chronic Peritonitis • 59S 

Chronic Adhesive Sclerotic Peritonitis 598 

Morbid Growths of the Peritoneum 599 

Cancer of the Peritoneum 599 

Other Growths of the Peritoneum 599 

Ascites 599 



xii CONTENTS 



DISEASES OF THE LIVER. 

Inflammation of the Liver 602 

Acute Hepatitis or Hepatic Abscess . 602 

Cirrhosis of the Liver 606 

Atrophic Cirrhosis 607 

Hypertrophic Cirrhosis 610 

Syphilitic Cirrhosis 611 

Perihepatitis (Capsular Cirrhosis) . . 612 

Affections of the Hepatic Bloodvessels 612 

Amyloid Liver 614 

Fatty Liver 614 

Tumors of the Liver 614 

Acute Yellow Atrophy of the Liver 616 



DISEASES OF THE BILIARY TRACT. 

Acute Catarrh of" the Bile-ducts, or Acute Cholangitis 617 

Chronic Catarrh of the Bile-ducts 618 

Suppurative Inflammation of the Bile-ducts 619 

Occlusion and Constrictions of the Bile-ducts 619 

Acute Cholecystitis 620 

Cholelithiasis 621 

Malignant Growths of the Gallbladder and Biliary Passages 627 

Icterus Neonatorum 630 



DISEASES OF THE PANCREAS. 

Pancreatitis 630 

Acute Pancreatitis , 630 

Chronic Pancreatitis 634 

Pancreatic Calculus 636 

Pancreatic Cysts 636 

Pancreatic Tumors 637 

Hemorrhages into the Pancreas 637 



DISEASES OF THE KIDNEYS. 

Malformations of the Kidneys 638 

Movable Kidney 638 

Circulatory Disturbances in the Kidney 640 

Acute Hyperemia 640 

Chronic Hyperemia 640 

Acute Nephritis 641 

Chronic Nephritis 643 

Chronic Parenchymatous Nephritis 645 

Chronic Interstitial Nephritis 650 

Amyloid Disease of the Kidneys 657 

Uremia 658 

Pyelonephritis and- Pyelitis 662 

Hydronephrosis 665 

Cystic Disease of the Kidney 667 

Tumors of the Kidney 668 

Nephrolithiasis 669 

Perinephritic Abscess 672 



CONTENTS xiii 

Disorders of Urinary Secretion 672 

Anuria 672 

Hematuria 673 

Hemoglobinuria 674 

Hematinuria 674 

Albuminuria 675 

Pyuria 678 

Chyluria 678 

Phosphaturia 679 

Oxaluria • 679 

Indicanuria 679 

Lithuria 680 

Melanuria 680 

Myelopathic Albumosuria 680 



DISEASES OF THE DUCTLESS GLANDS AND LYMPHATIC SYSTEM. 

Diseases of the Thyroid Gland 681 

Goitre 681 

Swelling of the Thyroid 682 

Tumors of the Thyroid Gland 683 

Exophthalmic Goitre 683 

Myxedema 688 

Cretinism - . 689 

Diseases of the Parathyroid Gland 691 

Tetany . 691 

Diseases of the Thymus Gland 693 

Status Thymolymphaticus 694 

Diseases of the Suprarenal Gland . 695 

Addison's Disease 695 

Diseases of the Pituitary Body 699 

Dyspituitarism 699 

Acromegaly 699 

Infantilism 702 

Diseases of the Spleen 702 

Splenic Anemia * 704 

Banti's Disease 705 

Gaucher's Disease 705 

Hemolytic Splenomegaly 706 



DISEASES OF THE BLOOD. 

Anemia 707 

Secondary Anemia 707 

Primary or Essential Anemias 708 

Chlorosis 708 

Pernicious Anemia 710 

Aplastic Anemia 713 

Chronic Splenomegalic Polycythemia (Erythremia) 713 

Leukemia • 714 

Splenomedullary Leukemia . 715 

Lymphatic Leukemia 716 

Chloroma 718 

Anemia Infantum 718 

Purpura 719 

Hemophilia 721 



xiv CONTENTS 



DISEASES OF NUTRITION. 

Diabetes Mellitus 723 

Bronzed Diabetes 739 

Diabetes Insipidus 739 

Gout 740 

Acute Gout 745 

Chronic Gout 746 

Irregular Gout 746 

Arthritis Deformans 749 

Chronic Rheumatism ■ 753 

Muscular Rheumatism 754 

Rickets 755 

Scurvy 759 

Obesity 762 

Adiposis Dolorosa . • 764 

Osteitis Deformans 765 

Hypertrophic Pulmonary Osteo-arthropathy ■ 765 

Leontiasis Ossea 765 

Scleroderma 765 

Ochronosis 766 

Ainhum 766 

Beriberi 766 



INTOXICATIONS. 

Alcoholism 771 

Acute Alcoholism 771 

Subacute and Chronic Alcoholism 772 

Morphinism 775 

Arsenical Poisoning 777 

Lead Poisoning, or Plumbism 778 

Food Poisoning 781 

Bromatotoxismus 781 

Sitotoxismus 781 

Mytilotoxismus ...*.... 781 

Ichthyotoxismus 782 

Kreotoxismus . 782 

Tyrotoxismus and Galactotoxismus 782 

Pellagra 782 



DISEASES OF THE NERVOUS SYSTEM. 

DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE BRAIN 

AND ITS MEMBRANES. 

Hemorrhage into the Brain, Cerebral Thrombosis, and Embolism 785 

Infantile Cerebral Paralysis . 795 

Little's Disease ' 799 

Aphasia 799 

Tumors of the Brain and its Membranes 801 

Abscess of the Brain 809 

Acute Cerebritis or Encephalitis 811 

Thrombosis of the Venous Sinuses 812 

Cerebral Meningitis 813 

Pachymeningitis 813 

Pachymeningitis Interna 814 



CONTENTS xv 

Cerebral Meningitis: 

Leptomeningitis 814 

Dementia Paralytica 816 

Disseminated Sclerosis 820 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE 

SPINAL CORD. 

Locomotor Ataxia 823 

Friedreich's Ataxia 830 

Marie's Cerebellar Hereditary Ataxia 833 

Chronic Anterior Poliomyelitis 833 

Bulbar Paralysis 835 

Lateral Sclerosis 836 

Syphilitic Spastic Spinal Paralysis 838 

Amyotrophic Lateral Sclerosis 838 

Myelitis . . - 840 

Acute and Subacute Myelitis 840 

Chronic Myelitis 842 

Senile Paraplegia 844 

Myelomalacia 844 

Syringomyelia 844 

Hemorrhage into the Spinal Cord 846 

Hemorrhage into the Spinal Membranes 847 

Compression of the Spinal Cord 848 

Spinal Meningitis 851 

Chronic Spinal Meningitis 853 

Acute Ascending Paralysis (Landry's Paralysis) . 854 

Caisson Disease 855 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE NERVES. 

Neuritis 857 

Special Forms of Neuritis 859 

Cervicobrachial Neuritis 859 

Obstetrical or Birth Palsy '. 860 

Sciatica 860 

Multiple Neuritis 860 

Diseases of the Cranial Nerves 865 

The Olfactory Nerve 865 

The Optic Nerve 865 

Optic Atrophy 866 

Hemianopsia 867 

The Third or Oculomotor Nerve 870 

The Fourth or Trochlearis Nerve -. ' 871 

The Fifth or Trifacial Nerve 871 

Paralysis of the Sixth Abducens Nerve 873 

Disturbances of Motility in the Ocular Muscles Depending on the Third, 

Fourth, and Sixth Nerves . 873 

Ophthalmoplegia or Paralysis of the Internal and External Muscles of the 

Eyeball 874 

The Seventh or Facial Nerve 875 

Facial Spasm 878 

The Eighth or Auditory Nerve 878 

The Ninth or Glossopharyngeal Nerve 880 

The Tenth or Vagus Nerve 8S0 

Eleventh or Spinal Accessory Nerve 882 

Twelfth or Hypoglossal Nerve 883 



xvi CONTENTS 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE MUSCLES. 

Muscular Dystrophies 884 

Pseudomuscular Hypertrophy 884 

Erb's Juvenile Muscular Dystrophy 885 

Landouzy-Dejerine Type of Muscular Dystrophy or Facioscapulohumeral Type . 885 

Muscular Atrophy of the Peroneal Type 886 



FUNCTIONAL NERVOUS DISEASES AND DISEASES OF DISPUTED 

PATHOLOGY. 

Myotonia Congenita 886 

Paramyoclonus Multiplex 887 

Paralysis Agitans 888 

Chorea Minor 890 

Other Forms of Chorea 893 

Huntington's Chorea 893 

Dubini's Disease 894 

Hysteria 894 

Neurasthenia 899 

Epilepsy 901 

Petit Mai, or Minor Epilepsy 909 

Jacksonian Epilepsy 909 

Eclampsia 909 

Infantile Eclampsia 909 

Puerperal Eclampsia 910 

Latah 911 

Amok (Running Amok) 911 

Astasia-abasia • 912 

Traumatic Neuroses . ' 912 

Occupation Neuroses 914 

Raynaud's Disease 916 

Angioneurotic Edema 916 

Erythromelalgia 917 

Migraine 918 

Sunstroke . 920 

Heat Exhaustion 922 

Facial Hemiatrophy 922 

Periodical Paralysis 923 



PRACTICE OF MEDICINE. 



DISEASES DUE TO A SPECIFIC INFECTION. 



TYPHOID FEVER. 

Definition. — Typhoid or Enteric fever, sometimes called Autumnal or Gastric 
fever, is an acute infectious disease due to the entrance into the body of a susceptible 
individual of the specific bacillus of Eberth, commonly known as Bacillus typhosus. 
The entrance of this organism into the system results, after a period of from one 
to three weeks in some persons, but not in all, in the development of fever, anorexia, 
headache, mental heaviness, and more or less severe pain in the bowels, back, and 
limbs. The tongue is coated, and the bowels are loose or constipated. With 
these symptoms are developed enlargement of the liver and spleen, and swellings 
and ulceration of the lymphoid structures of the small and large intestines, and a 
rose rash on the skin. 

History. — Typhoid fever for many years was confused with typhus fever and 
malarial fever, and its very name means "like typhus." In 1813 it was considered 
as a separate disease, but this separation was not generally known by the profession 
until Louis, of Paris (1829), first emphasized a number of its cardinal points. Not 
until 1837 was the identification complete, when Gerhard, of Philadelphia, published 
results achieved under the guidance of Louis which proved the malady to be a 
distinct entity. More than forty years later (1880) Eberth isolated the specific 
bacillus and proved it to be the sole cause of the disease. Up to that time various 
causes had been thought to exist, but it had been recognized for many years as 
a "filth disease," and, therefore, preventable to some degree. 

Distribution. — Enteric fever is one of the diseases which may be said to be pan- 
demic, since it is found with some degree of constancy all over the world, its preva- 
lence depending upon the introduction into the body of the specific bacillus, usually 
with water or food. It is estimated that about 150,000 cases of typhoid fever 
occur in the United States each year, with a mortality of 25,000. 

Etiology. — The cause of this disease, as just stated, is the specific bacillus of 
Eberth, a short, thick, actively motile bacillus, with rounded ends and flagella, 
growing readily in ordinary suitable media. It is killed by exposure to 60° C. 
(140° F.), but it can withstand a freezing temperature for many days. Exposed 
to sunlight it is slowly killed, but drying, except in very thin layers, does not destroy 
it. It remains alive for months, and even for years, in clothing and in soil, if 
the conditions are favorable. It is readily destroyed by the stronger germicides, 
such as carbolic acid (1:200) and bichloride of mercury (1:2000). The bacillus 
of Eberth bears a close resemblance to the Bacillus coli communis, which is always 
present in the intestine, and to the so-called paracolon bacillus and the Bacillus 
dysenteric. 

2 (17) 



18 DISEASES DUE TO A SPECIFIC INFECTION 

The second etiological factor in the development of the disease is the mode 
by which the bacillus gains access to the body. Almost invariably this access 
is through the mouth, stomach, and intestine, more rarely by inhalation of the 
bacillus in dust by the lungs. Infection takes place by the mouth in a host of 
ways, as by infected water, or milk diluted with infected water, or chilled by infected 
ice; by vegetables and oysters and clams, which, when eaten raw, are often the 
means of carrying infection. It has recently been proved at Ogdensburg, New 
York, that infected ice may transmit the organism after it has been stored in an 
ice-house for at least nine months. In still other instances persons nursing cases 
of this disease get the finger-tips infected and so, on putting the fingers to the 
mouth, introduce the organism into the body. A very important cause of enteric 
fever is the so-called "typhoid carrier." A carrier is one who continues for many 
years after an attack, in some instances as long as thirty years, to throw off the 
specific bacillus in the stools although in perfect health. Usually the patient 
has a clear history of an attack of the malady, but in some a mild attack has never 
put the patient in bed and no diagnosis of typhoid fever has even been thought 
of. Klinger traced to this source 1397 cases of enteric fever. Of these 1272 were 
infected by convalescent carriers and 125 cases by healthy carriers. "Typhoid 
Mary" in New York, a cook, apparently in perfect health, caused no less than 
seven outbreaks (28 cases) of enteric fever in five years at widely separated points. 
She denied that she had had typhoid fever, but examination of her stools showed 
them to be laden with typhoid bacilli. In other words, she was a chronic typhoid 
disseminator. Sawyer has reported ninety-three cases of typhoid fever infected 
by one "carrier," who prepared one dish at one meal. More and more such cases 
are being reported as time goes by. The bacillus of Eberth has been found in the 
stools of healthy attendants on typhoid-fever cases, who have never had the dis- 
ease, but who are, nevertheless, "carriers." Again, it has been proved beyond 
doubt that flies after lighting upon the discharges of a case of typhoid fever may 
carry the bacillus to otherwise pure food, and so spread the infection as long as 
twenty-three days after feeding on infected stools (Fischer) . Stokes describes an 
epidemic in a factory employing 1500 women and 400 men. As many as 200 of 
the women were ill at one time with typhoid fever, but none of the men fell ill. 
All the men drank beer at luncheon, whereas all the women used milk. The milk 
was found to have been infected by flies from a neighboring privy. Cockroaches 
may also spread the bacillus. 

Whipple states that typhoid fever is due to contaminated water in 40 per cent., 
infected milk in 25 per cent, and to contagion in 30 per cent., including fly trans- 
mission. 

Every great epidemic of the disease has been due to contamination of the water 
supply. In the Maidstone epidemic in England 1 person in every 17 in the town 
was infected; while in the Plymouth epidemic in Pennsylvania 1 in every 7 was 
stricken, for there were 1200 cases in a population of 8000. As only a part of 
these 8000 persons used the contaminated water, the proportion of actual infection 
to exposure was far higher than 1 in 7. The influence of bad and good water 
supply is shown in Figs. 1, 2 and 3. 

In 1888 the use of filtered drinking-water was begun in the French army, as a 
result of which the morbidity of typhoid fever was diminished 49 per cent, in 
1890, and the mortality 34 per cent. 

Prevention. — From what has just been said it is evident that typhoid fever is 
an entirely preventable disease, provided that the bacilli as they escape in the 
feces, the urine, the sputum, and, perhaps, in the sweat, are destroyed as soon as 
they pass from the patient's body. The destruction of the discharges and so of 
the bacilli is therefore absolutely essential, and in addition careful antisepsis on 
the part of the attendant as to personal cleanliness and the protection of the dis- 



TYPHOID FEVER 



19 



charges from flies are to be enforced. As careless or ignorant persons do not 
disinfect the stools, the additional measures of prophylaxis are the boiling of all 
water that is to be placed in the mouth, and the use of nothing but well-cooked 
foods, which have not been exposed to flies or dust after cooking. The vessel 
which receives the discharges of the patient should contain carbolic acid (1:200), 
corrosive sublimate (1:2000), or chlorinated lime (a heaping teaspoonful to the 
pint). Formaldehyde solution (40 per cent.) may also be used. If the stool is 
formed, it should be broken up by stirring it with a rod, so as to expose all the fecal 
matter to the germicide. 



Fig. 1 



Fig. 2 



Fig. 3 





es 

5T5 




TO 

a 

ao 


es 




to 
ao 


Si 

ao 


QTj 


es 

Of) 


o 
o 


1 






















1000 

1 




















2000 
1 


















3000 
1 


















4000 
1 


















5000 
1 


















6000 
1 


















7000 
1 
















8000 
1 









tese«i/ia!)»aoao»nri 



a s s a r. s s a s c 



9000 




1 




















1000 

1 




















2000 
1 




















3000 
1 




















4000 
1 




















5000 
1 




















6000 
1 




















7000 
1 




















8000 
1 




















9000 
1 




















100001 


T 


mi 


■ 

















10000 



Fig. 1. — Mortality in Chicago of typhoid fever. In 1891 and 1892 the water was contaminated with 
sewage and the death rate was about 1 to 450 to 1 to 1500. With a change in water supply the mor- 
tality has fallen to 1 to 6000 or even 1 to 9000. (Seibert.) 

Fig. 2. — Mortality of typhoid fever in Berlin before the supply of drinking-water was filtered. In 
the decade 1843 to 1853 the average yearly mortality was 1 per 900 of inhabitants. 

Fig. 3. — Mortality of typhoid fever in Berlin after water was filtered. (Seibert.) 



Physicians and nurses are not careful enough about the destruction of the stools, 
and the average individual is willing to take his chances on the use of unboiled 
water. Another of the difficulties is that patients may, when no longer kept* in 
the house by the disease, continue to cast off bacilli in the urine or feces which 



20 DISEASES DUE TO A SPECIFIC INFECTION 

are capable of infecting water supplies. This danger is of great importance, because 
at each urination or defecation the convalescent patient may produce a new source 
of infection. Further, it is toward the close of the attack and during convalescence 
that the urine contains these specific organisms in pure culture and in enormous 
numbers, and they may remain persistently present, not only for days but for 
months and even years. The patient should be told of this danger, should be 
directed to disinfect his discharges, and should receive daily doses of uritone or 
urotropin to destroy the bacilli in the urine before they are passed in that fluid. 
If he is also informed that bacilluria is a danger to himself, in that it may result 
in secondary diseases in his genito-urinary tract, he may be interested enough to 
aid the physician in arresting the spread of the bacillus by adhering to a plan of 
careful medication. Purjesz and Perl report the finding of typhoid bacilli in 
tongue-scrapings and upon the tonsils (more often the former) of half the conva- 
lescents examined. The examinations were made at times between the fifth and 
forty-seventh day after active symptoms had ceased. 

All clothing, instruments, bedding, pillows, utensils, bath-tubs and ordinary 
wash-tubs, which may be contaminated by the discharges of a patient, should be 
disinfected thoroughly as soon as their function is performed. The hands of the 
nurses should be repeatedly disinfected. 

Antityphoid Vaccination. — Another preventive of typhoid fever consists 
in the injection or inoculation in the arm or back of the individual with dead 
Bacillus typhosus, the organisms being destroyed by heat. Such an injection 
produces no effects, or, rarely, local swelling and some pain, a sense of nausea and 
depression, and some febrile movement, which symptoms speedily disappear, 
the patient at the end of twenty-four to thirty-six hours being well again. Ten 
days later the individual is injected a second time and ten days later a third time, 
each dose being larger than its predecessor. The dose is 500,000,000 increased 
to 1,000,000,000 or to 1,500,000,000. The dose for a child of 50 pounds is 
considered to be approximately one-third of the dose for an adult of 150 pounds. 
This prophylactic treatment is perfectly safe and has been used successfully in 
so many hundreds of thousands of cases as to be assured as firm a place in 
medicine as diphtheria antitoxin. The Commission of the French Academy of 
Medicine advises that no subject shall be vaccinated in whom typhoid seems 
imminent or at the beginning of an attack, as vaccination may aggravate the 
disease. It should be practised only upon perfectly healthy subjects, free from all 
organic or other defects and from local or general affections, no matter what their 
nature, especially tuberculosis, as vaccination may cause a temporary predisposi- 
tion to infection. Every person vaccinated against typhoid fever should take the 
strictest precautions to avoid the chances of typhoid infection by a careful watch 
upon the water that is drunk and the food that is eaten. The period during which 
such precautions must be taken has a duration of two or three weeks at the most. 

The group of persons designated as likely to be particularly benefited by anti- 
typhoid inoculation are: 

(a) Physicians, medical students, male and female nurses in military and civil 
hospitals. 

(6) Members of families in which typhoid fever is present or in which " bacillus 
carriers" have been demonstrated. 

(c) Young persons of both sexes who have come from salubrious regions in the 
country to cities in which are habitual foci of typhoid fever. 

(d) The population of cities where the latter disease is frequent. 

(e) Soldiers and sailors (rank and file). 

The immunity induced lasts, so far as is known, about three years. Probably 
antibodies do not exist, but the body is ready to prepare them in the presence of 
infection. 



TYPHOID FEVER 



21 



Fig. 4 

ADMISSION AND DEATH RATES FOR TYPHOID FEVER, 
UNITED STATES (ENLISTED MEN) 



Out of 130,000 antityphoid inoculations in the United States Army, 97 per cent, 
showed no disagreeable symptoms. In 1913 the general typhoid-fever morbidity 
throughout the United States was 12.70 per 100,000. In the United States Army it 
was per 100,000 under inoculation. 

In order to protect not only from the typhoid bacillus but also from both the 
Bacillus paratyphosus a and /3, a typhoid-paratyphoid vaccine has been employed, 
each injection containing 500,000,000 typhoid 
bacilli, 250,000,000 paratyphoid a, and 
250,000,000 paratyphoid /3. It produces 
little if any more reaction than the use of a 
single strain, but its use is probably needless 
unless there be present an epidemic of para- 
typhoid infection. 

Frequency. — Typhoid fever affects males 
oftener than females, and occurs most fre- 
quently between fifteen and thirty years of 
age. It may, however, affect infants or aged 
persons. It occurs more frequently in August, 
September, and October than any other quar- 
ter of the year, but is by no means limited to 
this period. (See Fig. 5.) 

Typhoid fever is becoming less and less 
frequent, and less severe all over the world. 
In Munich the mortality in the decade from 
1851 to 1861 ranged from 123 in 100,000 
inhabitants to 453 in 100,000 inhabitants, 
whereas in the years from 1890 to 1897 the 
mortality was from 57 or 14.8 in 100,000 
people to 10 or 2.5 per 100,000; in Vienna it 
has fallen from 120 per 100,000 to 10 per 
100,000; in Dantzig, from 100 per 100,000 to 
10.5. In Massachusetts the mortality from 
typhoid fever in 33 cities in 1901 was only one- 
fourth of what it was thirty years before. In 
Philadelphia a similar decrease has occurred 
in both mortality and morbidity. In Mel- 
bourne, Australia, there has also been a de- 
crease in the mortality rate which is very 
noticeable, being over 50 per cent. These de- 
creases are due chiefly to care in regard to 
water supplies. 

The general mortality rate of the world 
may be said fifty years ago to have been 
almost universally 25 per cent., whereas it is 
now from 15 to 10 per cent. 

With advancing years of age the morbidity decreases, but the mortality greatly 
increases. (See Fig. 6.) 

That typhoid fever is still the cause of an enormous number of deaths is empha- 
sized by Whipple's statistics of the United States, in which it is shown that in 
1910 there were 35,379 deaths due to this disease, a loss of life which was computed 
by him as equivalent to a pecuniary loss of $212,000,000 for that year alone. 

Pathology and Morbid Anatomy. — In studying the morbid anatomy of typhoid 
fever it must be remembered that it is not, when fully developed, a local infection, 
restricted to one or more foci from which the Bacillus typhosus distributes its toxin 




ANTI-TYPHOfB VACCINATION BEGUN VOLUNTARILY 
IN 1909 WAS MADE COMPULSORY IN 1911 

Chart showing decreasing morbidity and 
mortality from enteric fever in the United 
States Army under so-called antityphoid 
vaccination. (Courtesy of the Surgeon- 
General, United States Army.) 



22 



DISEASES DUE TO A SPECIFIC INFECTION 



through the body. On the contrary, the typhoid infection is practically universal, 
and the bacillus may be found in varying numbers in every organ of the body, includ- 



Fig.. 5 




Chart from the United States census, showing the period of the year when the mortality from 

typhoid fever reaches its maximum. 

ing the bone-marrow and skin. Contrary to general belief, they may not be demon- 
strable in the intestinal contents in large numbers until the disease is well advanced, 

Fig. 6 




Showing the increased mortality of typhoid fever with age. (Curschmann.) 

and their presence in the stools depends largely upon the intensity of the changes 
which take place in the intestinal lymph nodes. It is true, however, that the 



TYPHOID FEVER 



23 



agminated follicles (Peyer's patches) and the solitary follicles of the small bowel 
are the parts of the body which usually are the seat of the most evident and constant 
lesions. On the other hand, it is not to be forgotten that cases of undoubted typhoid 
fever occasionally occur in which no ulceration of the intestinal mucosa takes place. 
The alterations from the normal in the bowel may be discussed under three 
heads: (1) a diffuse catarrhal inflammation of the intestinal mucosa of varying 
severity, but usually resulting in desquamation of epithelium; (2) hyperemia, 
swelling, endothelial and lymphoid hyperplasia, necrosis, and finally ulceration 
of the agminated follicles or Peyer's patches; and (3) a similar change in the so- 
called solitary lymph follicles of the intestine, although the changes in the agminated 
follicles are distinctly the more conspicuous. These changes begin in the very 

Fig. 7 




2 cm. 



Ulceration of a Peyer patch in typhoid fever, with associated swelling of solitary glands. 



earliest stages of onset, and do not wait until the symptoms of the disease are well 
developed. If the patient comes to autopsy at this time, the intestinal mucosa 
will not only be found inflamed, but in addition the lymphoid structures just named 
will also be found swollen and reddened by hyperemia. Their edges are not well 
defined, and the entire gland is hyperplastic and spongy. A little later in the 
progress of the disease these areas become less red in hue and begin to look some- 
what gray in color; they are firmer and project above the surrounding mucous 
membrane to a marked degree, so that they extend well into the lumen of the bowel. 
Sometimes the hyperplasia within the gland is so great that its edges overhang 
the surrounding tissue. These elevated, circumscribed masses, made up of pro- 
liferated lymphoid and endothelial cells, are known as typhoid nodu/es. In addition 



24 DISEASES DUE TO A SPECIFIC INFECTION 

to being elevated above the surface of the intestine, these cells extend into the 
wall, usually involving the submucosa and at times the muscle coat.. Owing to 
disturbances in nutrition and the action of the typhoid toxine the nodules become 
necrotic, the dead tissue sloughs, and the typhoid ulcer is formed (Fig. 7) . The 
most extensive ulceration usually takes place in the lower part of the ileum. 

While ulceration of the tissues composing Peyer's patches is the usual result of 
this infection, necrosis does not always ensue. The gland may become red and 
swollen and the inflammatory process go no farther, proceeding from this state 
to that of resolution and healing. Not infrequently this agminated patch is not 
equally affected in all its parts, and this gives it an uneven appearance, which is 
emphasized when the portions which are most affected ulcerate, so that small 
ulcers are dotted over the surface of the swelling, which, if the process is severe, 
finally coalesce. In severe types of the disease the process is so well diffused that 
a huge slough forms which, when it drops off, leaves a swollen, ulcerated surface, 
the excavation being usually very deep. It is this type of necrosis that results in 
perforation, the opening in the bowel wall being usually found at a point directly 
opposite the mesenteric attachment. Rarely the perforation takes place between 
the layers of the mesentery and causes a retroperitoneal abscess. Harte states that 
in 140 cases out of 190 the perforation occurred in the small bowel within twelve 
inches of the cecum. 

If the patient survives the severer periods of the disease, the swelling of the 
glandular tissue gradually diminishes, granulations develop, new connective tissue 
largely takes the place once occupied by the gland, and the ordinary intestinal 
epithelium covers the exposed area. While it is true that the solitary glands are 
rarely so markedly affected as the agminated follicles, they may suffer much more 
severely and be found diseased over a larger area than are the patches of Peyer. 

The number of ulcers in the bowel in typhoid fever varies greatly. Usually 
they are limited in number, but occasionally they are many and cover very large 
areas. They may be more numerous in the cecum than elsewhere in the colon. 
Out of 577 autopsies upon cases of this disease in Hamburg and in Leipzig, the 
cecum was ulcerated in 510, or 88.39 per cent.; the cecum and appendix in 247, 
or 42.81 per cent.; the colon in 184 cases, or 31.89 per cent.; the jejunum in 41 
cases, or 7.10 per cent.; the rectum in 12 cases, or 2.08 per cent. The percentage 
of cecal lesions, in these statistics of Curschmann, just given, is much higher than 
is generally noted; 40 per cent, is more nearly correct. As already stated, the 
lower part of the small bowel is the area chiefly affected. 

Next to the changes in the intestine the most noteworthy alterations may be 
said to take place in the lymph nodes of the mesentery, which lie between the intestinal 
lesion and the general system. These tissues go through a similar process of 
hyperemia, swelling, and endothelial proliferation, which usually falls short of 
extensive necrosis. Small necrotic patches are not infrequent. More rarely 
large foci of softening or even suppuration may occur in these nodes, and as recovery 
takes place small septic areas are gradually walled off by lymph, become encysted, 
or are absorbed. Rupture of enlarged mesenteric nodes has been observed. 

The spleen, in addition to its swelling, which begins early and lasts for the first 
three weeks or more of the illness, is full and tense, and of a darker hue than normal. 
Later, as the attack wanes, it becomes soft and darker in hue. The splenic blood 
sinuses are distended by erythrocytes, the endothelial cells proliferate, and the 
pulp here and there becomes the seat of small areas of coagulation necrosis. The 
splenic lesions may also consist in infarction and rupture, but the latter accident 
is very rare. 

Until a few years ago the presence of the typhoid bacillus in the blood was un- 
known, but we now know that this organism is present in this part of the body 
with great constancy, probably invariably during an attack of typhoid fever. It 



TYPHOID FEVER 25 

is usually present as early as the fifth day and persists until the close of the third 
week, or even longer than this. Rosenberger collected 535 cases of typhoid fever 
in which the blood was examined for the bacillus. It was found in 80 per cent, 
of these cases. In a still more recent study Coleman and Buxton obtained the 
following results: 

Second Week. Of 484 examinations made in the second week of the disease, 
353 (73 per cent.) were positive. 

Third Week. Of 268 examinations made in the third week of the disease, 178 
(60 per cent.) were positive. 

Fourth Week. Of 103 examinations made in the fourth week of the disease, 39 
(38 per cent.) were positive. 

After the Fourth Week. Of 58 examinations made after the fourth week of the 
disease, exclusive of relapses, 15 (26 per cent.) were positive. The examination 
of the blood has therefore become of great importance in the early diagnosis of 
the disease. (See Diagnosis.) The bacillus probably gains access to the blood 
through the mesenteric lymph nodes, and the destruction of myriads of the bacilli 
by the blood thereby sets free their endotoxin, which produces the symptoms and 
many of the lesions of the malady. 

The liver is usually somewhat swollen, but the changes in its appearance are 
not peculiar to this disease. The hepatic cells manifest more or less cloudy swelling, 
and the areas of coagulation necrosis containing endothelial cells are present. The 
cells lining the bile-ducts may be swollen, granular, and, in some cases, undergo 
a process of desquamation. Abscess of the liver may develop or gallstones may 
by their presence aid in the production of a cholecystitis, but more commonly 
typhoid fever probably induces the formation of gallstones. (See Complications.) 

The heart muscle nearly always suffers from typhoid infection in direct proportion 
to the severity of the toxemia present. The myocardium is granular and may 
suffer from fatty or hyaline changes. Very rarely the endocardium becomes 
affected and the specific bacillus has been obtained from vegetations on the valves. 

The kidneys show no typical changes. They usually show cloudy swelling, 
and even an acute nephritis may be present. Sometimes as the result of a terminal 
infection multiple abscesses may form in the kidneys and a croupous exudate in 
the pelvis of these organs may develop. 

Reference is made elsewhere to the lesions of the respiratory tract which may 
complicate the course of the malady, such as laryngeal perichondritis, ulcerative 
laryngitis, hypostatic congestion, pneumonia in both its forms, pulmonary infarc- 
tion, simple pleurisy, and empyema. (See Complications.) 

An endarteritis (which may be a thrombo-endarteritis) has been shown to occur 
in a small percentage of cases, and it is reasonable to assume that the thrombotic 
processes occasionally observed in the veins depend upon a similar involvement 
of the lining membrane of these vessels. 

Longcope has shown that the lesions in the bone-marrow closely resemble the 
changes in the lymphoid tissues of the mesentery and of the bowel. There are 
present many lymphoid cells, large phagocytes, and foci of necrosis. 

A very important factor to be recalled in the study of the pathology of typhoid 
fever is the presence of additional infecting microorganisms which aid the Bacillus 
typhosus in producing severe lesions and often are equally responsible for a fatal 
termination. This view is, however, based on postmortem findings, and is not 
supported by the results of antemortem examinations of the blood, for of 150 
cases of typhoid fever in which the blood was examined during life Cole found but 
one in which mixed infection was present; the case was one of staphylococcemia, 
with multiple boils, and terminated in death. 

Incubation. — The period of incubation of the infection by typhoid fever is generally 
stated to be from one to three weeks. That the period of incubation may be much 



26 



DISEASES DUE TO A SPECIFIC INFECTION 



shorter than this would seem to be proved by the case reported by Duflocq and 
Voisin of a girl nineteen years of age who deliberately swallowed a virulent culture 
of the typhoid bacillus with the intention of committing suicide. She began to 
feel ill on the third day, had fever on the fourth day, rose spots on the fifth day, and 
the Widal reaction appeared on the sixth day. 

Symptoms. — Typhoid fever usually begins with a sense of wretchedness and 
general illness, no particular symptom being especially well marked, unless it be 
more or less severe frontal headache and aching in the back and limbs. The facial 
expression very early in typhoid fever usually becomes listless and later stupid 
and heavy, and the patient is often a little deaf because his mental state is benumbed 
rather than because there is any actual trouble with the auditory apparatus. Not 
infrequently there may be a considerable amount of cough without expectoration, 
and there may be exaggeration of the sounds of bronchial breathing on auscultation. 

The tongue is somewhat coated, and very early its edges become clean and red, 
while the central coating remains. This appearance of the tongue is very character- 
istic, even in mild cases. 

Headache, thirst, and sleeplessness are usually prominent symptoms during 
the first week. A mild fever develops simultaneously and nose-bleed may occur 
repeatedly. Usually the liver and spleen become swollen toward the end of the 
first week, and the belly becomes somewhat tumid and tender. 

The characteristic enlargement of the spleen in enteric fever may be undemon- 
strable because of the distention of the stomach and intestine with gas; but while 
the presence of an enlarged spleen is of some importance in reaching a diagnosis 
of typhoid fever, inability to discover any increase in its size does not negative 
the diagnosis of typhoid fever in any degree. 

An undue amount of gurgling can be felt and heard in the right iliac fossa. 

Constipation is usual in the first week, but diarrhea may be marked, and, if loose, 
the stools may be brownish, but later resemble okra-soup or pea-soup. 

Fig. 8 





M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


c 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


105° 

104° 

IT 
X 

if 103° 

ui 

DC 

5 102° 

IX. 
Ill 

a. 

5 

£ 101° 
100° 
99° 




















































































































































































































































































































































































1 




















































































A 




















































































/' 








































































A 




A 








/ 




















1 
















































A 




A 




l\ 








/ 


1 


A 








A 








/ 
















































A 




/\ 




\ 








/ 


\ 


\ 








/ 




1 




/ 
















































/ 






i 


' \ 




A 






\ 


' I 




l\ 




/\ 




A 




/ 


, 














































/ 


L 




L / 






A 


, 




I 


i 




n 


l 


' 




\ 




/ 


\ 










































A 




/ 


\ 




\/ 






/ 


\ / 




V 




I 




i / 






/ 




/ 


\ 










































A 






V 




V 




, 


' 


\/ 








\ 




\ 






' 




/ 


| 


A 








1 
































V 


| 




Y 








\l 




Y 








\i 




Y 








\ 




\ 


/ 




k 




/ 
































\ 


J 












\J 












w 












\ 




\ 


/ ! 




P 




/ 




. 








, 




















' 


\ 












V 












v 








\ 




\ 




V 


' i 


/ 




/ 




A 








h 






















V 
































\ 




\ 




V 






/ , 


/ 




A 




!\ 




\ 
















A 


, 




































V 




V 










/ 


/ 




/\ 




/ 




\ 
















/ 


, / 




































1 


















/ 




/ 




n 


/ 
















/ 


,/ 




















































\ 










/ \ 


/ 
















/ 


v 






























































I 






/ 


































































\ 








1 










/ 








l\ 


i 
























































\j 




li 




, / 










/ 








\ 


\ 
























































y 




/ 




/ 




, 






/ 








' 


\ 




























































U 




/ 




















\\ 




























































I 




V 




v 




1 












V 




































































r 












J 












































































/ 








/ 












































































u 






,A 


/ 












































































f 






/ 


\ 
















































































i 




V 
















































































/ 




















































































/ 




















































































£ 




































































































































































































































































































































































































































DAY OF 
DISEASE 


1 


2 


3 


4 


5 


6 


7 


8 


9 


10 


li 


12 


13 


14 


15 


16 


17 


1& 


19 


20 


21 


PULSE 


90 TO 120-DICROTIO 


M. 


/ *^- 


\. 



























Course of typhoid fever. (Modified from Musser.) 



The temperature in typhoid fever during the first week rises step by step. Each 
morning it is higher than on the previous morning, and each evening higher than 
on the night before, although the morning temperature is often lower than that 
of the preceding evening. (See Fig. 8.) Usually by the end of this week it reaches 



TYPHOID FEVER 



27 



in the morning 102° or 103°, and at night 103° to 104°, and remains at this level 
until the fourteenth or twenty-first day. 

The pulse is more rapid than normal, ranging from 90 to 100 beats per minute, 
and it is usually soft and compressible; the pulse of debility, not of vigor. Often 
the pulse is a little dicrotic. As the disease progresses the pulse rate usually 
increases to about 110, but the pulse force distinctly diminishes. 

At about the seventh to the ninth day a very important diagnostic sign first 
makes its appearance, namely, the so-called rose spots, which usually develop on 
the skin of the abdomen and chest, sometimes on the back, and more rarely on 
the limbs. These spots are small, faint macules, usually scanty in number, which 
lose their color momentarily when pressed upon or when the skin on which they 
exist is stretched between the finger and thumb of the physician. As a rule these 
spots are isolated, but very rarely they may be so profuse as to produce the appear- 
ance of an ordinary rash. 

Fig. 9 



o 

105 



104 

o 

103 

Q* 

X 

v3 102 

UJ 

en 

r> 

H o 

< 101 

UJ 

a 

UJ 


















I 


































S 

a. 


S 
< 


0. 


S 
< 


s 
a 


5 
< 


s 

a. 


< 


s 

O- 


s 
< 

CO 


s 

Q. 


5 
< 


a. 

CO 


2 
< 


5 


s 
< 


2 

Q. 




5 S 

< a 


s 
< 

CO 


CL 


S. 
< 


5 
Q. 


< 


s 
a 


5 

< 


























































































































































































; 




















































-L 




















































3 




















































): 
















































J 




















































\ 




T| 




















































J 1 




















































I 1 


r 
























I\ 


















1 








M 


j 
























/\ 


















K 








| 


i 
























/ 


\ 
























J 


1 
























' 


\ 
























; 


1 






























Jt 




1 


















1 1 


















\ 








\ 




A 




1 








\ 










1 1 


















\ 


y 






\ 




/ 








1 I 










1 




















\ 


1 




\ 












I 










I 




















\ 


/ 




1 










I ' 












1 


















— 


* 


\ 






- 


U 




- 




-] 














( 


















v 














































| j 


















































1/ 


















1 






















H 100 



99 

o 

98 












y 


















f 
































V 


































































i\r 






































1 


II 1 


















































i 
























































; 














































































































j 


































y 


















.7 




















































I 






























I 






















.1 




















































f 




















































_t 






































































































a 


















































! 






| 








DAY OF 
DISEASE 


3 


CM 


CO 


-■* 


iO 


o 


i- 


00 


Cl 


O I -1 




CO 


** 
iN 


PULSE 


M 


f4 


M 


f4> 


f4 


f4 


$4 


f4 


^¥^ 


4f4 


94 


% 


■M- 


RESP. 


f4 


94 


f4 




S4 


M 


54 


f4 


f4f 


4f4 


*>*% 

/i? 


f4 


H 


DATE 


CO 


<M 


co 


■*& 


w 


K3 


i- 


CO 


C5 


O T-l 


<5i 


co 


■># 



Jan. Feb. 



Part of a chart showing the period of steep curves from the fourteenth to the twentieth day 

of an attack of typhoid fever. 

The tongue becomes dry and it may be fissured, the mental stupor increases, 
diarrhea is also active, and the moderate tympanites of the earlier days becomes 
more marked. If the patient has received little care, or if the case is essentially 
severe, his condition is manifestly one of profound toxemia, and by the end of the 
second week he is evidently at the very acme of his infection. Death not infre- 
quently takes place during this period as a result of profound toxemia, hemorrhage, 
perforation, or pulmonary complications. 

Because of the toxemia delirium may be marked, and it is usually of the low 
muttering type, the patient seems to be in a semi-stupor, the teeth are covered 
with sordes, and the tongue is foul and dry. 

These symptoms gradually carry the patient into his third week, with increasing 
diarrhea, greater tympanites, deeper stupor, and more manifest signs of profound 



28 DISEASES DUE TO A SPECIFIC INFECTION 

toxemia, with muscular tremors or true subsultus tendinum. Emaciation by this 
time is marked and the skin dry and harsh. The heart is feeble, its sounds distant 
and muffled, and myocardial degeneration is manifestly advanced. To the possi- 
bility of the appearance of the fatal complications named in the succeeding pages 
as appearing at the end of the second week are added at this time still greater 
danger of pulmonary hypostatic congestion and pneumonia. The patient may 
be so profoundly poisoned by the toxic products of the disease that he seems almost 
moribund. 

If the pathological process is not so severe that recovery is impossible, the first 
sign of the ending of the malady may develop at any time between the fourteenth 
and twenty-eighth day, according to the severity of the disease. This consists in a 
slight modification of the temperature range and the development of a low morning 
temperature with a well-maintained high evening temperature, so that the daily 
range may amount to from 2° to 3°. This is called the "period of steep curves" 
and the appearance of these steep curves at this time in the course of the disease 
is usually a promise of approaching convalescence. An equally good description 
of this period is that of Murchison, who called it the "stage of changing fortunes," 
or that of Wunderlich, who described it as the "period of ambiguity." 

The last stage of the acute febrile period having been reached, the temperature 
falls to normal during the next few days by lysis, and then may be subnormal 
until convalescence is well established, the patient being wasted and feeble, but 
usually ravenously hungry. 

Atypical Fokms. — While the train of symptoms just described may be con- 
sidered typical of an attack of typhoid fever occurring under conditions favorable 
for its full development, it is often so modified by various causes that a large pro- 
portion of cases do not present many of the most prominent and diagnostic symp- 
toms, but, in their place, manifestations so at variance with those of ordinary 
cases as to greatly perplex the physician. Thus, very marked variations in onset 
may occur and completely mislead the medical attendant if he be not on his guard. 
In some cases instead of manifesting itself gradually the disease has a sudden onset 
with a sharp chill followed, it may be, by a profuse sweat and a continued fever. 
This variation is perhaps most apt to occur in children. Headache may be so 
severe in the beginning as to rouse the suspicion of meningeal inflammation, and 
active delirium may be an early symptom, being severe enough to be maniacal 
in type. In other instances a pneumonia is the earliest sign of the malady, while 
in still others a severe choleraic diarrhea may begin the illness. It is also important 
to recall the fact that well-developed signs of appendicitis may appear, due to 
the swelling of the lymphoid tissues of the intestine and appendix by reason of the 
infection. This has frequently resulted in enthusiastic surgeons removing the 
appendix only to find it slightly diseased as part of the general lymphatic change, 
the speedy appearance of the rose rash and persistent temperature soon showing 
the true character of the case. Rarely a severe attack of vomiting begins the 
illness, and still more rarely acute renal disease, nephro-typhoid, or the fievre typhdide 
a forme renale of the French observers, develops. 

Although diarrhea was correctly considered at one time to be one of the most 
constant symptoms of enteric fever, it is now absent in more than half the cases 
during the whole course of the disease, and splenic enlargement in many instances 
is too slight to be discovered, so that it is to be borne in mind that while these two 
symptoms possess a positive diagnostic value when present, their absence in no 
way contradicts the diagnosis of typhoid fever. 

In other instances the course of the fever greatly varies from that just described. 
It may rise very abruptly, and it may end equally suddenly, the lysis being com- 
pleted in twenty hours. Sometimes the morning temperature is the higher of the 
two, although this is rare. The regular course of the temperature may also be 



TYPHOID FEVER 



29 



greatly altered by intercurrent chills. (See Chills.) Very rarely, strange as it 
may seem, no febrile movement is present at any time in the course of the malady. 

The most important variations from 
what may be called the normal course 
of the temperature in the second and 
third week of this disease are those pro- 
duced by free hemorrhage from an in- 
testinal ulcer and by perforation of the 
bowel. A sudden fall of several degrees 
should always arouse suspicion of one 
of these accidents, for the drop in the 
fever may be noted before any of the 
other signs of hemorrhage or perforation 
manifest themselves. 

Marked rises and falls of temperature 
are also often seen in patients who are 
markedly anemic as the result of hemor- 
rhage. Abortion also causes a marked 
fall of the fever. 

The course of the temperature may 
resemble that of remittent malarial 
fever, and it has frequently misled phy- 
sicians into the belief that malarial in- 
fection and not typhoid infection was 
present. (See Chills.) Infectious com- 
plications of the disease, such as otitis 
media, phlebitis, furunculosis, menin- 
gitis, and erysipelas, may also cause 
sudden variations in temperature. And 
in cases which have been gravely ill it 
not rarely happens that fever continues 
after the typhoid infection has run its 
course because of post-typhoidal septi- 
cemia — that is, a multiple infection due 
to the presence of pyogenic organisms, 
which have found a favorable field for 
growth in a patient whose vitality has 
been impaired by the specific fever. 

As the stage of convalescence ap- 
proaches, or when it is reached, a sharp 
return of active febrile movement may 
come on for a day or two, the temper- 
ature being as high or higher than ever 
before. It then returns to its ordinary 
level. This is called a recrudescence, 
and possesses no grave significance. It 
often follows mental excitement and 
the taking of improper or too much 
food. When this rise of temperature 
perists, it usually is indicative of some 

complicating malady, or of a relapse called an "intercurrent relapse" if it takes 
place during the continuance of the primary febrile period. (See Fig. 10.) After 
the fever has disappeared there may be a prolonged continuance of a slight 
evening rise of temperature as the result of nervous irritability and anemia, or it 




3TV0S XI3HN3yHVd 



30 DISEASES DUE TO A SPECIFIC INFECTION 

depends upon the abuse of strychnine, with the mistaken idea that it is a valuable 
heart tonic at this time. In other cases a subnormal temperature for the entire 
twenty-four hours may persist for days. This is of no importance save that it 
indicates that the patient is feeble and needs good feeding and fresh air. The 
other variations met with depend upon the age of the patient. Old persons often 
have an irregular febrile movement, and children may have marked rises and 
falls of temperature which do not necessarily indicate any complications. 

Persistence of distinct febrile movement after the fourth week in any case of 
typhoid fever in which a relapse has not occurred nearly always means a complicat- 
ing or secondary infection. The number of cases of rapid tuberculosis called 
typhoid fever, until the persistent loss of flesh and fever forces the correct diagnosis 
upon the physician, is by no means small. The possibility of ulcerative endocar- 
ditis, cholecystitis with ulceration, with or without impacted gallstones, and septic 
infection due to suppuration as causes of fever are to be borne in mind and their 
presence carefully looked for. (See Complications.) 

That a patient with this disease may suffer not only from the infection due to 
the bacilli of Eberth, but from multiple infections by other organisms which aid 
in decreasing his vital resistance should be borne in mind. 

Closely associated with the study of the temperature is that of chills. They 
may usher in an acute complicating inflammatory process, or be entirely without 
such significance. Somtimes they occur in cases which suffer from constipation, 
apparently as a result of the absorption of fecal poisons. (See Fig. 11.) In other 
cases they are due to a true coincident malarial infection, but it is a noteworthy 
fact that during the course of typhoid fever, even if the patient is also suffering 
from malarial infection, the latter usually remains in abeyance until the former 
has about run its course. It is better for the physician to regard such chills as 
being an indication of some acute complication than to consider them as malarial, 
unless he can prove the existence of the last possibility by finding malarial organisms 
in the blood. 

The skin is sometimes covered by a fugacious scarlatiniform rash in the early 
stages. In certain cases it desquamates in large flakes or in fine, branny scales, 
the latter appearing oftenest in those who have been actively bathed and rubbed. 

Very commonly if sweating takes place, sudamina, or tiny sweat-drops retained 
beneath the superficial epiderm, are found on the abdomen, chest, or limbs. Herpes 
about the mouth is very rare in typhoid fever, but it does occur, notwithstanding 
the denial of this fact by some observers. 

Under the name of tache blenatre, or peliomata, faint blue or steel-gray spots 
of fairly good size, are sometimes met with. They are not due to the disease, but 
are found only in those who are infested with lice. The so-called tache cerebrale 
is not characteristic of this disease, but is sometimes seen during its course, and 
consists in a red line with white borders produced by drawing the finger-nail over 
the skin. It is probably due to palsy of the cutaneous vessels. 

Of the deeper lesions of the skin, we meet with bed-sores, which rarely occur in 
cases seen from the first and which receive proper care. They appear usually 
over the sacrum. Cases of superficial gangrene of the skin have been reported by 
Stahl and the author. Erysipelas occurs, usually of the face, by reason of infection 
through fissures in the buccal or nasal mucous membrane. Sometimes erysipelas 
migrans develops. In very malignant cases petechia may be present. 

Patients suffering from typhoid fever rarely suffer from other eruptive diseases, 
but instances of scarlet fever, chickenpox, and measles occurring as complications 
are on record. In women in particular the hair often falls out freely during or 
after an attack. Boils are by no means rare lesions, and even carbuncles may 
develop as a result of multiple infection. 

The blood in typhoid fever suffers from an increasing degree of anemia in respect 



TYPHOID FEVER 



31 



to the number of the red cells and of their richness in hemoglobin. Indeed, the 
color-index is more markedly lowered than the corpuscular count. When an 
inadequate supply of liquids has been allowed the resulting concentration of the 
blood may produce an apparent corpuscular richness not actually present. 






•K'T 6 
















































































/ 


1 












R6 


OS 


-K-Y9 












































































,; 


/ 
















S6 


8T 


•K'T g 












































































< 
















n 


06 


RT 


•KIT J! 














































































< 














96 


RT 


•m-a 6 






























































































TOT 


OS 


•km 9 




























































































0TT 


OS 


Tl g 






























































































T6 


RT 


•"ST 




























































































ROT 


SS 


•rc-v e 






























































































06 


OS 


I'JO 




























































































001 


OS 


•K-T £ 




























































































?.?■ 


001 


OS 


•KKgl 
















































































\ 












00T 


SS 


•ri6 
















































































s 


\ 












SIT 


RS 


•KM 9 


















































































i 


s. 








on 


T-S 


•re -a g 






















































































^ 


» 






on 


T-S 


'"SI 


















































































< 










ROT 


RS 


•k-t 6 






























































































SO 


T-S 


•WT0 




























































































SOT 


T-S 


•K'r }: 




























































































zz 


06 


T-S 


■KKSl 




























































































9TT 


T-S 


•K'J6 






























































































SOT 


OS 


•HM9 




























































































80T 


OS 


■rc-d g 






























































































T-0T 


OS 


•KSl 


















































































1 


• 








9TT 


SS 


•M'T R 




















































































^N 










SOT 


OS 


TK'Y p 






















































































> 






ROT 


SS 


■JTV g 




























































































\z 


8TT 


T-S 


•NKSl 




























































































00T 


T-S 


■TCM 6 






























































































m 


8f 


■B'J 9 






























n 


m 


) 


8 


F 


V 




















































00T 


99 


•It'I 


































































































•re 'a g 










































q 




u 








































ROT 


T-S 




[i 


j- 




Ul 






■Hgl 




























































































80T 


n 


•k"t <i 




























































































0TT 


n 


•WY9 






























































































9TT 


zz 


■K-Vg 




























































































9TT 


9S 


■h re z\ 




























































































oz 


STT 


SS 


•m-a r 




























































































0ST 


T-S 


•km 9 






























































































9TT 


RS 


•re m g 




























































































STT 


sc 


•rc;u 




























































































8ST 


T-S 


•K-T 6 


























































































OCT 


T-S 


TY m 














































i 


IT 


[C 


J 


0} 


n 


?• 


































OCT 


TS 


•re'T cj 
































i 


I! 


[C 


i 


u 


Ul 


H 


[ 


















































TTTg 




























































































6T 


9£T 


T-S 


■NK^X 




























































































9ST 


So 


re a fi 






























































































0ST 


sc 


•K'a 1 




























































































9ST 


0G 


OVO 






























































































9ST 


0C 


05"0 




























































































OPT 


9C 


•re-a 9 




































II" 


13 


"JA 
















































T-CT 


SC 


•re - a g 






















11 


" 





a 


in 
l 


JT 


a 1 




IT 




















































F. 

106° 
105° 
104° 
103° 
102° 
101° 
100° 
. 99° 
98° 

97° 
Day of Dis. 

Pulse 
Resp. 



03 

-5 



o3 



73 



T3 

S3 
o3 



cjO 



-^ 03 

S3 "S 
O O 

T3 >i 

03 pD 

§^ 

r-=i 03 

03 X3 

> G 

03 03 

-° M 
03 03 

=1 > 



!> 
03 

'o 



a 
o 



u 

03 
O 



The bacteriolytic power of the blood in severe cases is probably always dimin- 
ished. The leukocytes are slightly decreased in number, the large mononuclear 
and transitional cells are relatively increased, and, according to Thayer, the poly- 
morphonuclear cells are decreased. Cabot asserts that a leukocytosis, non-inflam- 
matory in origin, sometimes occurs. 



32 DISEASES DUE TO A SPECIFIC INFECTION 

Complications and Sequelae. 1 — Circulatory Complications. — The heart, as 
already stated, is weakened, and if severely affected may develop embryocardia 
or fetal heart-sounds. There are few, if any, diseases which do not have special 
predilection for the heart muscle or its valves, which so greatly interfere with this 
organ as does typhoid fever. A pulse rate above 125 is ominous, and one of 130 
or 140 dangerous. The danger is usually in direct proportion to the feebleness 
of the first sound of the heart. When the cardiac sounds are those of the foetus 
in utero (embryocardia), the prognosis is grave. A very rapid pulse and irritable 
cardiac action are sometimes seen in cases in which strychnine has been used to 
excess with the idea that it is a stimulant. A soft systolic murmur is occasionally 
audible, which may be hemic in origin or due to relative insufficiency of the mitral 
valves. Rarely it may be due to endocarditis or pericarditis, but pericarditis is a 
very rare complication of typhoid fever. Gaudy and Gourand state that pericar- 
ditis arising during the course of typhoid fever occurs in two forms, namely, the 
fibrinous, which is characterized by an abundant pseudomembranous exudation 
with only slight serous effusion, and the fibrinopurulent form, in which a consider- 
able effusion may occur. Pericarditis may exist alone or may occur in connection 
with endocarditis, myocarditis, pleuritis, or pulmonary complications. As a rule, 
it develops very slowly and may remain latent, so that only most careful auscultation 
over the precordial region will reveal the presence of friction fremitus, and later 
careful percussion may be required to distinguish an effusion. The pathogenesis 
of this complication is obscure. The purulent form when it occurs may be due 
to secondary infection, although the fibrinous variety is probably due to a direct 
infection with the Eberth bacillus. Typhoid fever complicated by purulent 
pericarditis is always fatal, but the existence of the serofibrinous pericarditis 
influences prognosis slightly if at all, unless the effusion be profuse. 

Sudden cardiac failure may occur as the result of myocarditis, or of embolism 
or thrombosis of the coronary arteries, from heart-clot, thrombosis of the cava? and 
pulmonary veins or from pericarditis with effusion. Sometimes the cardiac failure 
is gradual when due to these causes. 

So far as the bloodvessels are concerned the most common lesion is phlebitis, 
which usually affects the veins of the left leg, especially the femoral vein. The 
frequency of involvement of the veins in the left leg depends upon the pressure 
exercised by the right common iliac artery upon the left common iliac vein, which 
tends to obstruct the flow of blood. Sometimes the tendency to the formation 
of a thrombus is greatly increased by a local infection of the endothelial lining of 
the vessel, and it is not uncommon for a severe chill or chills to mark the onset of 
the lesion. Wright and Knapp have recently shown that the tendency to the 
formation of a thrombus in typhoid fever is augmented by the increase of calcium 
in the blood. When milk is the exclusive diet the rise in the proportion of calcium 
oxide supplied to the body is very noteworthy. They also recommend that for 
the prevention of this state the physician add 20 to 40 grains of citrate of soda 
to each pint of milk taken by the patient in order to decalcify it. 

Thromboses of extraordinary size and number may form and extend from the 
femoral vein to the vena cava. When venous plugging seriously interferes with 
the circulation, the gangrene which results is usually moist, but in the vast majority 
of cases of phlebitis of the leg partial recovery takes place, although varicosity 
of the veins of the limb may persist after convalescence is completed. The rarity 
of plugging of the veins of the upper extremity is remarkable. 

Arterial thrombosis is much more rare than is venous thrombosis. This complica- 
tion usually develops after the second week of the fever, and is manifested by pain 
and tenderness along the course of the vessel affected. Usually the leg is the 

1 See Medical Complications and Sequelae of Typhoid Fever, by the author and Beardsley, 2d ed., 
Lea & Fcbigcr. 



TYPHOID FEVER 33 

limb involved. After a temporary increase in the force of pulsation in the affected 
vessel the pulse becomes small and may be lost. The part becomes cold and 
discolored, and finally gangrene ensues. In other cases, in which the vessel which 
is involved is small, recovery takes place by the establishment of a collateral circula- 
tion. Even in the mild cases the patient suffers afterward from fatigue in the 
affected limb on exertion, and intermittent claudication may develop. The con- 
dition is due to an arteritis. 

Thayer has published statistics which seem to indicate that typhoid fever is 
prone to produce early senile changes in the bloodvessels in after years. 

Complications in the Alimentary Canal. — The complications in the upper 
digestive tract are pharyngitis, which is rarely severe enough to cause much dis- 
comfort, and esophagitis, which is still more rare, although several observers have 
recorded ulceration of the esophagus. Inflammation of the parotid gland is a rare 
complication of typhoid fever, and usually occurs about the third week in cases 
of severe infection. This inflammatory state may be due to infection of the gland 
from the mouth by ordinary pus organisms, or more rarely be due to the specific 
bacillus. Rarely parotitis occurs in the first week. In the only case the author 
has seen in which this complication developed at this time there was no pain. or. 
redness, and the swelling disappeared in about ten days. It was also bilateral. 
In advanced typhoid fever it is usually bilateral; is often followed by ugly sloughing, 
and is a very dangerous complication. 

The stomach in typhoid fever is rarely much affected. Digestion in this viscus is, 
as a rule, feeble because in all fevers there is a lack of gastric secretion, and this is 
particularly true of typhoid fever. Vomiting may come on usually as a result 
of indiscretions in food and medicine. Sometimes, however, late in the disease a 
persistent, pernicious vomiting develops which only ends with exhaustion and 
death. A few cases of gastric ulcer occurring in typhoid fever are recorded. 

When there are more than three or four stools a day diarrhea is to be considered 
excessive. When a far greater number occur, it is usually the result of improper 
feeding. The stools are thin and resemble pea-soup save that they are apt to be a 
little more yellow. They are alkaline in reaction, offensive, and may contain 
particles of undigested food, as curds of milk, and also small shreds of lymphoid 
tissue from the sloughs of the bowel. The specific bacillus usually is not to be 
found in the stools until about the seventh or tenth day. The significance of 
active diarrhea as to the gravity of the case has been much discussed, some believing 
that it is a sign of a severe infection. The real significance is not of severity of 
infection, but of severity of intestinal involvement, catarrhal or ulcerative, although 
in some cases even the latter state does not provoke active diarrhea. General 
diffuse pain in the bowels is often present early in the disease, but is apt to disappear 
later. 

Hemorrhage from the bowel in typhoid fever is one of the inevitable complications 
in a certain percentage of cases, and usually takes place after the second week 
of the disease. Very rarely slight loss of blood may occur in the first week. Proper 
treatment of the patient all through his attack may diminish toxemia and prevent 
a fatal terminal infection, but no form of treatment so far devised has materially 
diminished the frequency of hemorrhage or the mortality from this cause, although 
the frequency of the occurrence and mortal effects vary greatly in different epi- 
demics. The general average of its occurrence may be placed at 5 per cent. In 
52,196 cases of typhoid fever collected from several series of cases reported by 
French and German physicians, and from the official reports of hospitals in the 
United States and Canada, England and Ireland, Germany, Austria, South Africa, 
and Australia, hemorrhage is stated to have occurred in 2725 cases, which gives a 
percentage of 5.22. The mortality in persons suffering from it is about 35 to 50 
per cent., although in 271 cases of intestinal hemorrhage complicating typhoid 
3 



34 DISEASES DUE TO A SPECIFIC INFECTION 

fever, collected from the official reports of hospitals in the United States, Canada, 
England, and Germany, 71 case,s proved fatal, which gives a percentage of 26.2. 
Hemorrhages usually arise from ulcers in the small intestine and are very rare 
in children. The symptoms consist of sudden fall in the temperature and it may 
be in the pulse rate, but this primary decrease is usually followed by a more rapid 
pulse than existed before the accident occurred. A diagnosis of hemorrhage is 
to be reached not only by the observance of the symptoms just described, but in 
addition by the presence of blood in the stools and by examining the blood to 
discover a paucity of hemoglobin. The gravity of a hemorrhage depends upon 
the relation of the quantity of blood lost to the vitality of the patient and the 
frequency with which the bleeding occurs. Thus a fairly profuse hemorrhage 
in a strong patient may be followed by no severe symptoms, whereas repeated 
small hemorrhages may greatly exhaust the most lusty individual. When the 
patient is at the end of a long and severe attack of the fever, even a comparatively 
small hemorrhage may be fatal. The existence of small losses of blood not sufficient 
in size to be manifest to the eye when the stools are examined, may be discovered 
by the tests for occult blood. 

Perforation of the bowel, the most serious of all the complications of this disease 
that is commonly met with, has no relation to the severity of the general symptoms, 
for it occurs as often in mild as in severe cases. Indeed, in nearly 50 per cent, 
of recorded cases this accident occurred in mild cases. The statistics of Brown 
indicate that 25,000 deaths occur annually in the United States from this complica- 
tion of typhoid fever. It takes place far more commonly in men than in women, 
71 per cent, against 29 per cent, and in the majority of cases the lesion is in the 
ileum. When perforation occurs the symptoms may^be ushered in by agonizing 
pain, which may be severe enough to rouse the patient from a considerable degree 
of stupor. If the patient is not too apathetic the pain is often described as being 
in the lower zone of the belly near the median line, and most commonly slightly 
to the right. The belly-wall is sensitive to palpation, speedily becomes tense 
and all the symptoms of a general diffuse peritonitis may quickly ensue. The pain 
may, however, be very slight and pass away or become modified, as the peritoneal 
condition resulting from the escape of fecal matter into its cavity becomes more 
and more septic. The pulse becomes rapid and running, and collapse may speedily 
assert itself. When this occurs, death speedily comes on, the patient dying in a few 
hours, or, again, he may rally and survive for several days. Early death is, however, 
the more common result. Thus in the collection of 34 cases made by Fitz, of Boston, 
37.3 per cent, died on the first day, 29.5 per cent, on the second, and 83.4 per cent, 
in the first week. During the second week 9 died, in the third week 4 died, and 2 
other cases lived thirty and thirty-eight days, respectively. If collapse does 
not ensue, the rally of the system results in a rise of the temperature to a point 
higher than before the accident, and this movement is often accompanied by chills 
and rigors. Usually by the second or third day the peritoneal symptoms become 
more and more marked, the condition of the patient more and more asthenic and 
depressed, and death results by the fourth day from a general peritonitis with 
toxemia from the absorption of toxic materials. In other cases the onset of the 
perforation is insidious; the belly before the perforation may have been moderately 
tympanitic, but now becomes intensely hard and rigid; the pain, which in some cases 
is so severe, does not develop, but the great fall in fever followed by a rise, and 
this again by rigors, it may be, give evidence of the grave accident which has 
occurred. The pulse becomes increasingly rapid and running, and the respiration 
more and more costal and less and less diaphragmatic, until the patient sinks out 
of life, without much, if any, suffering, in generally the same manner as one sees 
death come to a case of diffuse septic peritonitis due to a pyosalpinx or to septic 
appendicitis. In such cases the perforation is usually very small, and is so sur- 



TYPHOID FEVER 35 

rounded by adhesions that the escape of the intestinal contents is very gradual 
and insidious, infecting the peritoneum without the escaping fluid being copious 
enough at any one time to produce great pain or reaction. 

In this connection it is important to note that a sudden fall in temperature is 
not a symptom necessary to the diagnosis of intestinal perforation. On the con- 
trary, there are many cases on record in which a rise of temperature has followed 
this accident. 

The diagnosis of perforation is to be reached by the following signs in addition 
to those just given: The hand of the physician, when lightly placed upon the 
abdominal wall, not only develops the fact that it is hypersensitive, but that its 
muscles are unduly tense. If the perforation has occurred, the abdomen, here- 
tofore rather swollen and tumid, may be slightly scaphoid. There is usually a 
sharp increase in pulse rate. Percussion may indicate the presence of gas in the 
peritoneal cavity, and the liver may be pushed away from the abdominal wall in 
such a manner that the ordinary area of liver dulness is largely decreased. Percus- 
sion of the right hypochondrium is, therefore, an essential procedure in the physical 
diagnosis of these cases. A fallacy underlying this test is the possibility of a 
portion of the colon, when greatly distended with gas, slipping up between the 
liver and the belly wall, and thus giving resonance; but this is a rare occur- 
rence. 

In some cases, however, as intimated, the symptoms are so insidious that the 
absence of this sign does not negative the diagnosis of perforation. Indeed a 
positive diagnosis may not be possible, and cases are sometimes met with in which 
the perforation has not been suspected, and is found only at the autopsy. Other 
cases have been operated upon for perforation and no opening found. 

The diagnosis of peritonitis due to perforation is aided, but not confirmed, if 
an examination of the blood reveals a leukocytosis of polymorphonuclear cells, 
but the absence of leucocytes does not negative perforation. 

There are several conditions causing pain which must be carefully excluded 
before the physician can arrive at the diagnosis of perforation, even if the symptoms 
and signs just described are present. These are diaphragmatic pleurisy, pneumonia 
of the bases, appendicitis, iliac thrombosis, and intestinal obstruction. Further 
than this, peritonitis may develop from extension of the inflammatory process 
in the bowel or by reason of the migration of microorganisms through those parts 
of the bowel wall which have been impaired by the ulcerative process. In such 
cases the pain, swelling, and diaphragmatic paralysis may all be present without 
being due to perforation, and so closely may the symptoms of perforation be aped 
that operation has been performed, with the discovery that no perforation had 
occurred; thus in a case under the care of Herringham, nothing was found at the 
section and the patient recovered. Perforation may also be simulated by suppura- 
tion and rupture of a swollen mesenteric gland. Other causes of peritonitis are 
necrosis of the mesenteric glands, infarction of the spleen, or the development of 
abscess in an ovary or Fallopian tube. Very rarely peritonitis arises from cholecys- 
titis or cholangitis, with or without gallstones. Liebermeister has recorded two 
cases in which rupture of the gallbladder with escape of gallstones into the abdom- 
inal cavity took place. An ulcer in the appendix may perforate or an intercurrent 
appendicitis may complicate the case. 

The percentage of frequency of occurrence of perforations is generally stated to 
be about 2.2, but in 30,966 cases of typhoid fever collected by me from several 
series of cases reported by French and German physicians, and from the official 
reports of hospitals in the United States and Canada, England and Ireland, Ger- 
many, Austria, South Africa, and Australia, perforation is stated to have occurred 
in 1144 cases, which gives a percentage of 3.69. The percentage of its mortality, 
when surgical interference is not resorted to at the most favorable time, is 90 to 



36 DISEASES DUE TO A SPECIFIC INFECTION 

95 per cent., and with operative interference it may be as high as 81 per cent. (See 
Treatment.) 

Perforation is very much more frequently seen in men than in women. Fitz 
in 444 cases found 71 per cent, in men and 29 per cent, in women. In 21 cases of 
perforation in Basle, 15 were men and 6 were women; and Griesinger in 14 cases 
had 10 men and 4 women. Murchison also found in 24 cases 16 men and 8 women, 
although the general mortality of the disease among women was slightly higher 
than among men. So, too, Bristowe, of London, met with this accident in men 
in 11 of 15 cases, and, again, Nacke collected 106 perforation cases, of which 72 
were in men and 34 were in women. 

Perforation is responsible for a large proportion of the deaths which occur from 
typhoid fever. Out of 1721 cases which came to autopsy the percentage of deaths 
due to perforation was 11.3, according to Murchison. According to Holscher, it 
was found in 2000 Munich cases 114 times (5.7 per cent.), and in 20 out of 80 of 
his cases which ended in death. In 4680 cases tabulated by different writers, 
Fitz found the proportion to be 6.58 per cent., which agrees with Holscher's 
statistics. Hoffman found that out of 250 deaths in typhoid fever 20 were due to 
perforation. 

Perforation occurs in the ileum in at least two-thirds of all the cases of this acci- 
dent and in the colon or appendix in about 4 per cent. It takes place most com- 
monly in the third and fourth weeks of the malady, but is by no means rare in the 
second week. It occurs most commonly in patients between twenty and thirty 
years of age. Elsberg has reported a case of a child of three and a half years who 
suffered from this accident, but whose life was saved by abdominal section. 

The relation of typhoid fever to appendicitis is one of great interest. It has 
been thought by some that appendicitis arising in typhoid fever was a mere coin- 
cidence; by others, that its origin depended upon a general infectious process; 
and, again, by others, that it was due to the direct infection of the appendix with 
the bacillus of Eberth. Probably all these views hold true in individual cases. 
The richness of the appendix in lymphoid tissue, and the fact that typhoid fever 
is particularly prone to attack such tissues, renders this organ peculiarly susceptible 
on theoretical grounds. That this view is correct is proved by the research of 
Hopfenhausen, who collected the appendices obtained from 30 cases of typhoid 
fever and studied them under Stilling in the University of Lausanne. She concludes 
that moderate changes in the appendix may be found in nearly all cases of this 
disease, that it is most marked in the earlier stages of the malady, and consists 
chiefly in cellular infiltration, specific lesions being rare and not sufficient to produce 
the more severe forms of appendicular disease. 

True appendicitis complicating typhoid fever, in the sense of inflammation of 
the appendix severe enough to produce abscess, is undoubtedly a very rare affection. 
Hopfenhausen has collected statistics of 743 cases of appendicitis, of which 5 per 
cent, were due to typhoid fever. This must be a very much larger percentage 
than usually exists. 

It is a noteworthy fact that appendicular symptoms are not infrequent in early 
typhoid fever, and often disappear under rest in bed, and with the full development 
of the infection. Rarely the inflammation goes on to the formation of an appendicu- 
lar abscess or perforation. The swelling of the lymph node in the meso-appendix 
and the presence of ulcers in the cecum explain why it is that pain in the appendicu- 
lar area is by.no means rare. (See Plate I.) Sudden pain in the lower zone of 
the abdomen may be indicative, not of appendicitis, but of the presence of an iliac 
thrombosis. 

Tympanites in typhoid fever is always present to some degree at some stage of 
the disease. When very marked, it is an evil symptom because it indicates active 
fermentation in the bowel, and the presence of intestinal atony, and because the 



PLATE I 




Showing Typhoid Ulcers in Small Bowel and near the 
Appendix. ( Kast and Rumpler. ) 



TYPHOID FEVER 37 

gas presses on the abdominal thoracic viscera and disturbs their functions. By 
distending the intestine it may also predispose the patient to a hemorrhage or 
perforation by the strain on a severely ulcerated Peyer's patch. 

Hepatic Complications.— The liver and gallbladder rarely show signs of active 
infection during the early part of an attack of typhoid fever. Jaundice is one of 
the rarest complications of this disease. Aside from some swelling and tenderness 
in the hepatic region, no symptoms in the hypochondrium are usually observable. 
It is, however, important to note that secondary involvement of the gallbladder 
as a sequel of this malady is by no means rare, a true cholecystitis developing in a 
goodly proportion of cases as a result of infection of this viscus by the bacillus of 
Eberth. This cholecystitis may be severe enough to result in empyema of the gall- 
bladder and perforation of its walls, with symptoms resembling intestinal perforation. 
A still more interesting fact is that such a cholecystitis due to this organism may 
develop many years after the attack of typhoid fever, and again the clumping of 
these organisms in the gallbladder may give rise to the formation of gallstones. 

Louis, in his work on typhoid fever, published in 1836, states that changes in 
the bile and gallbladder occur more frequently in typhoid fever than in other 
acute diseases, and cites 3 fatal cases in which cholecystitis, unrecognized during 
life, was found at autopsy. Grisolle and Andral mention similar cases. In 3 
instances French found the gallbladder of persons who had died of typhoid fever 
filled with turbid albuminous fluid, and Rokitansky speaks of having found "fibrin- 
ous exudations" in the gallbladder of several patients who died from the disease. 
Murchison refers to the cholangitis and cholecystitis which may accompany typhoid 
fever, and reports a case of rupture of the gallbladder, followed by general peritoni- 
tis. In 1876 Hagenmiiller reported 18 cases of cholecystitis complicating typhoid 
fever. He concluded that it was a more frequent complication than had generally 
been supposed. Holscher, in the 2000 Munich autopsies, found empyema of the 
gallbladder 5 times. 

In 1889 Bernheim suggested that typhoid bacilli might give rise to gallstones 
by producing alteration or stagnation of the bile. In 1893 Defourt reported 19 
cases of cholelithiasis, in which the first attack of biliary colic occurred at varying 
periods after typhoid fever. Osier has reported a case of hepatic colic occurring 
for the first time in the fifth week of typhoid fever. At operation nothing could 
be found to account for perforation of the gallbladder, but nine months later a 
gallstone was discharged. 

Fournier found bacteria in 38 out of 100 gallstones which he removed at autopsies. 
The colon bacilli predominated, while the typhoid bacilli were found to be second 
in frequency. Milian, Chantemesse, and Horton Smith report similar experi- 
ences. 

Chiari found typhoid bacilli present in the gallbladder in 19 out of 22 cases, 
and obtained pure cultures from 15. In 9 out of 10 cases at St. Bartholomew's 
Hospital, London, Bacilli typhosi were found. Cushing mentions 5 cases of 
cholecystitis complicating typhoid fever, in which pure cultures of colon bacilli 
were obtained from the pus. Marsden reports a case in which cultures resembling 
Bacillus typhosus were obtained. Van Dungern obtained pure cultures of typhoid 
bacilli from pus surrounding the gallbladder fourteen years and a half after an 
attack of typhoid fever. Pure cultures have often been obtained from six to 
eight months after the attack (Chantemesse, Dupre). This is a fruitful source of 
infection. 

Mason thinks that the bacilli gain entrance through the biliary ducts. Council- 
man believes that they are carried through the blood, and that areas of necrosis 
in the liver afford them portals of entrance. Hagenmiiller, Mayo Robson, and 
Mark Richardson believe that biliary complications, especially cholecystitis, are 
due to ascending infection of the ducts. Marsden is of the opinion that the most 



38 DISEASES DUE TO A SPECIFIC INFECTION 

important passage of bacilli into the gallbladder is through the blood, the liver, 
and the biliary ducts. He is undoubtedly correct. 

Typhoid cholecystitis during the course of the fever is frequently latent. In 
more than one-half the recorded cases, either on account of latency of symptoms 
or typhoidal stupor, nothing unusual was observed during life. 

The two most constant symptoms are pain and swelling, the former being paroxys- 
mal and most marked in the region of the gall-bladder and under the scapula. 
Maurice Richardson says that it may be in the epigastrium or over McBurney's 
point. According to Mayo Robson, if a line be drawn from the umbilicus to the 
ninth rib on the right side, there is almost always tenderness at the beginning of 
the second third of this line. Jaundice is rarely met with, but there may be repeated 
chills and sweats. 

Genito-urinary Complications. — Albuminuria in typhoid fever is quite a 
constant condition, occurring as frequently as in 70 per cent, of all cases, and being 
most marked in the second week. Usually its presence is not associated with 
that of tube-casts unless the patient is already a sufferer from nephritis prior to 
the attack. When casts are present, the albumin is usually present in large amount. 
Albuminuria without casts is not a serious complication. Probably true nephritis 
is present in almost 20 per cent, of the cases, but this is usually not productive of 
renal symptoms. An antecedent nephritis may take on renewed activity and a 
true hemorrhagic nephritis may occur, usually in severe cases only. The urine 
is apt to be scanty and of high specific gravity unless the physician insists upon 
the patient drinking freely of water. 

Pyuria in slight degree is common. Blumer says it occurs in 17 per cent., but 
it is a noteworthy fact that pyelitis due to typhoid fever is almost unknown. While 
this is true, it is also of interest to note that enormous numbers of the bacillus 
of Eberth are to be found in the urine after the second week of the disease, and 
often far into convalescence. Petruschky has estimated that 1 c.c. may contain 
170,000,000 bacilli. A profuse polyuria is often present when the stage of con- 
valescence is entered upon. 

Orchitis and epididymitis rarely occur as a result of a direct infection with the 
specific bacillus. They differ from the changes due to gonorrhea in that they are 
less painful and more rapid in their course to suppuration or recovery. They are 
usually unilateral and the testicle is first affected. Typhoidal cystitis due to the 
presence of the bacillus of Eberth rarely occurs. 

Respiratory Complications. — The respiratory disorders met with in connection 
with the course of typhoid fever, aside from the bronchitis already mentioned, 
are quite numerous. In the later stages of the disease we may meet with severe 
laryngeal ulceration, which in turn may be complicated by perichondritis or edema 
of the glottis. Hoffman found 28 cases of ulcer of the larynx in 250 autopsies in 
this disease, and Griesinger in 26 per cent, of those dying of the malady, so that it 
is by no means rare. Keen collected 146 cases of severe laryngeal disease due to 
this cause, and found that necrosis of the laryngeal cartilages when it occurred was 
a very fatal complication, death occurring in 95 per cent, of the cases. 

Intense hypostatic congestion is one of the most constant pulmonary changes 
seen at autopsy; in some cases the blood may inundate the air vesicles, causing 
solidification. How often this change is agonal cannot be determined with any 
degree of certainty, but as it depends on more or less prolonged maintenance of 
one position aided by an enfeebled circulation the danger can be greatly lessened, 
if not avoided, by frequent changes in posture. 

Pneumonia develops in typhoid fever in three forms and in different stages of 
the disease: (1) As an acute lobar pneumonia ushering in the attack of enteric 
fever, and due to the pneumococcus, or, it is thought by some, to the infection 
of the lung by the bacillus of Eberth, the so-called "pneumotyphoid." True 



TYPHOID FEVER 39 

croupous pneumonia in the later stages is very rare. (2) Bronchopneumonia, 
probably arising from terminal infection or by hypostatic congestion due to the 
profound toxemia and cardiac degeneration and feebleness, is more common. 
(3) Acute tuberculous pneumonia sometimes seizes the typhoid-fever patient 
when he seems about to begin his convalescence. 

It is not to be forgotten that infarction of the lung may occur as the result of 
cardiac or venous emboli. Such an infarction may mislead the physician into a 
diagnosis of lobar or lobular pneumonia by reason of the dulness on percussion, 
the rise of temperature, and blood-tinged sputum. An infarction may, if the 
patient survives, result in pulmonary abscess or gangrene. 

Pleurisy arises very rarely as a primary lesion. It is usually secondary to 
infarction, pneumonia, or gangrene. Cases of empyema due to the specific bacillus 
have, however, been recorded. 

Nervous Complications. — The nervous disturbances vary very greatly. In 
the average case there is in the early part of the onset no mental change save that 
of unfitness for mental occupation, with dreamful sleep which is apt to be restless. 
Later the patient continually dozes off, yet awakens easily, and for a moment 
may be a little confused between the mental impressions left on his brain by the 
dream and the conditions he finds about him on returning to consciousness. Still 
later, if the infection is severe, he becomes more apathetic when awake, less easily 
aroused when asleep, and often delirious in his sleep, his dreams being evidently 
vivid, so that he keeps muttering the conversation he thinks he is actually having, 
or calls out loudly, as his dream seems to lead him to a point where an imperative 
call or sudden action is needed. Sometimes the delusions in the delirium amount 
to imperative conceptions, and the patient believes that he is away from home 
and must return there at once, or that he is being restrained by force, or, again, 
that some member of his family is in distress and needs his aid or is calling for 
him. Often this form of mental disturbance is painful to witness, difficult to 
overcome, and harassing to the patient. In these cases the hands may be moved 
continually in active motions, as if to illustrate the ideas of the patient. Such 
cases are apt to be grave if for no other reason than that they exhaust themselves 
if relief is not given. The more encouraging type of delirium is of the quiet, mutter- 
ing form, as if the patient was gently "speaking in his sleep" as in health, and this 
may be taken as the natural form of delirium in the disease. Later the stupid 
condition becomes more and more marked in some cases, and absolute mental 
stillness is reached, in which only rough shaking or loud calling will arouse the 
patient. In severe cases with marked toxemia we find at times a state of mental 
confusion, staring eyes, and semi-stupor, with persistent muttering — the so-called 
coma vigil. 

During convalescence mental aberration, depending usually upon exhaustion, 
may develop. The prognosis in such cases is usually good. 

Rarely in the course of typhoid fever symptoms of irritation or inflammation 
of the meninges of the brain develop, and it is important to remember that these 
symptoms may arise from several causes. The most common of these is congestion 
and engorgement of the meningeal vessels without any true inflammatory process; 
the next most common form is that due to the extension of an infection from abscess 
in the middle ear; the third form is that in which there is infection with the strepto- 
coccus or pneumococcus, and very rarely the meningitis is due to the bacillus of 
Eberth. Cole has recorded three instances in which the typhoid bacillus was 
obtained from the cerebrospinal fluid by lumbar puncture in typhoid fever. In 
one the meningitis was serous, in another purulent; the character of the other is 
not stated. The frequency of this complication in the different periods of the 
disease when due to true typhoid infection of the meninges is in direct ratio to the 
length of the malady, namely, in the third or fourth week. In the great majority 



40 DISEASES DUE TO A SPECIFIC INFECTION 

of instances in which the complication has appeared the patient was under thirty 
years, and usually between twenty and thirty years. That is the period in which 
typhoid fever is most commonly seen. 

In every case of true typhoid meningitis, so far recorded, death has occurred, 
but this is a statement which does not possess as great prognostic value as would 
appear at first glance, since an absolute diagnosis of true typhoid meningitis can- 
not be made during life, for the positive test is the bacteriological examination of 
the skull contents. Nevertheless, the presence of marked meningeal symptoms 
is of the gravest import in all cases. 

Sometimes, because of degenerative changes in the vessels, a hemorrhagic effusion 
into the meninges of the brain takes place, but this does not commonly produce 
marked symptoms unless it is profuse. 

Convulsions, generalized or localized, with coma and delirium may arise from 
thrombosis of the cerebral sinuses or of the cerebral arteries, but they are very 
rare from any cause. Murchison met with them in only 6 cases out of 2960. If 
due to the lesions named, they indicate a fatal termination in the near future. 
In Osier's case death followed convulsions, produced by thrombosis of the branches 
of the left middle cerebral artery, in twelve hours. If they occur in neurotic 
children or females, the outlook is not so gloomy, as they probably do not depend 
upon an actual lesion in the brain. 

Sometimes acute otitis media produces violent headache and finally symptoms 
of meningitis, but its presence is often unrecognized as a cause until a discharge 
takes place from the ear. 

Neuritis, generalized or localized, is met with occasionally in the later stages, 
producing wrist-drop or toe-drop, and sometimes causing severe pain. When 
there is a multiple neuritis the symptoms may closely resemble locomotor ataxia 
or anterior poliomyelitis. Sometimes the skin of the toes or of the whole foot 
becomes exquisitely sensitive. 

When hemiplegia occurs, which is quite rare, it results from cerebral embolism 
or thrombosis or very rarely from actual hemorrhage. 

Complications in the Bones, Joints, and Muscles. — Secondary disease 
of the bones, consisting of post-typhoidal osteomyelitis due to the specific bacillus 
or to infection by associated microorganisms, may occur. The tibia and the ribs 
are the bones most commonly involved, and the changes are subacute or chronic 
rather than acute. So, too, arthritis may be due to pyogenic microorganisms or 
to the Eberth bacillus, and is usually of a subacute or chronic type. Spontaneous 
dislocation of the hip may occur in very rare instances. 

Many years ago V. P. Gibney, of New York, described, under the name of 
typhoid spine, a condition in which there develops, often some days after the patient 
is up and about, and often only after some very slight jar or trauma, great tenderness 
of the spine, with pain in the back, and in the legs when they are moved. It has 
been held that this condition is not dependent upon a spondylitis, neuritis, or 
Pott's disease, and is probably a neurosis closely allied to the neuroses seen in 
cases of severe trauma, but in most cases it is probably spondylitis. In most cases 
it is probably due to periostitis. Fraenkel has recently shown that in fatal cases 
of typhoid fever the bacillus may be obtained from the cancellous tissue of the 
bodies of the vertebrae and some of these cases of so-called typhoid spine may be 
instances of osteomyelitis involving these structures. 

Sometimes in the stage of convalescence a curious state is developed in which 
the muscles of the lower extremities become painful, somewhat brawny, and even 
slight redness may appear in the skin covering them. Usually this is unilateral, 
but it may be bilateral. Most commonly it affects the calf of the leg, and pain is 
developed on pressure or on movement, acute or passive. This is due to a myositis. 
It should not be confused with phlegmasia dolens due to thrombosis. 



TYPHOID FEVER 41 

Typhoid Fever Complicating Pregnancy. — In a very large number of cases 
of typhoid fever complicating pregnancy, abortion or premature labor comes on. 
Corbin collected 364 cases of typhoid fever occurring in pregnant women, and 
Fellner, of Vienna, has added 7 others to this number, making a total of 371 cases. 
Of these 371 cases 228, or 61 per cent., ended in premature births, and in 202 cases 
pregnancy terminated before the sixth month. Most of the full-term children 
were born dead, and those who were born alive were weak and did not long survive. 
The mortality in the mother under these circumstances is about 16 per cent. 

Diagnosis. — The diagnosis of typhoid fever is to be based on the characteristic 
ascent of the temperature, the general malaise of the patient, the peculiarly coated 
tongue with red edges, the tumid belly, and the development of the rash about the 
seventh to the ninth day. If to these symptoms are added an enlargement of the 
spleen and liver, the diagnosis becomes still more certain, and is confirmed if the 
laboratory tests mentioned on the following pages are positive. The laboratory 
aids to diagnosis are the Widal or agglutination test; the isolation of the bacillus 
from the blood, from the stools, from the urine, and from the rose spots, and the 
diazo-reaction. The objection to these tests is the difficulty as to technique for the 
general practitioner, and, more important still, the fact that some of them are 
obtainable in many instances so late in the course of the disease as only to confirm 
the clinical diagnosis already made. (See page 43.) 

Typhoid fever must be separated from a number of maladies which closely 
resemble it. Pure typhoid infection may result in the production of a fever which 
closely follows the remittent or intermittent malarial types, and which is often asso- 
ciated with so much gastric disturbance and vomiting and so lacking in the more 
prominent typhoid symptoms usually seen that the picture of remittent malarial 
fever is clear, while the true picture of typhoid fever is clouded. Again, there can 
be no doubt that cases of true malarial infection occur in which the symptoms so 
closely resemble those of typhoid fever that a purely clinical diagnosis is almost 
impossible if an epidemic of typhoid fever is in full swing at the time. Finally, 
there can also be no doubt that it is possible for the patient to have a double infection 
with the bacillus of Eberth and the Plasmodium of Laveran, in which case, however, 
the malarial manifestations are usually dwarfed by the typhoid poison, and are 
marked only at the onset of the enteric fever and at its termination. To this mixed 
infection the term typhomalarial fever may be correctly applied to indicate not a 
separate disease, but a double infection. Etymologically, this term might also 
be used to define a condition of malarial fever in which, because of profound debility, 
the patient was in a typhoid state — that is, in a condition of which typhoid fever 
is a type. Practically, however, it should be discarded or limited in its use to 
the double infection just described. 

How far constant fever occurring day after day and associated with manifestations 
of general loss of strength and debility can be relied upon in the diagnosis of typhoid 
fever is hard to determine. Certain it is that if a physician makes a diagnosis of 
enteric fever upon these symptoms alone, without bearing in mind the fact that 
similar conditions are equally well developed under other forms of infection, he 
will find himself in error in not a few instances. Chief among these conditions 
may be mentioned tuberculosis of the lungs or peritoneum, that form of influenza 
in which the chief symptoms are abdominal, cases of ulcerative endocarditis, 
septicemia, and pyemia, and those of cholecystitis with ulceration, as from impacted 
gallstones. It must not be forgotten, too, that syphilitic fever may in very suscept- 
ible persons resemble typhoid infection. The febrile movement, rose rash (if it 
be scanty), malaise, and signs of general infection in this disease may readily mislead 
the physician. Again, in the more advanced, or tertiary, stages of syphilis a 
prolonged low, septic fever may be present. Any case of so-called typhoid fever 
which lasts more than four weeks without the attack being prolonged by a relapse 



42 



DISEASES DUE TO A SPECIFIC INFECTION 



is almost certainly suffering from another disease, often tuberculosis. It is not to 
be forgotten that trichiniasis may resemble typhoid fever, for in it we have fever, 
pains in the limbs and back, headache, stupor, and nausea, with pain in the belly 
and diarrhea. The differentiation of typhoid from other fevers is aided by a study 
of the following table : 



Typhoid Fever. 

Onset gradual. 

Face dull and apathetic. 

Delirium a late symptom. 

Coma a late symptom. 

Eruption very late. 

Eruption chiefly on trunk, well defined, and 

appears in several crops of small rose-red 

spots. 
Leukocytes decreased. 
Widal test positive. 
Bacilli of Eberth in blood. 

Typhoid Fever. 

Rash appears in crops. 
Profuse sweats rare. 
Temperature curves regular. 
Pulse rarely over 100. 
Bacillus of Eberth in blood. 
Widal test positive. 
No eye changes. 
Respirations slightly increased. 
Cyanosis rare. 



Typhus Fever. 

Onset abrupt. 

Face livid, anxious, swollen, conjunctiva red- 
dened. Pupils contracted. 

Delirium an early symptom. 

Coma an early symptom. 

Eruption early. 

Eruption over trunk and limbs and ill- 
defined. Does not appear in crops, and is 
dusky red or petechial in character. 

Leukocytes increased. 

Widal test negative. 

Bacilli absent. 

Acute Miliary Tuberculosis. 

Rash, if present, not in crops. 
Profuse sweats constant. 
Temperature curves irregular. 
Pulse usually rapid. 
Absent from blood. 
Negative. 

Choroidal tubercles. 
Greatly increased. 
Cyanosis common. 



Typhoid Fever of the Cerebral Type. 

Regular temperature. 
No marked blood change. 
Herpes very rare. 
Rose rash on trunk chiefly. 
Cerebrospinal fluid negative, 

Typhoid Fever. 

Onset gradual. 
Fever gradually rises. 
Chills rare in onset. 
Unaffected by quinine. 
Heavy facial expression. 

Herpes rare. 

Early delirium rare. 

Anaemia moderate. 

Moderate reduction in leukocytes. 

Rose rash. 

Bacilli in blood. 

Typhoid Fever. 

Onset gradual. 
Enlarged spleen. 
Rose rash. 
Prostration gradual. 
Lasts several weeks. 

Typhoid Fever. 

Onset gradual. 

Nervous symptoms moderate. 

No leukocytosis. 

Widal test positive. 

Bacilli in blood. 

Lasts weeks. 

Disease of youth. 



Cerebral Meningitis. 

Irregular temperature. . 

Increase in polynuclear white cells. 

Very common. 

Petechia? over whole surface. 

Positive for the specific bacillus. 

Estivo-autumnal Fever. 

Onset acute. 
Fever rises irregularly. 
Severe chills common. 
Improved by quinine. 

Anxious facies with slightly icteroid conjunc- 
tiva. 
Herpes common. 
Early delirium common. 
Anaemia marked. 
Great reduction in leukocytes. 
No rash. 
Plasmodium in blood. 

Influenza. 

Onset sudden. 

No enlargement of spleen. 

No rash. 

Prostration rapid. 

Lasts a few days. 

Typhoid Pneumonia. 

Onset more rapid. 
Nervous symptoms severe. 
Some leukocytosis. 
Widal test negative. 
None in blood. 
Lasts a shorter time. 
Disease of old age. 



TYPHOID FEVER 



43 



Typhoid Fever. 

No cardiac murmurs. 
Regular temperature. 
Sweats rare. 
No leukocytosis. 
No cardiac dyspncena. 
No petechias. 
No infarctions. 
No leukocytosis. 
Widal test positive. 
No retinal emboli. 
No chills. 
Bacilli in blood. 

Typhoid Fever. 

Rose rash. 
Face not swollen. 
Muscles normal. 
Eosinophiles decreased. 
A common disease. 



Ulcerative Endocarditis. 

Cardiac murmurs. 

Irregular septic temperature. 

Sweats common. 

Marked leukocytosis. 

Cardiac dyspnoea. 

Petechias. 

Infarctions. 

Leukocytosis. 

Negative. 

Retinal emboli. 

Repeated chills. 

No bacilli in blood. 

Trichiniasis. 

No rash. 
Face swollen. 
Myositis. 

Eosinophiles numerous. 
A rare disease. 



For the diagnosis of paratyphoid fever from typhoid fever, see the article on 
that disease. 

Tests. — The so-called Widal test depends upon the fact that if a small amount 
of blood, or blood-serum, or even the breast milk or tears from a patient having, 
or recently having had, typhoid fever, are brought in proper dilutions in contact 
with living typhoid bacilli, these organisms soon cease to move, that is, lose their 
motility, and gradually come together in clumps, or, in other words, agglutinate. 

The typhoid bacilli to be employed in the test are not such as have been recently 
isolated from a case of typhoid fever, but those which have been modified by 
repeated transplantation on artificial media. These bacilli are kept in sealed 
tubes of nutrient agar-agar in an ice-chest; from such a stock culture inoculations 
are made, and when the test is to be used are placed in broth-bouillon, incubated 
for twenty-four hours at a temperature of 37° C, and then employed for the test. 
It is essential that it be proved beforehand that this culture is composed of organisms 
reacting to known typhoid serum and not to healthy serum. From this test 
culture a proper dilution is made by adding the bacilli to blood diluted with normal 
salt solution. A hanging drop is now placed under the microscope and examined 
with a magnifying power of about 800 diameters. The bacilli should appear as 
actively motile organisms which do not clump. 

The finger-tip or lobe of the ear is pricked, and by means of the "white pipette" 
of a blood-cell counting apparatus the blood is drawn up to the mark 0.5. Then 
the pipette is dipped in distilled water and the water is drawn up till the figure 11 
is reached. This gives us a dilution of 1 : 20. One drop of the mixture of bacilli in 
salt solution and one drop of the diluted blood are then placed on a cover-glass, 
which is inverted over a hollow slide and the drop examined. A positive reaction 
consists in an absolute immobilization of all the bacilli and of a clumping of a 
majority of them. This reaction should occur in five minutes if the dilution of 
blood has been 1 : 20, and in thirty minutes if it has been 1 : 40, and in two hours if 
the dilution has been 1 : 60. A rapid clumping with a weak dilution is to be regarded 
as a very positive test. On the other hand, it is to be remembered that a dilution 
of blood in the porportion of 1 :10 may give a reaction even if normal blood is used. 
An exact estimate of the strength of the solution and of the time of reaction is 
therefore of importance. 

This test is an exceedingly accurate one, if properly employed. The chief 
difficulty about it is that the reaction is often absent until the seventh or even 
the twelfth day of the disease. Out of over 8000 cases reported by a number of 
observers, the test was positive in 94 per cent. A negative result is unimportant if 



44 



DISEASES DUE TO A SPECIFIC INFECTION 



it is obtained prior to the third week. But cases have been recorded in which bacilli 
were isolated from the blood during life and at autopsy the lesions were those 
of typhoid fever, yet at no time during the course of the disease did the blood 
yield the agglutinative reaction. Repeated tests should also be made before it is 
decided that the blood does not give the reaction. When dried blood is used 



Fig. 12 




Agglutometer for the agglutination test for typhoid and paratyphoid fever. 



its volume as near as may be should be restored by the addition of distilled water, 
and from this the proper dilution is to be prepared and the resulting dilution used 
as already indicated. The fallacies of this test lie in the possibility that the patient 
may have had typhoid fever at some previous time and so give the reaction, and 
in mistaking irregular and delayed clumping as true agglutination or as a partial 
reaction. The time of appearance of the Widal reaction has distinct prognostic 



TYPHOID FEVER 45 

as well as diagnostic value. When it occurs in high dilution and early, that is in 
the first week of the illness, the course is usually mild, and when it occurs as late as 
the fourteenth or sixteenth day the illness is usually a severe one and lasts longer. 

This test has now been brought within the reach of everyone by the use of an 
agglutometer which has been placed on the market by a well-known house. (See 
Fig. 12.) 

This apparatus is designed to obviate the use of the microscope and the fresh 
live culture of typhoid bacilli necessary in the Widal test when made in the old 
way. Laboratory experiments have shown it equal in delicacy to the former 
method. The limits of the reaction are more distinct than in the old process. 

One bottle of a sterile permanent suspension of typhoid bacilli is furnished, 
together with four test-tubes, one lancet and tube for collecting blood, one vial for 
diluting the serum, one small pipette for distributing the diluted serum, and one 
large pipette with two graduations (each corresponding to ten drops of the size 
delivered by the small pipette) for filling the tubes with suspension. The three 
tubes labelled 50, 100, and 200, are to be used for the test; the fourth is a control 
tube to which no serum should be added. 

Let blood flow into the blood-tube until the bottom is covered with a layer 
one-eighth to one-fourth inch thick. The blood will flow much more rapidly if 
the lobe of the ear is squeezed imtermittently between the thumb and index finger. 

Cork the tube and replace in an upright position. 

In a short time (an hour) the serum will have separated, or may be readily 
made to do so by carefully loosening the edges of the clot with the lancet. 

After the serum has separated, insert the pipette into the blood-tube, the point 
resting in the lateral depression, and incline both slightly, when the serum will 
readily enter the pipette. 

Add one drop of serum to ten drops of clear water in the diluting tube, and shake 
well. If the diluted serum is cloudy, let it clear by standing a few minutes before 
distributing to the tubes of suspension. 

By means of the large pipette put 20 drops (two graduations) of the suspension 
of typhoid bacilli in each of the four test-tubes. 

Add the serum dilution to the typhoid suspension by means of the small pipette, 
in the following amounts : four drops added to the tube marked 50 gives a dilution 
of 1:50; two drops added to the tube marked 100 gives a dilution of 1: 100; one 
drop added to the tube marked 200 gives a dilution of 1 : 200. 

No serum should be added to the control tube. 

After adding the serum dilution, cork the tubes and shake well. Put away in a 
warm place. 

Examine the tubes at the end of one and four hours, and again on the following 
day. The rapidity of the reaction depends both upon the agglutinating power 
of the blood-serum and the temperature at which the tubes are kept. The reaction 
may be seen with the greatest distinctness when one stands near the middle of 
the room facing a window. The tubes should be held on a level with the eye and 
inclined slightly away from the observer. 

When the reaction is positive, floccules appear in one or more of the tubes, 
depending upon the agglutinating power of the serum tested. These flakes are 
small at first and disseminated through the fluid. They gradually increase in 
size and settle to the bottom of the tube. 

In a complete reaction the supernatant fluid is perfectly clear. 

In a positive but incomplete reaction, floccules are seen in the still cloudy fluid. 

In a negative reaction the fluid in the tubes remains uniformly clouded, as in 
the control. 

All apparatus and corks should be thoroughly washed before using a second time. 

The diazo-reaction, sometimes called Ehrlich's reaction, depends upon the fact 



46 DISEASES DUE TO A SPECIFIC INFECTION 

that in typhoid fever the urine of the patient contains a chromogen which, when 
treated with diazo-benzine-sulphonic acid and ammonia, produces a distinct 
red hue in the urine, which may be as deep as garnet red. Other diseases give 
this reaction, such as tuberculosis and some cases of pneumonia, but it is of consider- 
able value in determining the presence of typhoid fever if taken in conjunction 
with other signs. It is usually present as early as the sixth day, and lasts until 
about the eighteenth day. The test itself consists in using two solutions. One 
of these consists of a 5 per cent, solution of hydrochloric acid to which has been 
added sulphanilic acid in the proportion of 1 gram for each 100 c.c. The other is 
a 0.5 per cent, solution of sodium nitrate. When the test is to be made the two 
solutions are mixed in the porportion of 40 :1. Equal parts of urine and this mixture 
are then shaken together and rendered alkaline by the addition of ammonium 
hydrate, which is allowed to flow down the side of the tube, forming the layer 
above the mixture just named. At the dividing line between these two fluids 
the reaction appears. If typhoid fever is present a garnet-red hue develops. If 
it is not present, only an orange tint is seen unless one of the other maladies which 
give this test is present. After the test tube containing these liquids has stood 
for some time a green sediment forms, which Ehrlich considers very characteristic 
of a true reaction. 

Another method of reaching a positive diagnosis is the examination of the blood 
itself for the specific bacillus, which, as already stated, is present in this fluid in 
nearly all, if not all, cases of typhoid fever. While it is true that this examination 
is not possible for one who is not trained in its technique from the bacteriological 
stand-point, it is also a fact that this test is not open to the fallacies of the Widal 
test, and that the bacilli are often found as early as the fifth day, whereas the Widal 
test is frequently not positive till the ninth day, or even later. The urine and 
stools may be examined for the specific infecting microorganism, but they are 
rarely discoverable in these discharges early enough to aid the diagnosis. 

The Widal test and the discovery of the bacillus of Eberth in the blood enable 
us to differentiate true typhoid fever from paratyphoid fever. 

Finally, it is to be remembered as a valuable diagnostic fact that the fever of 
the first stages of typhoid fever is more resistant to the cold bath than in any 
other malady, although it yields readily enough later on in the course of the malady 
to this therapeutic measure. 

Prognosis. — The prognosis in typhoid fever depends upon several important 
factors. One of these is the time at which the patient comes under medical care, 
not because active medication is of great advantage, but rather because patients 
that go to bed late in the onset of the disease usually become more seriously ill 
than those who conserve their vital forces by rest from the very beginning of the 
malady. Patients who travel long distances in the early stages of typhoid are 
wont to have severe attacks, and if, after the disease is well developed, travelling 
is resorted to the illness nearly always increases in violence. Another factor is 
the state of the patient at the beginning of the malady, as to his vital resistance 
and general health. Fat persons usually do not bear typhoid fever well. Children 
nearly always recover from typhoid fever in its uncomplicated forms, and aged 
persons, while rarely affected, succumb when attacked in direct proportion to 
their years. (See Fig. 6.) 

A third factor is the degree of toxemia which develops in severe cases, particularly 
if they are not -treated skilfully at first. 

Aside from these general considerations it is impossible to make an accurate 
prognosis as to the severity of the attack or probable recovery of the patient in 
the first week of the disease, because the malady develops slowly and because a 
fatal termination is nearly always due to some intercurrent complication which 
cannot be foreseen. Even when the disease is ushered in with violence of all the 



TYPHOID FEVER 47 

symptoms, particularly an exceedingly high temperature, it often happens that it 
follows a very short and fairly mild course, so that a severe onset indicates a 
speedy recovery in many instances. When, however, complicating conditions 
such as pulmonary, cerebral, or meningeal manifestations develop, the prognosis 
is of course correspondingly grave. 

Recovery in typhoid fever, under the modern and favorable methods of treat- 
ment, takes place in about 93 per cent, of cases in the best types of private practice 
and in hospitals in which the patients are received early and in fairly good condition. 
In private practice among the poor the mortality is much higher. In army practice 
the mortality may vary from 2 or 3 per cent, in time of peace to 50 per cent, in 
time of war, illustrating very well the fact, already stated, that early rest in bed, 
perfect quiet of mind and body, and proper nursing are most favorable in their 
influence, whereas an absence of these aids to recovery is most harmful. Under 
the cold-bath treatment of typhoid fever, when it is instituted early, the mortality 
of about 7 per cent, is largely due to those unavoidable accidents, hemorrhage 
and perforation of the bowel. 

Much depends in all cases upon the severity of the infection. In some widespread 
epidemics the mortality is singularly low even when the care of the patients is 
not very skilful; in others it is correspondingly high. In the United States army 
in the Spanish war it was only 7 per cent., a remarkably low rate for war time; 
whereas in the Boer war the English troops suffered from a death rate of nearly 
21 per cent. 

Sudden death sometimes occurs in typhoid fever without the autopsy revealing 
any adequate cause, the real cause being in all probability an acute cardiac 
dilatation. 

Treatment. — The following is the plan pursued by the author in the treatment 
of this disease. As soon as the patient comes under observation, unless his bowels 
have already been moved by the aid of calomel, he is given 1 to 2 grains of this 
drug in quarter-grain doses every hour. If his bowels are not moved in twelve 
hours, a movement is produced by the aid of a large rectal injection of soap and 
water, and if need be by the ingestion of a Seidlitz powder. Twelve hours later 
he receives 5 to 10 minims of dilute hydrochloric acid with a teaspoonful of essence 
of pepsin; this is repeated regularly every six hours throughout the disease after food. 

Hydrotherapy. — An order is given that if the temperature rises as high as 
102.5° the patient is to be rubbed with tepid, cool, cold, or ice-water, or even with 
a piece of ice, according to the degree with which his temperature resists the bath 
and according to the degree of toxemia present. If toxemia is very great, it is 
often necessary to give a thorough, brief and brisk, rub-off with a small piece of 
ice, not so much to reduce the fever as to cause reaction and arouse the patient's 
vitality. With this application of cold, in different degrees according to the needs 
of the case, there must be employed by another nurse, or by the free hand of the 
nurse who uses the cold, active friction to the skin as the cold comes in contact with 
the integument, because friction increases the heat loss 50 per cent., aids in produc- 
ing those most essential conditions reaction and equalization of the capillary 
circulation, and prevents the patient from being chilled. It is a cardinal rule that 
if the patient has been ill so long that reaction does not occur under the bath, it is 
contraindicated and we must endeavor by gentle measures and the use of tepid 
or even of hot water to redevelop the power of the body to react. In other words, 
that temperature of water should be used which is necessary when combined with 
active friction to reduce the temperature at least 2° in fifteen to twenty minutes, 
provided reaction can be produced. Without reaction we simply increase internal 
congestions by the use of cold water. It is interesting to note that Hirschfeld has 
treated over 1000 cases with tepid immersion baths of 80° to 90° and friction with 
a mortality of only 3.4 per cent. 



48 DISEASES DUE TO A SPECIFIC INFECTION 

Whenever cold is used, an ice-bag or cold cloth should be applied to the head to 
prevent cerebral congestion. 

While the method of bathing just described is that nearly always pursued by 
the writer, it is proper to give definite information concerning the so-called Brand 
method of cold bathing, a plan which was introduced by Brand, of Stettin, many 
years ago, but which has only received its full share of credit during the past thirty- 
five years. This plan consists in immersing the patient, when his temperature 
reaches 102° or 102.5°, in a tub of water the temperature of which is 70°, and keeping 
him there with active friction for fifteen or twenty minutes, until the temperature 
is reduced to 100°. In order to combat chilling and aid the circulation it is custom- 
ary to give the patient one-half to one ounce of whiskey before, during, or after 
the bath. The bath is repeated whenever the temperature rises to 102°. Usually 
it is needed every two or three hours. In order that the patient's strength may 
be conserved he should be lifted into and out of the tub. 

This so-called plunge bath, or Brand bath, is a remedy of the greatest possible 
value, but is not needed in every case as a matter of routine. When used it is 
essential to produce reaction and to use friction, and to apply ice to the head. The 
indications for its use are identical with those just named. It is actually contra-indi- 
cated in the very young and very old, in whom it is often difficult to produce 
reaction, and if the case comes under treatment so late as the beginning of the third 
week, since reaction to cold is usually then lost. The presence of a complicating 
pneumonia also contra-indicates it. Its disadvantages are that the back cannot be 
rubbed, although the muscles in that part of the body contain much heat; this part 
of the skin is most prone to suffer from bed-sores, and the patient must be lifted 
or raise himself out of the tub. The temperature of the plunge bath when its 
use is deemed wise should not be placed at a tepid level and then reduced while 
the patient is in the water, as this does not administer a stimulating and awakening 
shock to the system, but simply chills the patient, thereby doing no good, for the 
object in using water in typhoid fever is to produce reaction, eliminate poisons, 
and reduce temperature, and the means by which this is best accomplished can 
be determined in each case by the physician. 

Personally the writer has never failed to successfully accomplish all these results 
by cold rubbing, with friction, if it is properly given, but many physicians prefer 
to follow the method of Brand as a routine pratice. An enormous array of statistics 
prove its value as a life-saving agent. 1 

When cold is properly used it should, after the first week of the disease, produce 
changes in the temperature, as shown in the following chart (Fig. 13). 

Some form of bath at least once a day is absolutely necessary, even if the tempera- 
ture never exceeds normal, to establish cleanliness and equalize the circulation 
everywhere, and he who treats typhoid fever without resort to efficient hydrother- 
apy, if it can be used, is not doing all for his patient that can be done. 

The use of hydrotherapy greatly lowers the mortality, saving about 10 in every 
100 cases, but it does not diminish the frequency of perforation or hemorrhage, 
and it apparently increases the frequency of relapse. This may be due to the 
fact that more are saved to run the chance of relapse, but also may depend upon 
the fact that mild cases are more prone to relapse than severe ones. Hydrotherapy 
does not shorten the duration of the fever, but it often shortens the length of the 
illness by preventing complications. 

Diet. — The diet consists of milk in the first week and often for most of the 
second week, about a quart to a quart and a half a day being given, so divided 
that the patient gets it every three or four hours. It is followed by the acid and 
pepsin already named, unless the stomach is irritable, when a little lime-water 

1 See article by the author in Therapeutic Gazette for March, 1898. 



TYPHOID FEVER 



49 



may be given as a substitute, or a little Celestins Vichy water may be used. When 
the digestion of milk is difficult it is well to add to it hot water or to dilute it with 
an alkaline or carbonated water. If the taste of the milk is unpleasant to the 
patient, it may be flavored by the addition of vanilla, nutmeg, coffee, tea, or cocoa 
in small amounts. After the first week or ten days the patient is allowed from 
one to two soft-boiled eggs twice a day, so soft that they can better be taken as a 
drink than eaten with a spoon, and flavored with a little salt. Well-boiled rice 
strained through a fine sieve, and even thin cornstarch or barley-gruel, if well 
cooked, may be given several times a day at this time with advantage, particularly 
if at the same time a little taka-diastase is used to aid their digestion. The author 
is firmly convinced that by this means terminal infections and general feebleness 
can be largely avoided and the patient brought to the stage of convalescence ready 
for speedy return to health and with greater vital force. Broths and other liquid 
animal soups are inadvisable, for they are good culture media, and often tend to 
increase tympanites and diarrhea. They are largely used by many physicians, 

Fig. 13 



BOWELS, 
HT1MBER OF 
MOVEMENTS 




CI 




- 










1 


























- 














« - 












- 






r^ 


















r^ 




- 




- 












URINE 
DAILY AM'T 




















n 




























CO 











































-*< 
























105° 

101° 

t- 103° 

■< 

ui 

° 102° 

LU 

m 
gl01° 

CE 

w 

| 100° 

LU 

M 99° 

NORMAL 
98° 






























































































































































































































































































































2 

cJ 




•s 


-i 


a 
2 


2 
< 


•5 

< 


i 

< < 


.' 2* 


2 

<- 


2 

< 


2" 


2 


2 : 


• 2 

- cl- 


5 

clc 
















-: 


E 


2 


~2 


i: 

0,0 






















































l|qT 


OS- 


2 


2 


2 


g 


sssa 


5 c S 


5*1 






S'2^ 
tJ<T 


; 2 


& 


a 


2 

Cl 


2 

CL 


2 

a 


d2. 


= 2 


5- 


2 
<- 


< 


■2 


2 

a. 


-5 


-2 

CL 


2r 

CL 


a 


2-2 




2 


< 


< 


« 


< 


< 


<- 


< 


.- CL4CL CL 


CL S< 


















































































. ^ 
















T-7 


i 


cnin 




^ m 






















■'- 












r?V 


tsr 










S 


-«- 
































! -, 




:, 


CT 


- 








































cn^c 
















































































































































































! 










































































































































































■ 


r 
























































— ■ h — 






















































































































































































































































































1 


























f 




1 
















jJl [ 








"■ — 








































t 




-/ 
























































































































































1 
































































"~ 


--- 


., 














a 





-1- 






|i 




H 




'4 






1 




H V 


J 






















•l^. 


^T 
















11 




G 




1+ 




c 

r 




— 1- 








r-- = 










■ 




'li 


+ — 


f- 




V 




1- 


f 




-H 


- 


H- 


~nh 1 


— H — 






-; 


4 T — 


- — 


V 




-T- 






-p; 


r-4- 












J4 




-H 




-j-*- 




■* 


~t 




! 














| . < 




I 














1 








i 


















f 






1 


l! 
















J 


- 




= 










































































il 














d=jfc 


























































































-2 
o 
























1 








! 












| 








K 










1 ! 












































o 




j 










1/ 














r_7 


-II 




















i 
















































































































1 1 




r= 














— 


* 








--'- 






- 4-f 








T- 








4-- 






- 






r 


|4= 


i= 


- 


f = 
































-O 


















































































































i 


















-i 


















1 






























i- 
i- 


E 


i - 










jj 






















































1 




























* 


rl 




































































f, 




1 




i 


] 




h 


— 




1— 






^ 
























UJ 


























































































































































































', 
































! 




1 














j 










! 






j 




i 




















! 






























(1 








































































































if 












, 


1 
















( 








3 










) 










v 






I 


























































































































































































































































































J 


























- Z, 


if 
































! 
































cn 










in 












^ct 




^ 




- 








u 


















4 




OJ 




SI 




IN 


— 


n - 




- 


— 


)> 








m 








ro 




Z- - 


















































































j 


■ 




i 




















































n 


























































i 




















































z 




























































1 














































































































- 1- 




















































a. 




























































-;— 






















































































































































DAY OF DIS. 


cc, 




-f 














lO 














CO 
















c- 
















vz 


PULSE 


2 3 


glw 


§'3 


s|sts 


g 


■?. 


g 


g 


-* 




?: 


fe 


=,= 


s 


2 


§ 


5 


g 


§ 


a 


§ 


gla 


a ? •£ 


s °2 




5 " 




J 


ai 




r 


^S 


rE 






r'S 


32 


= Q 


o ^ 




- 




S3 
t- 


RESP. 


s r 


3s 


gS 


3§.8'3 


a 


.=, 


s 


s 


S~ 


ss 




^ 




3 


s 


5 


* 


5 


s 


3 




s; 


Ts^S 


SSS 


=?; 


IS 






X 


s 


a 


■P 




5s; 


ss 




2a 


SjtS 


s 


n 


5 5 


3 


DATE 


CO 
CO 




CO 
CO 


1 












CO 














ml 1 












o 

CO 

















Mar. 



Chart showing the falls in temperature and reactions following the use of cold spongings in a case of 
typhoid fever. The dotted lines show the fall. The broken, nearly horizontal line shows the morn- 
ing and evening range unaffected by sponging. Thirty-four baths were given in eight days. 



but never by the writer. When curds appear in the stools, the quantity of milk 
should be diminished or it should be peptonized, or its digestion aided by the use 
of pancreatin given after it is taken. The use of 5 to 10 grains of citrate of soda 
in the milk will also prevent the formation of curds. 

Medicines.— Drugs are not to be given if they can be avoided— that is, they 
are not to be used unless they are certainly needed to combat some definite condition 
which should be alleviated. In the great majority of cases, if not in all, the so-called 
antipyretic drugs are not only useless but harmful, and particularly harmful if 
their use is resorted to simultaneously with bathing. Their only justifiable use 
in a case which can be properly nursed and bathed is for the purpose of relieving 
headache and backache, when they may be given in small doses, such as 2 grains 
of acetanilid three or four times a day. Quinine is of little, if any, value except 
as a tonic in small doses. 

Stimulants are to be used when the pulse is actually weak and the cardiac first 
sound distant or feeble. The best of them is whiskey or brandy, diluted with 
4 



50 DISEASES DUE TO A SPECIFIC INFECTION 

milk or water, and given in doses of half an ounce every three to six hours as needed. 
Many cases do better without any stimulation, whereas others need much larger 
doses of alcohol than those just named. Digitalis is rarely of any service because 
it does not act well in the presence of fever, rarely supports the degenerated muscle 
fibers of the heart, and is apt to disorder the stomach. When the cardiac condition 
is desperate, Hoffmann's anodyne in dram doses every two hours in cool water 
is very valuable. When profound adynamia develops and the patient is critically 
ill, much good may result from the injection hypodermically of 1 grain of camphor 
in 30 drops of sterilized olive oil every eight hours for five or six doses. Another 
method of value when the vascular system is relaxed and the patient adynamic 
is the use of normal salt solution by hypodermoclysis. Strychnine may also be 
used, but it is a mistake to employ it for more than a few doses in the active 
stage of this disease. It is better to keep it in reserve for attacks of sudden 
circulatory failure. 

Antisepsis. — Absolute intestinal antisepsis cannot be produced by any known 
means, although it is possible to modify very materially the growth of micro- 
organisms in the bowel by the use of proper remedies. If the physician takes the 
ground that by the use of these substances he destroys the Bacillus typhosus and 
so benefits the patient, he is largely in error, and his use of them is not rational 
because the bacillus is widely distributed in every part of the body. If, on the 
other hand, these remedies are given to combat intestinal fermentation, as shown 
by foul-smelling stools and tympanites and other evidences of an excessive growth 
of the non-specific bacteria which throng the bowel during the progress of this 
disease, his use of them is rational in that by this means other toxic materials are 
prevented from being generated in excess. Often the Bulgarian lactic acid bacillus 
may be given with advantage in these cases. Another remedy is the sulphocarbo- 
late of zinc in the dose of 2 to 3 grains in pill form three or four times a day. Still 
another drug of far older use is turpentine in emulsion in the dose of 10 to 20 drops 
three or four. times a day. The latter I prefer. In many of these cases also the 
use of a few small doses of calomel or salol is advantageous. 

Antityphoid Vaccine. — The employment of antityphoid vaccine in the treatment 
of a patient suffering from typhoid fever is an entirely different proposition from 
its use to protect an individual by rendering him immune. In the patient who 
is ill the Bacillus typhosus has already more or less overwhelmed the patient, who 
is suffering from having set free in his body the poison of the invaders, for the 
poison of the bacillus of Eberth is endogenous and is not set free until the germ is 
destroyed. Given to a healthy man the vaccine puts him in such a condition that 
he is an unfavorable field for the growth of the infection, but given to one who 
is ill we only add to the number of dead bacilli and the poisons already present. 
It is conceivable that the use of vaccine may rouse dormant protective processes 
to active effort, but it is more conceivable that the dose may be "the last straw 
that breaks the camel's back." The use of antityphoid vaccine after the disease 
is developed has been quite largely resorted to, but the results have not been very 
encouraging, probably for the reasons given, although there are some who advo- 
cate its use. 

Treatment of Special Symptoms.— Constipation is to be relieved, preferably 
by the use of enemata of soap and water, to which may be added in obstinate cases 
a tablespoonful or two of glycerin. Many of these patients have no constipation 
in the sense that the ileum or colon is sluggish; but, on the other hand, the sigmoid 
flexure becomes packed with hardened feces, and mechanical obstruction occurs. 
The use of purgatives by the mouth is therefore useless unless very strong drugs 
are used, which are dangerous. If it is thought that the bowels are really sluggish 
a little cascara sagrada (20 to 30 minims of the non-bitter extract) may be given 
each evening. 



TYPHOID FEVER 51 

Diarrhea, if excessive — that is, more than three or four stools a day — may 
be controlled by 5- to 10-drop doses of aromatic sulphuric acid in simple elixir 
several times a day or by adding to these two ingredients a half-dram of fluid- 
extract of hematoxylon. If much fermentation is present, an intestinal antiseptic 
should be used, such as zinc sulphocarbolate. 

Vomiting is to be primarily prevented by regulating the diet as already referred 
to. If it persists, as little food and drink should be given as possible for a few 
hours to let the stomach rest; and if there be much nervous irritability, 60 grains 
of sodium bromide in a little starch-water should be given by the rectum to quiet 
the vomiting centre. Counterirritation should be applied over the epigastrium 
in the form of a mustard plaster or turpentine stupe. If alcohol is being used as a 
stimulant its use must be stopped, or, if this is impossible, then a very old brandy 
or wine should be substituted for the whiskey and given often in very small 
quantities. 

For tympanites a turpentine stupe is to be placed over the belly, if possible, 
before the gas accumulates in any amount, and if it persists a rectal injection of 
the emulsion of asafetida, with or without a dram or two of turpentine, should 
be given. The efficiency of this injection may be much increased in the way of 
expelling gas, and if marked adynamia is present, by adding half an ounce of Hoff- 
mann's anodyne to the injection. Turpentine in the dose of 10 drops, in emulsion 
or capsule, may also be given by the mouth for this condition. When the gas fails 
to come away, its passage may be aided by the introduction of a long rectal rubber 
tube. 

Hemorrhage from the bowel does not offer very much opportunity for direct 
rational treatment. In the majority of instances the best we can do in the way 
of real benefit to the patient is the maintenance of body heat by the application 
of hot bottles; and if the circulation becomes markedly feeble, the employment of 
normal salt solution by hypodermoclysis, a pint of it being given once, twice, or 
thrice in the succeeding twenty-four hours, according to the needs of the patient. 
Bandages may be applied to the limbs to limit the circulation to the vital parts, 
and the foot of the bed be raised for a similar purpose. The large number of 
remedies which have been suggested for the direct control of the hemorrhage 
indicate how feeble they all are. There is no more reason for supposing that 
astringents given by the mouth can check hemorrhage from an ulcerated vessel 
in the bowel than that they can check a hemorrhage from a branch of the anterior 
tibial artery; and when they are given and hemorrhage ceases, the arrest is due more 
to coincidence than to the effect of any drug. If any remedy of this type is of 
value, it is probably Monsel's salt (ferri subsulphas), which should be given in a hard 
pill or compressed tablet inclosed in a capsule, with the hope that it will escape 
from the stomach into the intestine without being dissolved, and thereby exert 
its styptic influence. Of course, if it is dissolved in the stomach, its chemical 
characteristics are altered. Many physicians apply a small ice-bag over the centre 
of the belly to influence the circulation in the small intestine, with the hope that 
in that way hemorrhage will be controlled. There is no objection to this plan 
of treatment, and the author often resorts to it; but it should be used with caution, 
if the hemorrhage is severe, lest it aid in devitalizing the patient by abstracting 
heat. Simultaneously with the application of the ice-bag to the belly, hot bottles 
should be applied to the other parts of the body, for it is to be remembered that 
the loss of bodily heat is an important factor, not only because the vital processes 
cannot be well performed at a low temperature, but also because the sudden 
reduction of temperature caused by the hemorrhage deprives the heart and other 
organs of the stimulating effect of the fever which has been present for days. An- 
other popular method of treatment is the administration of a pill containing a 
grain of opium and a grain of acetate of lead ; the opium being expected to diminish 



52 DISEASES DUE TO A SPECIFIC INFECTION 

peristalsis and so aid clotting, and the lead to act as a styptic. The opium is 
probably of value, but it is doubtful if the lead ever reaches the bleeding spot 
without becoming altered by the gastric and intestinal juices. When there seems 
to be continued oozing of blood from a large intestinal ulcer without free hemor- 
rhage, the administration of turpentine and the use of horse serum or coagulose is 
to be seriously considered, as there is reason to believe that they control capillary 
hemorrhage. Wright and his co-laborers have shown that the hypodermic use 
of calcium lactate and the internal use of calcium chloride increase the coagulability 
of the blood and these salts may be used. (See Purpura.) After the hemorrhage 
has ceased, particularly as convalescence is begun, small doses of iron should be 
administered to combat the anemia. 

The treatment of perforation of the bowel from a medical point of view consists 
in giving opium to relieve pain, and employing heat and stimulants to combat 
shock. If a skilled abdominal surgeon can be obtained, all such cases should be 
operated upon at once, since the mortality under operation is less than with no 
operation. Statistics seem to show a mortality of about 80 per cent, with operation 
and 95 per cent, without it. My colleague, Dr. Keen, has published 158 cases. 
They gave a recovery percentage of 23.41. I have collected 54 cases which have 
been reported since January 1, 1900, and find that 35 of the number were followed 
by recovery. This gives a recovery percentage of 61.54, which is far too high for 
the general run of cases. Harte and Ashhurst place the recovery after operation 
at 26 per cent. The statistics of Bagley, who extended the collection of cases 
from 1903 to the close of 1909, show that the recoveries after operation in this 
second period were 42 per cent.- Among children the results have been excellent. 
Out of 25 cases collected by Elsberg 16 recovered, a postoperative mortality of 
only 36 per cent. These figures are of value as showing that recovery may take 
place, but they do not give the real percentage of deaths, for most of the cases that 
are operated upon and die are not reported. I have seen 3 of these within a year. 
To be successful the operation ought to be performed at the earliest possible moment 
after perforation, although if the patient when seen is profoundly shocked it may 
be necessary to rally him by stimulation before the operation is commenced or 
even postpone operation until sufficient time has elapsed to allow him to rally. 

Statistics clearly prove that the prospect of recovery from perforation treated 
by operation steadily diminishes with each hour that passes after the accident 
occurs. Cases are on record, however, and I have seen more than one, in which 
perforation took place and recovery occurred without operation. 

Persistent insomnia is rarely a troublesome symptom in typhoid fever. Although 
patients complain of wakefulness at night, careful observation will usually show 
that they get sufficient sleep in twenty-four hours. In some cases, however, 
when they are wakeful, largely because of active delirium, and are rapidly exhausting 
their vital forces by continued nervous activity, life can be saved by the hypodermic 
injection of \ grain of morphine, to which may be added ^to" grain of nitroglycerin 
to prevent secondary nausea and depression. 

The application of an ice-bag to the head throughout the attack will usually 
prevent ordinary delirium from becoming excessive. 

Bed-sores are usually prevented by the friction applied to all portions of the 
skin in the baths which are given every few hours. If they appear over the sacrum, 
the patient should lie as much as possible on his sides, all bony prominences on 
which the patient rests being protected from contact with the bed by circular 
air-cushions. When the skin first reddens the irritation may be allayed by painting 
it with a solution of nitrate of silver, 20 grains to the ounce. If the bed-sore has 
begun to form, a useful dressing consists in equal parts of powdered chloretone and 
boric acid. If the slough becomes large, all that portion which is actually dead 
should be cut away, the part thoroughly sprayed with peroxide of hydrogen, dried 



PARATYPHOID FEVER 53 

by the gentle application of soft lint, and then dressed with the dusting-powder 
just named. 

The treatment of the other complications of typhoid fever will be found under 
the headings of the respective diseases, such as Pneumonia, etc. 

During convalescence the patient should be fed with increasing quantities of 
nutritious, easily digested food, but stimulants if possible should be avoided. If 
the patient is out of bed care should be taken that food is not ingested until after 
he has lain down to rest, in order that he may not be tired and so lack nervous 
energy during the progress of the digestive processes. 

As already pointed out when discussing the prevention of typhoid fever, urotropin 
or uritone should be given in doses of 5 to 10 grains four times a day in water, to 
destroy the bacilli which are usually present in the urine and bile. 

The ordinary diet should not be restored until from ten days to two weeks after 
all fever has ceased. The author has often been impressed with the fact that the 
use of green vegetables, such as lettuce, spinach, asparagus, and similar substances, 
seems to exercise a most valuable influence in convalescence in typhoid fever, 
perhaps because they antagonize scorbutic tendencies. 



PARATYPHOID FEVER. 

Paratyphoid fever is a disease caused by infection with the paratyphoid bacillus, 
and presents a symptom-complex closely resembling or indistinguishable from that 
of typhoid fever. 

Bacteriology. — The paratyphoid bacilli belong to a group of organisms inter- 
mediate between the Bacillus typhosus and Bacillus coli communis. Buxton has 
shown that by appropriate methods organisms occupying this position may be 
divided into several groups; one resembling the colon bacillus, for which he proposes 
to use the name paracolon; another group closely allied to the typhoid bacillus, 
called the paratyphoid, and producing the condition termed paratyhpoid fever. 
The last-named group may by appropriate cultural methods be further divided 
into a species culturally unlike the paracolon type, and a second distinct species 
resembling the paracolon group. 

The differentiation of these typhoid-colon groups and their components is a 
most complex bacteriological problem. It is probable that not a few paratyphoid 
infections are diagnosed typhoid fever. 

Prevention. — The same measures as are given for the prevention of typhoid fever, 
including the use of vaccine, are to be resorted to. (See Typhoid Fever.) 

Pathology. — Differing anatomically from typhoid fever in essential details, 
this disease possesses no characteristic morbid anatomy, resembling in this respect 
the other forms of septicemia. The most constant change is splenic enlargement, 
which is present in all of the cases coming to autopsy. Saltykow has collected 
22 cases of which 14 showed implications of the lymphoid tissue, ulceration being 
present in 9. He describes the lesions as similar to those of typhoid but not typical. 
The mesenteric glands are but slightly altered ; focal necroses, not containing endo- 
thelial cells, occur in the liver. The proliferative and phagocytic endothelial changes 
of typhoid fever are practically absent. There are no constant changes found 
in other organs, although toxemia in severe cases may induce its usual anatomical 
changes. Giitig examined the blood of six paratyphoid patients and found that 
the neutrophiles are diminished during the early stages of the disease. The lymph- 
ocytes also are diminished at first, but become increased later in the disease, and 
in convalescence they constitute more than half the entire number of white cells. 
The eosinophiles disappear from the blood during the fever, but reappear just 
before or shortly after the temperature becomes normal. 



54 DISEASES DUE TO A SPECIFIC INFECTION 

The bacilli have been found in the heart's blood, in a cardiac thrombus, in the 
liver, lungs, spleen, adrenal bodies, cerebral cortex, and in the fluid of pericardial 
and pleuritic effusions. 

Cases have been reported from France, Germany, Holland, Roumania, England, 
the United States, and the Philippine Islands. The disease affects chiefly young 
adults, and, like typhoid fever, is more prevalent in autumn than at other seasons 
of the year. V. Sion and V. Negal and De Feyfer and Keyser found that the 
epidemics under their observation were produced by drinking infected water. 
Hunermann traced several cases occurring among children to one of their number 
who had suffered from a mild infection. Of the other recorded cases nothing 
definite concerning the mode of infection is known. Watt reports 12 cases, from 
which Bacillus paratyphosus /3 was isolated, occurring in an epidemic of 100 cases 
of typhoid in Aberdeen. He believes that the two epidemics were independent 
and did not arise from a common source. 

Symptoms. — The disease may be mild or severe. The onset is gradual, and 
the symptoms of invasion are the same as those met with in typhoid fever, namely, 
headache, lassitude, and slight bronchitis. During the course of the disease the 
spleen becomes enlarged, rose spots may appear, and the patient develops the 
typhoid state. In Cushing's case a relapse occurred. Johnston states that 
diarrhea and termination of the fever by crisis are of more frequent occurrence 
than in typhoid fever. Brion found diarrhea in 18 per cent, of the recorded cases. 
In uncomplicated cases no leukocytosis has been observed. Hemorrhage from 
the bowel occurred in 5 per cent. 

Complications. — The complications of paratyphoid fever are of about the same 
character and frequency as those of true typhoid fever. 

Diagnosis.— The diagnosis depends upon the isolation and cultivation of a 
paratyphoid bacillus from the patient's blood, urine, or feces, or from a localized 
lesion. Bacilli thus obtained should be agglutinated by the patient's blood-serum, 
and the latter should agglutinate known paratyphoid bacilli. In case an organism 
cannot be recovered Pratt thinks a diagnosis of paratyphoid is justifiable if the 
patient's blood-serum agglutinates known strains of paratyphoid bacilli. The 
Widal reaction is usually negative, or positive only in very low dilution, but all cases 
in which it is negative must not be regarded as cases of paratyphoid rather than 
true typhoid fever. The agglutination test, when employed, in paratyphoid 
fever serves to separate this disease from true typhoid fever and, as in the 
Widal test for enteric fever, the earlier the reaction appears the shorter and milder 
is apt to be the course of the illness. 

Prognosis. — The prognosis would seem to be favorable, as only 3 deaths have 
occurred in 83 undoubted cases of the disease, and 1 of these was a mixed infection 
with the Bacillus typhosus. 

Treatment. — This is identical with that of true typhoid fever. 



TYPHUS FEVER. 

Definition. — Typhus fever is an acute, infectious, self-limited disease of sudden 
onset which is characterized by fever, mental apathy, and the development of a 
rash which does not recur in crops as does the rose rash of typhoid fever. It is 
particularly prone to attack large numbers of persons in unhealthy surroundings. 
The period of incubation of typhus fever, as a rule, varies from eight to fourteen 
days, but there can be no doubt that many cases have been attacked within seven 
days after exposure. A few cases are said to have developed as early as the 
fourth day. Under the conditions mentioned typhus fever is one of the most con- 
tagious of the acute infectious maladies. 



TYPHUS FEVER 55 

Some confusion has arisen in the past between typhus and typhoid fever, but 
at present, they are clearly differentiated, although it is worthy of note that the 
symptoms of enteric fever are so much like typhus fever in their degree of adynamia 
that it is called "typhoid" or like typhus, while German writers of the present 
day still call typhoid fever " ileotyphus ." 

Typhus fever is sometimes called Spotted Fever, Ship Fever, Putrid Fever, 
or Hunger Typhus. 

The infection which at one time was supposed to spread by direct contact with 
the patient or by his garments or discharges is in many, if not all cases, transmitted 
by the bite of the louse (pediculus vestimenti) . Possibly the bed-bug is also a 
transmitting agent. It is not certain, however, than an insect must always be 
the transmitting agent, although in the following text it will be readily seen that 
the conditions favorable to its transmission by the air are usually associated with 
lice, fleas or bed-bugs. 

History. — Typhus fever was first described as occurring in 1083 by Corradi, 
but it was not fully recognized as a distinct malady till 1546, when Gracastorius 
wrote of the affection as he had seen it in Verona in 1505 and 1508. Several epi- 
demics are reported as having occurred during the last half of the sixteenth century, 
in the eighteenth century, and in the early part of the nineteenth century in various 
parts of Europe; a most virulent epidemic ravaging Ireland and England in 1846. 
In America it first appeared in the New England States in 1807, and in Philadelphia 
in 1812, where it is said to have existed in isolated cases until 1836. (See Distribu- 
tion.) 

Distribution. — Typhus fever seems to occur in all parts of the world, if the con- 
ditions favorable to its development are present in the sense of unhealthy surround- 
ings and provided the necessary germ is introduced. Because of its intimate 
association with unsanitary conditions it has been epidemic in great armies, during 
famine, and on ships in which the crew or passengers often were huddled together 
for long periods of time. On the continent of Europe it spreads usually from east 
to west and is disseminated chiefly by the poorest classes when they travel from 
place to place. Persia, China, Hungary, and Turkey are never free from typhus 
fever, and small epidemics occasionally arise from these sources. Sometimes 
small epidemics or sporadic cases arise without it being possible to find any source 
of infection, probably because lice are carried great distances in clothing. In its 
classic form the disease is exceedingly rare in the United States, but the possi- 
bility of its occurrence must always be borne in mind by quarantine officers and 
physicians in charge of large hospitals in crowded cities. This is the more 
important because typhus fever in a modified form seems to be present in all 
large cities at times. Since Brill of New York, in 1898, reported several cases 
lacking certain characteristics of enteric fever and which he proved was not this 
disease, Brill's disease, so-called, has been proved by Anderson and Goldberger 
to be true modified typhus. Typhus fever varies greatly in virulence in different 
localities and in different epidemics. The so-called Manchurian Typhus of Asia 
is as mild in many cases as Brill's disease, both as to its dissemination and its 
symptoms. On the other hand Mexican Typhus (Tarbardillo) is exceedingly 
severe and lethal. 

Etiology. — As already stated, typhus fever is a malady which depends upon 
a specific cause and the presence of unsanitary conditions for its development. 
The specific contagion, whatever it may be, retains its virulence for long periods 
of time in garments and in furniture. Much difference in its infectiousness also 
exists, for in some epidemics nearly everyone exposed is taken ill, whereas in others 
but few are affected. The specific microorganism has never been isolated, although 
several investigators have claimed its discovery and Anderson and Goldberger 
have transmitted the disease to monkeys and thereby induced immunity to Mexican 



56 DISEASES DUE TO A SPECIFIC INFECTION 

typhus fever. Nicolle believes it belongs with the filtrable viruses, but Ricketts 
and Anderson in this country do not agree with this view. The disease can be 
transferred to monkeys and guinea-pigs. 

Exposure for a considerable period of time to the atmosphere of a room which 
is poorly ventilated and which contains typhus patients is the most effective way 
of contracting the disease, whereas, if ventilation is good and the exposed person 
in perfect health there is much less danger of infection. When a large number of 
cases of typhus fever are grouped together in a ward, the infection becomes very 
virulent and both the attendants and the physicians are extremely prone to contract 
the disease. 

The most infectious period of the disease is in the early stages and at the height 
of the fever, although Moore asserts that it is most contagious during convalescence. 
It is also infectious even during the stage of incubation. Mild cases are probably 
as capable of spreading the infection as severe ones. After the febrile condition 
has passed away there is reason to believe that the patient ceases to be a direct 
source of infection, and if an attendant who comes in contact with him for the first 
time now contracts the disease, it must be from the poison which has found lodg- 
ment in the clothing of the patient during his illness. So far as we know, the most 
common means by which infection gains access to the body is by the organs of 
respiration and perchance by the skin. Indeed, some clinicians of experience 
assert that actual contact between the body of the patient and that of the attendant 
is necessary for infection to take place, but this is not generally conceded. Cer- 
tain it is that a very brief period of exposure is sufficient for the transmission of the 
disease. The infectious agent or agents of typhus fever is rarely, if ever, carried 
by water or other liquid media. Lowered vitality of the individual naturally 
increases his susceptibility. The influence of age and sex is very slight, for all ages 
after early infancy seem equally susceptible, the greater predominance of the 
malady between twenty and forty probably being due to increased opportunities 
for exposure. 

The influence of climate and season upon the spread of typhus fever is only an 
indirect one, in that the poor ventilation of the houses of the lower classes during 
the winter months aids in the dissemination of the disease among the occupants, 
whereas in summer the better supply of fresh air and the greater amount of out-door 
life tends to diminish the danger of infection. 

Prevention. — There is no disease in the prevention of which fresh air plays so 
large a part as it does in typhus fever. Indeed, it may be stated that if a healthy 
man be supplied with plenty of fresh air while in the presence of the sick he will 
have a fair chance of escape, whereas if the air of the room be impure, infection 
is almost certain, for, as already stated, typhus fever is a malady of darkness and 
poor ventilation. Practical experience seems to indicate that the various disinfect- 
ants usually employed have little value in preventing its spread unless they are 
used in concentrated form upon the garments which have been infected. By 
far the best means of preventing the spread of typhus fever are the admission of a 
plentiful supply of fresh air and sunshine, the application of steam or scalding 
water to all woodwork and clothing, or the use of dry heat if steam heat cannot be 
employed. The bed-clothing and mattresses should be destroyed by fire. The 
value of formaldehyde gas as a disinfectant is still undetermined for preventing 
the spread of this disease. 

Pathology and Morbid Anatomy. — Typhus fever, unlike typhoid fever, has no 
peculiar morbid anatomy, and it is therefore impossible from autopsy findings 
alone to determine that the cause of death has been typhus. The skin, it is true, 
may show very soon after death numerous petechias, and early decomposition 
constantly occurs after death from this disease. The body is usually not greatly 
emaciated because the disease lasts so short a time. The muscles, which are 



TYPHUS FEVER 57 

somewhat dry, may also show, when examined under the microscope, signs of 
granular or fatty degeneration just as they do in typhoid fever. Waxy or Zenker's 
degeneration of the heart and skeletal muscles is a frequent finding. 

The respiratory passages may be inflamed or congested. Thus there may be 
laryngeal ulceration as in typhoid fever and a considerable degree of bronchitis. 
Often hypostatic congestion of the lungs is present. In other instances a true 
lobar pneumonia occurs. Indeed, Curschmann says it occurred in 15 per cent, 
of his cases. The heart muscle is friable and suffers from the form of myocarditis 
seen in all infectious diseases, and the blood is found to be darker and more liquid 
than normal. It is a noteworthy fact that the intestines show no lesions whatever 
either in Peyer's patches or in the solitary glands. If such lesions are present the 
disease is typhoid, not typhus, fever. The liver is usually swollen and is found to 
be the seat of cloudy swelling, while the spleen is also enlarged to some degree, but 
very soft. It may contain infarcts. The kidneys are also the seat of cloudy 
swelling. 

Symptoms. — The symptoms of typhus fever are quite characteristic. Unlike 
those of typhoid fever, the invasion is usually abrupt, the patient suddenly feeling 
ill about twelve days after exposure, and being seized by a chill or series of chills, 
with headache, backache, and general prostration. The fever rises rapidly, reaching 
its acme, it may be as early as the second day, but as a rule it rises steadily during 
the first four or Hve days, and during this period of rise the characteristic morning 
remissions of typhoid fever do not occur to so marked a degree. By the fifth 
day the temperature often reaches 105° or even 107°, but when the infection is 
not severe it may not go above 103°. After having reached its highest point it 
remains fairly constant with a slight decrease each morning, the evening tempera- 
ture, however, remaining high until the period of crisis, at about the fourteenth 
day. In cases characterized by severe infection the temperature may continue 
to rise until it reaches as high as 109°, when death usually occurs. To those cases 
in which the temperature reaches this very high point within the first few days 
of the illness the term Typhus Siderans is usually applied. 

The pulse is full and rapid, but usually not so feeble as in the early stages of 
typhoid fever. The face is deeply flushed, the conjunctiva congested, and the 
expression one of apathy, although in some cases delirium varying from mild 
wandering to actual maniacal violence may be met with. Sometimes the delirium 
is wild (delirium ferox), sometimes it is like that of delirium tremens, and sometimes 
it is low and muttering — the typhomania of Galen. If the toxemia is severe 
extreme prostration and feebleness may ensue by the tenth day. 

In from three to &ve days the eruption appears upon the abdomen and chest, 
and soon spreads to the legs, arms, and face. It possesses two peculiar character- 
istics. In the first place it is papular, as in typhoid fever, but the spots are rarely 
as rosy as they are in that disease, and may finally become as dark as actual petechias, 
which indeed they really are. The second peculiarity is that there seems to be 
a subcuticular eruption or area of congestion, or mottling, so that the skin is marbled 
or mottled. Unlike the rash of typhoid fever, that of typhus does not disappear 
on pressure, and is distinctly manifest after death. Even if the case is mild the 
petechial character of the rash is present. In some instances the skin is said to 
give off a peculiar, musty or mouse-like odor. In children the rash may be so 
profuse as to resemble an attack of malignant measles. 

As the disease advances to the second week the evidences of toxemia become 
more marked. The active delirium which perchance was present at first is replaced 
by stupor and coma vigil with subsultus tendinum, the tongue is dry and heavily 
coated, the teeth covered with sordes, and the heart's action rapid and feeble. 
The respirations are quickened but shallow, and diarrhea may be marked. This 
stage is called the " putrid," "malignant," or "typhoid" stage of the malady. It 



58 DISEASES DUE TO A SPECIFIC INFECTION 

is essentially one of profound toxemia, and the patient lies in a state of deep prostra- 
tion, indifferent to all sounds and objects in the immediate vicinity, mumbling 
a few disjointed sentences, his tongue being so coated and dry that it is almost 
impossible for him to move it. The pupils are often strongly contracted and the 
tendons twitch, while there may also be carphologia, or picking at the bedclothes. 
Finally, if the illness becomes more severe, the patient lies with open eyes, gazing 
into space, with dilated pupils, a thready, imperceptible pulse, and a cold, clammy 
skin, which heralds the approach of death, which is due to the toxemia, asthenia, 
and hypostatic pulmonary congestion. 

If the patient survives the early stages of attack, the fever usually ends by the 
twelfth or fourteenth day and the temperature undergoes much more rapid deferves- 
cence than it does in typhoid fever. Indeed, it is generally thought that the fever 
ends by crisis; so that the patient passes, during a prolonged sleep, from a state 
of severe illness with a clouded mind to early convalescence with a clear mind, a 
critical fall of temperature taking place. This remarkable change in the aspect 
of the case has been alluded to by some authors as quite pathognomonic of typhus 
fever, but the statement that the fall of the temperature is always by crisis is not 
universally conceded to be correct. Thus, Moore, of Dublin, states that the end 
is by crisis; while Curschmann asserts that in the great majority of cases it ends by 
lysis, although he admits that a critical fall occasionally takes place, covering a 
period of from two to three days. This is hardly a crisis in the usual acceptation 
of the term. 

Whatever may be the true method of the fall of temperature, it is certainly a 
fact that convalescence is rapidly established; so that the patient proceeds to 
complete recovery more rapidly than after typhoid fever, health being completely 
restored, it may be, by the end of a month. 

Relapse in typhus fever very rarely takes place, and in the vast majority of 
cases one attack produces immunity against further infection. 

The complications of typhus fever are those which we would expect to meet 
with in the presence of any severe infection. Bronchopneumonia or lobar pneu- 
monia may occur. In very poorly nourished individuals noma may develop, and 
symptoms of generalized paralysis develop as the result of neuritis. So, too, 
septic arthritis and infection of the parotid glands may occur. 

Diagnosis. — Several characteristics of typhus fever have already been emphasized. 
The most noteworthy of these are: the sudden accession of the disease, the rapid 
rise of temperature without morning remission, the development of a peculiar 
rash between the third and fifth day, the dusky appearance of the face, the musty 
odor of the skin, and the early appearance of active delirium or profound apathy. 
All these symptoms are quite different from those met with ordinarily in typhoid 
fever, but it is not to be forgotten that sometimes typhoid fever begins suddenly 
and presents manifestations closely resembling those of typhus; so that during 
the presence of an epidemic of typhus or typhoid fever cases of either one of these 
diseases may readily be overlooked. In the differentiation the early development 
of the rash (third to fifth day) in typhus fever is of great practical value, and the 
distribution of the rash is still more helpful in aiding a decision; for the rash of 
typhus fever, if profuse, involves the extremities as well as the trunk, whereas 
that of typhoid fever is chiefly limited to the body; a profuse and dusky rose rash 
on the hands and legs is therefore distinctly in favor of typhus fever. Again, 
the rash of typhus fever is constant,. whereas that of typhoid fever fades and recurs 
in crops. Sometimes however, the rash of typhus fever, like that of typhoid fever, 
is very scant, only a few rose spots being present. Indeed, the disease may occur 
without any exanthema being manifest. 

As the illness progresses much additional differential information can be gained 
if the case be one of typhoid fever by the discovery of the Widal reaction, the 



TYPHUS FEVER 



59 



recovery of the Bacillus typhosus in the blood and in the rose spots. Then, too, 
typhoid fever does not end so abruptly nor so early as does typhus fever. Malig- 
nant measles and variola may in their earliest stages resemble typhus, but their 
later course clearly separates them. 



Fig. 14 



H BETWEEN BETWEEN BETWEEN BETWEEN 
go THE AGES THE AGES OF THE AGES OF THE AGES OF 
^ " 20 AND 30 30 AND 40 40 AND 50 50 AND 60 


73 - — - - -L 1 Z 


<2 ....i ::::::: ; 


71 " i 


TO ~ J 


69 7 


08 / 


07 :_::::t:::::::::::::: j 


00 ' 


05 ^ / 


64 ___._^l / 


03 i 


fi2 ___ T __ 1 ^ 


01 ■ 1 1 ... . _|_ / '"" """ 


oo 1 I 


50 | , 


58 


57 | )/ 


56 _ _ _ __ 1 _ _ L' 


55 J J J T 


51 + / 


53 / 


52 f 


51 


50 / 


49 


48 . 


i7 f 


40 / 


45 / 


44 / 


43 / 


42 J 


41 / 


40 / 


39 / 


"88 / 


37 _ / _ _ 


30 1/ 


35 / 


34 ' 


33 '' 


32 / 


31 / 


30 |/ 


29 T _ 


28 | f 


27 . t 


.26 7 


.25 / 


21 1 V 


23 ■< ,f 


22 V 1 / 


21 V ' ' 1 


20 X / 


19 >. 


is /l \ 1 


17 ' 1 V. 


10 / \[ 


15 1 A 1 ^. 1 


14 t_L . _ - >^ 


13 /I T< 


12 / ■ | S V 


11 7 \ 


io J II S N 


9 '' 'IT >v 


8 "V 


7 N 


o T _ nt" 



Showing the decreasing morbidity and increasing mortality percentage of typhus fever with advancing 
years. Solid line represents morbidity from Murchison's statistics. Broken line, mortality percentage 
from the statistics of Murchison, Guttstadt, and Curschmann. 



Relapsing fever is separated from typhus fever by the clear mental condition 
of the patient notwithstanding his high temperature, by the lack of petechia?, and 
the absence, as a rule, of severe initial symptoms. 

Prognosis. — The prognosis in typhus fever varies greatly with the previous 
condition of the patient, and also to some degree with the severity of the epidemic. 



60 DISEASES DUE TO A SPECIFIC INFECTION 

Usually the mortality rate varies from 10 to 20 per cent, in young adults, but in 
children it is often much less than this. In advanced years the mortality is very 
high. 

Curschmann has stated that "old age makes itself felt as early as the fortieth 
year and that after fifty almost 50 per cent, die." The accompanying chart, 
Fig. 14, made from the statistics of Murchison, Guttstadt, and Curschmann indi- 
cates the influence of age on the prognosis. 

Death in typhus fever rarely occurs before the second week. After the end of 
the second week it seldom takes place except as the result of some untoward compli- 
cation. 

Treatment. — The treatment of typhus fever is in many respects identical with 
that now recognized as useful in typhoid fever. The patient should be isolated, 
of course, and provided with an abundance of light and air. As already stated, 
in no disease are these aids to health more essential for recovery. As the course 
of the malady is one toward profound asthenia, easily assimilated or predigested 
foods should be given as freely as the patient can utilize them. Milk to which is 
added a little pancreatin and sodium bicarbonate, barley- and rice-gruel in which 
is placed some takadiastase, and copious draughts of water to flush the kidneys 
and aid in the elimination of poisons are to be administered. The fever is to be 
treated by cool or cold bathing as the patient lies in bed, according to the directions 
given under typhoid fever, and cold is to be kept applied to the head continuously. 
The coal-tar antipyretics are not to be used if they can be avoided. When signs 
of cerebral and pulmonary hypostatic congestion manifest themselves the patient 
may be immersed in a bath of about 90°, and cold water at 60° poured over his 
head and shoulders as a douche, active friction of the body and limbs being performed 
by the nurse for several minutes before the sick man is returned to his bed. Should 
the circulation fail, alcohol in the form of whiskey or brandy, well diluted with 
water, is to be employed for the purpose of equalizing the circulation and quieting 
the nervous system. Camphor in 1-grain doses is useful for this purpose. If the 
nervous restlessness of the patient is sufficient to endanger life by the resulting 
exhaustion, a hypodermic injection of morphine may be given to produce sleep or 
nervous quiet. 

The bowels should be kept open by the use of gentle laxatives, or be evacuated 
by a saline purge if obstinately confined. The activity of the kidneys must also 
be maintained by the use of alkaline diuretics and sweet spirit of nitre and by the 
free administration of a pure drinking-water. As retention of urine often occurs, 
the state of the bladder must be carefully watched. 

VARIOLA. 

Definition. — Variola, or smallpox, is an acute infectious disease affecting the 
entire body, but manifesting itself chiefly by the development upon the skin, 
more particularly that of the face and forearms, of an exanthem which is at first 
macular, then papular, then vesicular, pustular, and finally umbilicated. 

History. — Smallpox is one of the ancient diseases, for records exist which show 
it to have occurred many centuries before the time of Christ. The first authentic 
medical record of the malady did not appear, however, before the tenth century, 
when Rhazes, of Bagdad, wrote his Treatise on Smallpox and Measles. It is 
generally considered that smallpox did not gain entrance to Europe till about 
a.d. 710, when the Arabs conquered the Spaniards. It reached Germany about 
the tenth century, at which time it also appeared in England. At times since the 
tenth century it has swept away thousands of persons in a single epidemic, and 
very few escaped its ravages. Indeed, a large part of the population of London 
were at one time pock-marked. It was first introduced into Mexico in 1520, 



VARIOLA 61 

destroying 3,500,000 persons, and into Massachusetts in 1633. Until the introduc- 
tion of vaccination it was one of the most death-dealing maladies known to man. 
(For the influence of vaccination in diminishing smallpox see article on Vaccinia.) 

Distribution. — Smallpox has occurred in all parts of the civilized world, from the 
Arctic to the Tropics, and is of equal virulence in very cold and in very warm 
climates. The disease affects persons who may be exposed to it at all ages, and re- 
markably few people who are unvaccinated are able to resist the infection, not more 
than from 1 to 5 per cent. The negro race is peculiarly susceptible, and in this race 
the rate of mortality from the disease is usually very high. Smallpox affects males 
more frequently than females. It is more common in the winter and spring than 
in the summer, perhaps because of the crowding in the homes of the poor during 
the cold months. 

Etiology. — Variola is believed by some to be due to a parasite named by Guar- 
nieri, in 1892, the Cytoryctes variola, and carefully studied by Wasielewski in 1901. 
Its evolution has become more fully known by the labors of Councilman, Magrath, 
and Brinckerhoff in 1903, and Brinckerhoff and Tyzzer in 1905, the latter research 
being an extensive investigation of experimental variola and vaccine in Philippine 
monkeys. These in every respect confirm the previous findings in human beings. 
Basing his views upon previously accomplished work, but especially upon the study 
of Councilman and his students, Calkins has attempted to formulate the different 
stages in the life history of the parasite. A full review of these and previous 
inquiries into the nature of the organism of variola and vaccinia will be found in 
the Journal of Medical Research, February, 1904, vol. xi, No. 1, pp. 8-360 and 
January, 1906, vol. xiv, No. 2, pp. 209-359. (For the process of the development 
of this organism see Pathology and Morbid Anatomy.) Notwithstanding these 
studies many authors still regard the cause as unknown. 

The contagion of smallpox is spread in several ways — viz., directly, that is, 
by contact with the patient's body and his clothing; and indirectly, by the air. 
Stokes has recently published a paper indicating that the infection usually enters 
the body through the lungs. A nurse may convey the disease from a patient to a 
healthy individual, and rats, mice, and flies may do likewise. The patient ill of 
smallpox is capable of infecting a healthy person from the initial stage of the disease 
to the moment when, recovery having occurred, every particle of pustule or desqua- 
mating skin has been cast off. The most contagious periods are, however, those 
of vesication, pustulation, and exfoliation. 

The fact that the disease is spread by aerial convection is never to be forgotten, 
and it may be carried in this way from a few feet to several yards (Fig. 15). Much 
difference of opinion, however, exists among those who have studied the question 
of aerial convection. Power, of Fulham, and Barry, of Sheffield, England, found 
a noticeable influence exercised by the propinquity of a smallpox hospital, but 
Savill, from investigations carried on at Warrington, came to the conclusion that 
aerial currents influenced the spread of the disease but little. It must be remem- 
bered, moreover, that before we accept figures as to aerial convection we must 
be sure that the contagion was actually carried by the air and not by insects or 
animals. I know of one smallpox hospital from which flies, mice, rats, and cats 
passed freely, and surrounding which smallpox was almost constantly present. 

Bodies dead of smallpox can also spread the disease among those who handle 
them. 

The severity of the infection depends not so much upon the violence of the 
disease in the giver as in the susceptibility of the receiver of the malady. A mild 
case may therefore be provocative of most virulent epidemic. 

Incubation. — The period of incubation of smallpox varies from five to twenty 
days, but as a rule it is about twelve days. Cases occurring in less than five days 
after exposure are very rare. 



62 



DISEASES DUE TO A SPECIFIC INFECTION 



Prevention.— There is one measure above all others to be used in the prevention 
of smallpox, and that is vaccination, which by its beneficent influence has changed 
smallpox from a common and fearful scourge of mankind to a disease so rare that 
many physicians practise a lifetime without seeing a case. (See Frequency and 
Vaccinia and Vaccination.) 

Fig. 15 

4000 feet. 




0.02 per esni. 
Diagram showing the percentage of aerial convection of smallpox. (Moore.) 



It is very important to bear in mind the clinical fact that vaccination not only 
protects the patient who may be subsequently exposed to smallpox, but also that 
it protects the patient who, having been so exposed, is subsequently vaccinated. 
Even if the vaccination be performed so long after the exposure that smallpox 
nevertheless develops, the severity of the disease will be modified, the degree of 
modification being in direct ratio to the length of time between vaccination and the 
appearance of the variola. 

A most interesting illustration of this has been sent me most kindly by Dr. 
Allan Warner, of the Borough Isolation Hospital, Leicester, England. The history 
of the cases is as follows: 

A boy, aged fourteen years, unvaccinated, sickened with smallpox on April 14. 
He was removed to the hospital on April 18, where he had a severe confluent attack. 
The father consented to his wife and three children being vaccinated, stating that 
personally he would not be vaccinated, but would be a "test," to see if there was 
anything in it. Ten days later his daughter, aged three years, developed smallpox 
eruption; she had less than one hundred spots and never appeared ill. No other 
person in the house suffered from smallpox except the father, vaccinated in infancy, 
his eruption appearing fourteen days after the son had been removed to the hospital. 
A photograph of the father and daughter, taken on the twelfth day of the father's 
eruption, may be seen in Fig. 16, and requires no comment. 



VARIOLA 



63 



In cases of urgency it is generally held that humanized virus is more valuable 
than calf virus, but as humanized virus is often difficult to obtain it is better to 
vaccinate the patient in different places with glycerinated vaccine made by different 
manufacturers, since in this way there is little doubt but that one will surely take. 



Fig. 16 




Father and child suffering from smallpox. The child was vaccinated in the incubation period. 

(Allan Warner's cases.) 



The second preventive measure of importance is the absolute isolation of the 
patient, and the third the complete disinfection or destruction of all garments 
and bedclothing which have been about the sick person, including those worn 
by his attendants. Finally, all individuals exposed to the contagion should be 
quarantined for a period of twenty-one days, in order that the physician may be 
sure that they are not going to be attacked and so spread the infection. 



64 DISEASES DUE TO A SPECIFIC INFECTION 

Frequency. — Smallpox is so constantly present in the poorer part of large cities 
that it may be said to be almost endemic in all of them, but to a very moderate 
degree. Occasionally when a considerable number of un vaccinated persons have 
accumulated in a city or country district, the disease bursts out in a small epidemic, 
and sometimes, without any such apparent cause, certain districts seem to be 
affected, many unvaccinated persons being attacked. During the winter of 1901 
and 1902 smallpox appeared almost all over the United States in scattered localities. 
It can, however, always be stamped out by house-to-house vaccination, and its 
spread depends upon imperfect quarantine and inefficient vaccination. 

As an illustration of the extraordinary effect of vaccination and sanitation upon 
this malady it is interesting to note that during the eighteenth century fully two- 
thirds of all children born in Europe were sooner or later attacked by smallpox, 
and an average of one-twelfth died of the disease. On the other hand, the death 
rate from smallpox in the latter part of the nineteenth century in London was 
98.5 per cent, less than one hundred years before. To put it differently, the death 
rate from smallpox in 1838 was 1064 per million, while in 1889 it was 1 per million, 
and in 1890 nil per million. 

During 1904 the disease was totally eradicated from New York and Philadelphia 
by vaccination and quarantine. 

Pathology and Morbid Anatomy. — -The most noteworthy lesion produced by small- 
pox takes place in the skin. The dermal pailla? become hyperemic, the cells of 
the rete Malpighii swell and so raise the epiderm, and under this epiderm serum 
exudes and pushes the stratum still farther upward. The cells of the rete are more 
or less elongated, pigmented, and form fibrils extending from the epiderm to the 
base of the inflamed zone in the derma, constituting the vacuolar focal degeneration 
described by Councilman, Magrath, and Brinckerhoff. Into this reticulum still 
further serous exudation occurs, and so forms a vesicle which increases at its margin, 
where the exudation takes place very rapidly, while degenerative and necrotic 
changes progress in the epithelium of the area involved. As a result the area 
under and around the vesicle becomes indurated and we have the characteristic 
hard pock of variola. The persistence of this free exudation at the margin of the 
pock and the greater density of the centre lead to depression of the latter, giving 
rise to umbilication. Wright has shown that the central depression in the pock 
may be due to diptheroid degeneration. It may also be due to retraction by a 
hair or small gland. Councilman, Magrath, and Brinckerhoff do not believe that 
the pock is always produced by the same cause, but that a number of factors enter 
into its formation. 

Following this stage, the serum in the pock is infiltrated with leukocytes, and 
these becoming great in number, the contents of the pock become opaque or 
turbid, and finally resemble pus. Sometimes if the inflammation in the adjoining 
pocks is very severe the deeper layers of the skin become involved, undergo necrosis, 
and so great local destruction of tissue takes place. After this stage epithelial 
regeneration progresses beneath the scab, which dries up and ultimately falls off, 
leaving a red or pink depression in the skin, which depends for its depth upon the 
degree of pustulation or necrosis present during the acute stage. Not only do 
vesicles form on the skin, but upon the mucous membrane of the mouth, pharynx, 
tongue, and even the rectum, anus, vagina, penis, and conjunctiva in some cases. 

Myocardial degeneration is present in most cases, and a variolous myocarditis 
has been described. 

In general the cardiovascular changes of smallpox resemble similar alterations 
occurring in other infectious diseases. 

Proliferative changes occur in the hematopoietic organs (spleen, lymph nodes, and 
marrow), associated with the production of basophilic mononuclear cells which 
enter the circulation and also phagocytic endothelial elements. The basophilic 



VARIOLA 65 

mononuclear cells infiltrate the testicle and usually the kidney, liver, and adrenals. 
Cloudy swelling occurs in the glandular viscera and a diffuse toxic degeneration 
takes place in the liver, kidneys, adrenals, and testicles. 

The kidneys are more or less altered in all cases; in milder degrees this may 
amount to little more than intense cloudy changes, but in other cases acute diffuse, 
glomerular, or, less commonly, suppurative nephritis occurs. 

Many of the lesions produced in the internal organs in smallpox are the result 
of a secondary infection from the skin and respiratory tract, and this usually 
depends upon the presence of the Streptococcus pyogenes. 

When hemorrhagic smallpox takes place we have transudations of blood into 
the pocks and into the conjunctiva, the retina, the muscles, the subpleural tissues, 
into all the abdominal organs, and into the kidneys and the perirenal fat. Submu- 
cous extravasations also take place in all the organs of the body lined with mucous 
membrane. Such cases are nearly always fatal. 

Symptoms. — After an incubation period of about twelve days the symptoms 
develop. As in many acute infections, headache and backache are the predominant 
initial symptoms of smallpox, but they are peculiar in their severity in this disease, 
so that their very intensity possesses diagnostic significance. Sometimes the pain 
in the back extends down the posterior portions of the legs. Rigors also occur 
and poAn in the epigastrium and vomiting may come on. Sometimes drowsiness 
and sleep with muscular twitching develops as a prominent initial sign in children. 
The urine is often scanty, loaded with urates, and usually contains some albumin. 
The temperature in smallpox is usually high from the onset, so that it may reach 
104° as early as the latter part of the first day, and 105° or 106° by the end of the 
first forty-eight hours. It maintains this high degree with very slight remission 
until the eruption is developed. The pulse is rapid, often as high as 120 per minute, 
in adults, and unless profound depression is very early manifested it is fairly strong. 
The abdominal organs present no signs of any importance, but constipation is 
more frequently present than is diarrhea. 

The true variolous eruption makes its appearance, in the majority of cases, on 
the third day, although many writers state that it appears most commonly on the 
fourth day, while others insist that it appears on the second. The facts are that 
the time of the appearance of the rash varies materially in different cases, for it is 
delayed in mild attacks and develops early in severe ones. Sydenham said of the 
confluent form of this disease: "This kind usually comes out on the third day, 
sometimes earlier, but scarcely ever later; whereas the distinct (discrete) form 
appears on the fourth day or later, but rarely before." Boerhaave said: "The 
slower the small pocks come out, the milder they prove and the better they ripen. 
Those appearing on the first day of the illness are esteemed the worst kind; those 
on the second, milder; those on the third, still more gentle, and on the fourth the 
more favorable." Very rarely indeed the rash may be delayed till the fifth day, 
but this is an unfavorable sign. 

It must be borne in mind that the first signs of the eruption may be very scanty. 
But one or two papules may be present on the face, or hand, or forearm. In other 
instances the papules are very numerous on the face, the extensor surfaces of the 
forearms, and then on the trunk, these being the parts which are particularly 
prone to present the first sign of the eruption. In still other cases the entire surface 
of the body is speedily covered and the mucous membrane of the mouth, pharynx, 
and vulva also are involved. The portion of the skin least affected in most cases 
is that of the anterior part of the thorax, the abdomen, and the flexor surfaces of 
the extremities. 

The eruption of smallpox proceeds through the following five stages of develop- 
ment with considerable rapidity : For the first few hours minute bright-red macules 
are present, which disappear on pressure. They soon become hard and elevated — 
5 



66 



DISEASES DUE TO A SPECIFIC INFECTION 



that is, the macules become papules. By the end of the first twenty-four hours 
of the eruption the papule begins to show at its apex a tiny vesicle, which rapidly 
develops so that by the fourth or fifth day of the rash the vesicular stage has reached 
its full development. This vesicle is, as a rule, less than a sixth of an inch in diam- 
eter, contains fairly pearly-looking fluid (lactescent), and is surrounded by a narrow 
areola of red. A peculiarity of the vesicle of smallpox is that though some serum 
may escape when it is pinched, it never empties itself or collapses, because of the 
fibrilla which are present in the cavity of the vesicle, as already described. With 
the advent of the fifth or sixth day the centre of the vesicle is seen to be slightly 
depressed, showing the beginning of the stage of umbilication. 

Fig. 17 




Well-developed variola. 



The fluid in the vesicle now rapidly becomes cloudy and purulent, the surface 
of the pock gradually loses its umbilication, and by the seventh or eighth day of 
the eruption exists as a pustule, which by the tenth day is dome-like and 
surrounded by an areola. This pustule, when it is punctured and pressed 
upon, discharges pus and cloudy serum. If the pustule is not meddled with it 
ruptures in about twenty-four to forty-eight hours and the pus escapes, dries, and 
forms a dirty-looking scab, so that by the eleventh day of the eruption the primary 
macule has advanced through its stages of maturation to the ruptured pustule. 
These scabs produce a disgusting odor. Sometimes the pustule does not rupture, 
but simply dries up; when the scab falls off it leaves under its former site a red or 
pink depression in the skin, the future pockmark. This stage of desiccation or 



VARIOLA 67 

drying, followed by exfoliation, may last in severe cases for several weeks, and it is 
followed by a period of desquamation of fine scales of epidermis, during which 
time the reddened pockmark gradually heals and cicatrizes. This desquamation 
rarely takes place earlier than the sixteenth and often about the eighteenth day. 

The eruption on the mucous membranes runs a much more rapid course than 
that on the skin, so that as early as the fifth day the pustule ruptures, leaving 
an ulcerated surface, which, if the eruption on the mucous membrane of the mouth 
has been confluent, may resemble the ragged, dirty-looking exudate of diphtheria. 

There are two additional facts of importance in connection with the eruption 
not yet named — viz., a peculiarity of the papule of smallpox is that when the finger 
is drawn over it, it feels indurated as if a shot were under or in the skin. The second 
point is, that the rash does not all appear at once, but different parts of the body 
are affected one after the other, so that one part may present vesicles while another 
is beginning to show pustules. 

Another point of interest from a diagnostic stand-point is the characteristic 
course of the fever. Primarily high until the eruption begins, it speedily falls to 
99° in moderate cases, or to 100° in confluent ones, and remains low until pustulation 
begins, when the so-called secondary fever develops, which rises to 102° or even 104°. 
This fever, unlike the primary fever, has morning remissions of 1° to 2°, and grad- 
ually ends by lysis, so that about the twelfth day, which is the period at which 
the pustules rupture or become dry, the temperature reaches normal. 

As would be expected from the severity of the eruption, the skin during the active 
stage of the disease is deeply inflamed and so greatly swollen that the features of 
the patient may be unrecognizable. (See Fig. 17.) 

In many cases the mind is clear throughout the illness, but in others it is clouded, 
and active delirium, which may be violent, is met with in severe cases. 

In the earliest stages of variola initial rashes may precede the true eruption 
and mislead the physician if he be not on his guard. In some instances an erythema, 
like that of early scarlet fever, is present, and in still others a rash appears which 
strongly resembles the early stages of the eruption of measles. These rashes 
may last from a few hours to a few days, and usually appear on the trunk and limbs 
and but slightly on the face. The scarlatiniform rash is to be separated from that 
of scarlet fever by the fact that it is not so punctate, nor so bright in hue, and is 
not associated with the presence of the sore throat of that disease. The rash 
which resembles measles is scarcely raised at all, as is the real rash of that disease; 
it develops much more rapidly, covering the entire body in a few hours, and dis- 
appears with a speed equal to that of its onset, rarely lasting over thirty-six hours. 

In some cases both the scarlatiniform and morbilliform rashes appear in very 
small patches on the wrists or about other joints. These initial rashes possess a 
considerable degree of prognostic importance, since they usually appear in mild 
cases. 

Still another initial skin lesion, of some importance because of its prognostic 
features, is an intensely red rash, which appears on the second day of the illness and 
spreads over the body so that the surface may after a few hours look as if it were 
affected by a generalized erysipelas in its early stages. Such a rash is said to indi- 
cate the future development of the hemorrhagic or malignant type of the disease. 

Petechial rashes also occur as initial or preliminary lesions. They usually 
involve the suprapubic or inguinal regions, but sometimes they appear in the 
infraclavicular areas. The individual petechia? may be bright red, or dull red, 
or purple in appearance. In still other cases an eruption which closely resembles 
that of true purpura develops. In very malignant cases death may occur before 
any typical eruption of smallpox appears. 

Something more must be said in regard to the variations which occur in the 
eruption of smallpox. In the first place, it is possible for smallpox to -occur without 



68 



DISEASES DUE TO A SPECIFIC INFECTION 



eruption, although, of course, such instances are exceedingly rare. In all probability, 
careful examination of such patients will reveal one or two papules which otherwise 
might be overlooked. Indeed, this type of smallpox may be considered as belonging 
to so-called varioloid, and to occur in those patients who have been imperfectly 
protected by early vaccination. 

Very rarely in the pustular stage, the epiderm at the base of a pustule may be 
displaced by the formation of a bulla, or bleb, which contains a clear, straw-colored 
serum, and which holds in its centre the pustule. 

Councilman, Magrath, and Brinckerhoff describe secondary vesicles usually 
formed on the surface of the primary vesicle, but occasionally seen in the base. 

Fig. 18 




Variola in a child with scant eruption. (Schamberg.) 



Confluent smallpox, as its name implies, may be localized or general ; that is 
to say, the confluence of the various pocks may occur only in certain portions of 
the body, while in other instances all portions of the body may be covered by a 
coalescence of the eruption. In these cases there is always an extensive dermatitis. 
There is usually great restlessness, delirium, marked circulatory disturbance, and 
death very frequently occurs from the ninth to the eleventh day. It is in this 
type of case, too, that the greatest degree of the edema of the subcutaneous tissues 
appears, and the temperature usually maintains a high degree. Sometimes, how- 
ever, in confluent smallpox, the vesicles do not seem to reach as great a degree of 
fulness as in ordinary cases, and there is not the same degree of swelling of the 
subcutaneous tissues, although the skin is apt to be harsh and thickened. This form 
of confluent smallpox is considered by experts to be more frequently followed by 
death than that form in which the eruption seems to be more completely matured. 

Under the name of hemorrhagic or black smallpox, which is by no means rare, 
and which takes place both in sporadic and epidemic cases, a form of the disease 
occurs in which the initial symptoms are always very severe, and in which hemor- 
rhages into the skin occur early. Not only do the spots become purpuric by extrava- 
sations of blood into the skin, particularly about the joints, but the hemorrhages 
also occur on the eyelids under the conjunctiva, and even on the tongue, the palate, 
the fauces, and the vagina. Bleeding also frequently takes place from the gums, 



VARIOLA 69 

and nosebleed, bloody vomit, and bloody stools may occur. Sometimes hematuria 
also develops. In these patients the temperature usually does not rise above 
100°, and the mind remains clear and unclouded, but they are distinctly typhoid 
in type, and death often occurs, sometimes as early as the third day, but more 
commonly between the third and sixth day, as the result of the profound toxemia 
and associated cardiac failure. 

Under the name variola pustulosa hemorrhagica, a form of the disease is described 
in which the eruption does not become hemorrhagic until the stage of pustulation 
is reached. This type is not so severe as that just described. 

Under the name of variola fulminans, an exceedingly fatal form, with a high 
temperature of 105°, delirium, coma, and collapse occur. In these cases death 
comes on within a few hours after the onset of the disease, and, while no hemorrhages 
are manifest in the skin, since the eruption is as yet scarcely developed, internal 
hemorrhages are, nevertheless, found at autopsy. It is much more apt to occur 
in unvaccinated than in vaccinated persons. 

Smallpox almost never occurs a second time in the same individual. In nearly 
every instance where a second attack is stated to occur, there has been an error 
in diagnosis, either at the time of the first or second illness. 

Varioloid. — While the symptoms detailed up to this point may be considered 
as those of ordinary smallpox which runs a natural course, it is not to be forgotten 
that a modified form of the disease quite frequently occurs, in which by reason of 
vaccination many years before, or natural immunity, or lack of virulence the mani- 
festations of the affection are quite markedly modified. To this type of the disease 
the term varioloid is applied. 

The whole of the eruption may appear within half a day after the first papule 
is developed. The vesicles which in an ordinary case reach their maturity by the 
fourth or fifth day, in these cases become fully developed in seventy-two hours, 
and they are often very small. Instead of the fluid in the pock becoming cloudy 
on the fifth day, this change develops as early as the third or fourth day, and many 
of the vesicles never become pustules, but dry up. Those that do develop into 
pustules reach this condition by the fifth or sixth day, instead of as late as the 
seventh or eighth in the unmodified form of the disease. It is evident, therefore, 
that, as most persons in all civilized countries have been vaccinated, physicians 
will often meet with a modified type of smallpox rather than the severe form. 

The temperature in these cases runs a very mild course, often remaining at 
the normal point as soon as the rash develops, and never partaking of a secondary 
rise. Indeed, the entire symptom-complex of the illness may be of the mildest 
possible type as to objective symptoms, suffering, or discomfort. The appetite 
is good, the patient sleeps well, no complications develop, and convalescence is 
rapid. 

The important fact to be remembered concerning these mild or modified cases 
is that they are quite as competent to spread the disease as are the more severe 
types of variola, and they require as strict quarantine as severe cases of the dis- 
ease. There is therefore every reason why a case of varioloid should be quaran- 
tined most strictly. Chapin points out that in 1896 such a mild type prevailed in 
the Southern United States, and rarely caused death, but gradually spread over a 
very wide area. Unrecognized it developed a host of ludicrous names such as: 
"Cuban itch," "elephant itch," "Spanish measles," "Japanese measles," 
"bumps," "impetigo," "Porto Rico scratches," "Manilla scab," "Porto Pico 
itch," "army itch," "African itch," "cedar itch," "Manila itch," "Bean itch," 
"Dhobie itch," "Filipino itch," "nigger itch," "Kangaroo itch," "Hungarian 
itch," "Italian itch," "bold hives," "eruptive itch," "bean-pox," "water-pox," and 
"swine-pox." 

Even in some cases of modified smallpox, coalescence or confluence takes place 



70 DISEASES DUE TO A SPECIFIC INFECTION 

with associated edema. In these instances the confluence is not to be regarded 
as a very grave omen, since the pocks mature early, frequently do not rupture, 
and convalescence may begin as early as the eighth or ninth day of the illness. 

Variola sine eruptione is a well-recognized mild form of the disease occurring 
usually in hospital attendants, about twelve days after exposure to a case of variola. 
There is general wretchedness, headache, backache, fever, and nausea. Often the 
patient is not ill enough to stop work. These symptoms last only two or three days. 
The initial rashes may appear but the pocks do not. This condition may be con- 
sidered as a modified form of mild smallpox or variola, but in the latter pocks 
appear and the disease differs from true variola only in its severity. Variola sine 
eruptione is infectious but does not cause smallpox as does varioloid in the un- 
vaccinated. Ashburn, Vedder, and Gentry believe it is due to the fact that vac- 
cination with cow-pox protects the individual from the eruptive pustular stage or 
form of variola but not from the whole infectious agent. (See Vaccinia). 

Complications and Sequelae. — When the severity of variola as an infectious disease 
is considered, it is remarkable that it has so few severe complications, and, aside 
from the state of the skin, so few serious sequelae. In some instances where the 
infection of the skin seems to be very severe, multiple abscesses may develop, varying 
in size from a small bean to a large slough. They usually do not appear until after 
the eruption has passed on to the stage of desiccation, but they may persist for a 
long period of time and so prolong the illness. Moore speaks of a case in which 
a patient who suffered from this condition could not be discharged from the hospital 
until after a period of nine months and nine days, because he had forty-two large 
abscesses following confluent smallpox. The most common seat for these abscesses 
is upon the extremities and about the buttocks and shoulders, and occasionally 
on the scalp. Much more rarely abscesses which are more deeply situated form, 
as, for example, ischiorectal abscess. Such abscesses may produce marked systemic 
symptoms, but ordinarily evidences of septicemia are not severe. 

Occasionally erysipelas occurs as a late complication of the disease, either upon 
the face and scalp or on the scrotum. Under these circumstances it is a most 
serious malady, and frequently destroys the patient, since he has not the vital 
resistance to withstand the new infection. 

Bed-sores are rare if proper nursing has been carried out, but boils may occasion- 
ally occur, and are caused most frequently by the Staphylococcus pyogenes aureus. 

Gangrene of the skin complicating smallpox is almost unknown. But when it 
occurs it usually affects the scrotum. The eyelids sometimes become the seat of 
abscesses, or more rarely slough, as the result of the swelling and edema, but actual 
disease of the eyeball complicating smallpox is not common. The ears, on the 
other hand, are not rarely affected, and deafness occurs in a certain proportion of 
cases. When earache is complained of, the possibility of an extension of the 
suppurative process to the mastoid should be borne in mind, as this sometimes 
occurs with serious results. 

So far as the respiratory organs are concerned, it is important to note that small- 
pox sometimes produces laryngitis, varying in severity from a catarrhal to an 
ulcerative type. As in typhoid fever, the development of aphonia, due to ulcerative 
laryngitis, is an exceedingly serious complication, since the cartilages of the larynx 
may become eroded. Bronchitis and bronchopneumonia may develop, and occasion- 
ally pleurisy results from an extension of the infection from the lung or by direct 
involvement of. the pleura by pyogenic organisms. 

The circulatory system does not suffer with anything like the degree of severity 
which we would expect. 

Pericarditis and endocarditis are exceedingly rare complications. 

Myocarditis, on the other hand, is more frequently met with as a result of the 
infection, as it is, indeed, in all of the acute infectious diseases. 



VARIOLA 71 

The kidneys, aside from the ordinary albuminuria of all acute infectious maladies, 
usually escape, as does also the nervous system. That there is irritation of the 
kidneys is evident from the fact that Arnaud, in 1898, found albuminuria in 95 
per cent, of his cases. 

Septic arthritis occasionally occurs. 

The occurrence of smallpox in a pregnant woman very frequently results in 
abortion, but if the mother goes to term, the child is to some extent protected 
from smallpox, although cases are on record in which children have apparently 
had smallpox in utero, and, extraordinary to relate, there are instances reported 
in which the child bore the eruption at birth, although the mother seemingly 
did not have smallpox. MacCombie even states that one case is recorded in which 
the mother contracted smallpox from her newborn infant. 

Diagnosis. — In the later stages of well-developed smallpox there is little difficulty 
in making a positive diagnosis; but in the early stages, when the initial skin lesions 
which have been named are present, the diagnosis may be for a time impossible. 
Indeed, great difficulty may be experienced in expressing a positive opinion as to 
the presence of smallpox, even when the papular stage is in its early development. 
The unusually severe headache and backache, with chills, and pain in the epigas- 
trium, are strongly in favor of smallpox, particularly if there is a history of exposure 
to this disease within the incubation period already named. The absence of throat 
symptoms, of enlargement of the cervical and submaxillary glands, and of the 
peculiar coating of the tongue of scarlet fever may enable us to determine that the 
initial scarlatiniform rash sometimes seen is probably to be followed by smallpox, 
and, furthermore, as has already been pointed out, this scarlatiniform rash lacks 
the punctated appearance of true scarlet fever. 

On the other hand, it is to be borne in mind that in persons in whom the protective 
effect of an early vaccination is waning, it not rarely happens that true smallpox, 
or varioloid, develops in so mild a manner as to present but a few pocks and very 
mild systemic symptoms. A similar state may also be present in those who possess 
a natural immunity even if they have never been vaccinated. (See Symptoms.) 

When the measles-like rash is present, the absence of the characteristic catarrhal 
symptoms of that disease, with its cough, running at the nose, and puffiness of 
the face, should cause the physician to hesitate in making a diagnosis until a suffi- 
cient time has elapsed for the eruption to be well developed. The papules which 
form in measles, while they are often confluent, do not possess the shot-like feeling 
so typical of the early papular stage of smallpox. Finally the measles-like rash 
preceding smallpox disappears in twelve to twenty-four hours, leaving no stain 
on the skin, while that of true measles pursues a course lasting several days. (See 
Measles.) 

Chicken-pox is one of the diseases which is most frequently confused with small- 
pox. In this disease, however, the initial symptoms are always mild, and the tem- 
perature does not rise as rapidly as it does in variola. Then, too, in variola, the 
eruption occurs on the arms and face ; whereas, in chicken-pox it is most abundant 
on the trunk, and sometimes on the scalp. It is always discrete, and it appears in 
successive groups. The vesicles of varicella, when punctured, collapse, since they 
are unilocular; while, as has already been pointed out, those of smallpox are multi- 
locular, and so do not completely discharge their contents when punctured. The 
vesicles in chicken-pox also reach their full development in twenty-four hours 
after the appearance of the papule; whereas, in smallpox they are not completely 
developed for five days. 

Next to varicella, syphilis may be considered as the disease which most frequently 
produces confusion in diagnosis, for variola must be separated from that form of 
pustular syphiloderm which is sometimes called variolaform syphilide. In most 
instances pustular syphiloderm is preceded by macular or papular syphilitic 



72 DISEASES DUE TO A SPECIFIC INFECTION 

eruptions, but in certain instances a history of these previous eruptions may not 
be present. Pustular syphiloderm is more frequently met with in negroes than 
in the white race, and occurs, as a rule, somewhere between the sixth month and 
the second year of the syphilitic infection. Important points in the differentiation 
are that in pustular syphiloderm, the patient does not present the well-marked 
prodromal symptoms of smallpox, such as intense backache, although there may 
be a moderate fever and some pain and aching. Again, in syphiloderm there is 
no marked remission of the temperature such as occurs when the eruption appears 
in smallpox, and syphilitic patients presenting such an eruption do not, as a rule, 
appear very ill or have to take to their beds. Further than this, the syphilitic 
eruption comes out in successive crops, is often profuse upon the trunk, and the 
individual pustules never become so large and deep seated as do those of variola. 
Again, they are practically always non-confluent. Many cases of syphilitic eruption 
have associated with the vesicles copper-colored papules, which should render 
the diagnosis easy. 

Drug eruptions, which are sometimes papular and pustular, are differentiated 
by the absence of fever and of constitutional symptoms. 

Prognosis. — The prognosis of smallpox differs greatly in different epidemics 
and in different individuals. The greatest difference, of course, exists between 
those who are vaccinated and those who are not vaccinated. The mortality 
present in the un vaccinated may be said to amount to nearly 45 per cent., and in 
the vaccinated to about 8 per cent. If a patient has been vaccinated more than 
once, the mortality of the disease is wonderfully decreased. Thus, while among 
those who have been vaccinated once the mortality may be 8 per cent., those who 
have been vaccinated twice have a mortality of less than 4 per cent. If the mark 
of both vaccinations is a satisfactory one, the prognosis is exceedingly favorable, 
for death very rarely occurs unless the patient is already suffering from some 
serious disease which has undermined his constitution and therefore aids materially 
in causing death. In most of the instances in which smallpox has occurred after 
even a single vaccination, the vaccination mark has been so unsatisfactory that 
there has been grave doubt as to whether the patient has been protected at all. 

The age of the patient influences the prognosis materially. It is much more 
grave in early infancy and after thirty years of age, and best at about the end of 
the second decade of life. Chronic alcoholism and the presence of any antece- 
dent disease in the heart, lungs, or kidneys makes the prognosis more grave. 

Marked severity of onset is an evil prognostic sign, but a mild onset does not 
necessarily promise recovery, for in many instances cases which seem mild afterward 
become severe and fatal. Petechial rashes are always of evil import, whereas 
early maturation of the eruption or an aborted maturation, so that it does not go 
on to pustulation, is a favorable omen. Confluent smallpox, if it has not been 
modified by previous vaccination, is more dangerous than the discrete form, and 
varies in its mortality with the age of the patient. Young children almost 
invariably die from it. Older children and adults often recover, and it may be 
said that prognosis is favorable in confluent cases in direct proportion to the age 
of the patient until after the third decade. 

Great swelling of the hands and feet, associated with salivation and swelling 
of the face, in confluent smallpox has long been regarded by physicians, who have 
had a large experience, as possessing considerable prognostic value, since if the 
eruption fails to appear the patient very frequently dies. The swelling is, of 
course, due to non-maturation of the pustules. 

Hemorrhagic smallpox, if well developed, always ends in death. 

When death takes place from smallpox, it most commonly occurs about the 
twelfth or sixteenth day, as the result of pneumonia, hypostatic congestion of the 
lungs, or from the profound exhaustion and septicemia. 



VARIOLA 73 

Treatment. — As in most infectious diseases, the treatment of smallpox consists 
chiefly in good nursing and the maintenance of vitality by the use of proper nourish- 
ment and care. The air of the room should be fresh and cool, and frequently 
changed. Draughts should be avoided, and food should be given frequently in 
small quantities. Water should be given freely for the purpose of allaying thirst 
and flushing the kidneys, and there is no objection to the patient receiving a small 
quantity of ice to relieve the dry condition of the mouth. If the urine is scanty 
5-grain doses of citrate of potassium or citrate of lithium should be given every six 
hours. Stimulants are not needed, unless there are evidences of circulatory feeble- 
ness, when alcohol is considered by most practitioners of experience to be valuable. 
Good brandy and whiskey are the best forms of alcohol to employ. For the relief 
of intense nervous irritation, opium or morphine may be administered in small 
doses, particularly if the condition of the skin seems to be the chief cause of the 
patient's suffering. These drugs are also, perhaps, the best for the purpose of 
allaying excessive delirium, since they do not irritate the kidneys as do some of the 
newer hypnotics. Where the delirium is active and threatens to exhaust the 
patient, a hypodermic injection of J to \ grain of morphine will often produce 
several hours of restful sleep, with benefit. 

For the relief of the intense irritation of the skin all over the body, a very useful 
dressing is ordinary carron oil — that is, lime-water and olive oil mixed in equal 
parts. To this may be added 1 per cent, of carbolic acid for its local antiseptic 
and anesthetic properties, and where great pain is experienced, because of the 
occurrence of the eruption in the thick skin of the hands and feet, prolonged hand- 
baths and foot-baths of lukewarm water may be employed, or hot poultices used. 
An ointment of aristol of the strength of one drachm to the ounce may also be used. 

It seems to be generally considered that local applications to the eruption are 
of little value in the sense of modifying its severity, although certain parts of the 
skin which seem to suffer from an excessive degree of irritation may be relieved 
by cool compress or by the application of antiseptic poultices. MacCombie 
states that the best dressing for the face is a mask with holes cut for the eyes, nose, 
and mouth. Upon this mask is smeared on its inner surface a small linseed poultice, 
over which is placed some vaselin which contains iodoform. This poultice should 
be changed every two hours. It aids materially in separating the crusts, and so 
leaves the skin free for the application of the dressings, which tend to prevent 
ulceration and the formation of scars. The local use of antiseptic drugs to the 
surface of the entire body has not met with favor. 

The mucous membrane of the mouth should be kept cleansed by mouth-washes 
of boric acid or chlorate of potassium and myrrh. When the mouth is exceedingly 
dry, flaxseed-tea, sweetened with a little white sugar and acidulated with lemon- 
juice, may be used. 

The primary fever of smallpox does not last long enough to require treatment, 
but the secondary fever may be sufficiently high to demand relief. Cold compresses 
may be applied to the head, and sponging the body with cool or tepid water may 
be employed, but the cold-bath treatment, so successfully employed in typhoid 
fever, has not apparently given good results in smallpox, and it is practically never 
employed. 

Should any irritation or inflammation of the eyes appear, they should be carefully 
washed every few hours with boric acid solution, and, if necessary, cold-wet com- 
presses should be applied, great care being taken that the warmth of the body 
does not speedily change the cool compress into a hot poultice. 

During the suppurative stage, it is exceedingly important that the nutrition 
and vitality of the patient be preserved by the frequent administration of easily 
digested and predigested food. 

In considering the general condition of a patient who is suffering from smallpox, 



74 DISEASES DUE TO A SPECIFIC INFECTION 

it must be borne in mind that the disease is essentially one which is prone to produce 
profound toxemia, since it is incredible that such widespread infection can take 
place all over the body without simultaneously resulting in septic absorption on 
the one hand, or profound exhaustion on the other. For this reason the degree 
of suppuration should be controlled as far as possible, measures should be introduced 
to aid in the escape of pus, and the treatment should be stimulating and supporting. 

Finally, mention should be made of the so-called red-light treatment of smallpox, 
in which patients are kept in rooms to which no light is allowed to enter save 
through red glass, it being claimed by advocates of this method that the severity 
of the eruption, and so indirectly the severity of the disease, is greatly modified, 
and, further, that scarring of the skin is diminished. Suffice it to state, that while 
certain European clinicians have claimed to have obtained excellent results from 
this method, Welch and Schamberg in Philadelphia, and others, have found it 
entirely useless. When repeated attacks of boils occur in convalescence, staphy- 
lococcus vaccine may be used. 

There are several points in the treatment of variola which should be carefully 
avoided. For the relief of the severe backache and headache, counter-irritation 
is sometimes employed in the early stages of the disease. Such treatment frequently 
results in severe ulceration or sloughing of the part to which the irritation is applied. 
Again, the application of powders, antiseptic or otherwise, is, as a rule, disadvan- 
tageous. The opening of individual pocks by means of a needle or the fine blade 
of a knife is not advisable. 

VACCINIA AND VACCINATION. 

History. — Little is known of the history of vaccinia, save that it has been recog- 
nized for many years as a disease which affects heifers and cows, and that it causes 
an eruption to appear on the teats and udder or neighboring parts. 

Although it was known, among those persons who milked these animals, or other- 
wise handled them, that the disease could be transmitted from the cow to the human 
being, and although many of these persons also knew that this transmission protected 
the human being from smallpox, it was not until Jenner, on May 14, 1796, first 
inoculated a patient with the contents of a cow-pock that the preventive influence 
of vaccination was first tried in a scientific manner. Two years before this an 
English farmer, by the name of Benjamin Jesty, inoculated his wife and two children 
in a similar manner, but at the time no report of the procedure was made. From 
this small beginning so-called vaccination, or the inoculation of human beings with 
vaccine virus, has spread all over the world, and is a well-recognized procedure, 
by which millions of lives have been saved. There are a few persons, not medical 
men as a rule, who still express doubt as to its efficacy, but they are not worthy 
of credence, and the statistics of every civilized land prove that vaccination is one 
of the greatest blessings yet discovered for mankind. It is only necessary here to 
state that vaccination is now obligatory in most civilized lands, and that the 
frequency of smallpox is in direct ratio to the laxity with which vaccination laws 
are enforced. Immense statistics as to its protective value are to be found in all 
works on public health. 

In the Philippine Islands, about Manila, with a population of about 1,000,000, 
there had been for years an annual mortality from this disease of about 6000. 
From 1907 when the United States Government instituted vaccination, until 1911, 
not one death from this disease occurred among vaccinated persons. Heiser also 
states that in May, 1904, the United States Army transport Liscum left Manila 
with 26 cabin passengers, 170 steerage passengers, 16 officers, and 80 members 
of crew, or a total of 292 souls on board. During the first week smallpox broke 
out aboard the vessel, in an unvaccinated child, in the steerage. An examination 



VACCINIA AND VACCINATION 75 

of the personnel on board showed that 3 members had never been vaccinated. 
Within a period of two weeks these unvaccinated persons were stricken with the 
disease and not one of the 289 remaining persons contracted it. If the patient 
contracts smallpox many years after a vaccination, the severity of the disease 
is usually modified. Thus in 58,278 cases of variola collected from various sources, 
occurring in individuals who had been vaccinated, but in whom the "takes" were 
not known to be good, there were 4872 deaths, a percentage of 8.35; whereas in 
23,360 cases of variola, occurring in individuals who had not been vaccinated, 
there were 8682 deaths, a percentage of 32.88. 

Vaccination, when properly performed, and when an active vaccine is used, 
may be said to be a sure preventive of smallpox for a very considerable space of 
time, if not for the lifetime of the individual; but it is safer to be vaccinated every 
few years, and every year if exposed during an epidemic. Not only does vaccination 
protect the individual for a long period of time, but it also modifies the severity 
of smallpox if the patient contracts this disease before the vaccinia can completely 
protect him. This has been proved by practical experience so often that it is a 
fact beyond all doubt, and it bears this important truth with it, namely, that when 
a person who has not been recently vaccinated is exposed to smallpox he should 
be revaccinated at once, since if the vaccine fails to confer complete immunity 
it will modify the disease if it develops. The degree of immunity, or the degree 
of modification, if smallpox develops, depends upon the space of time elapsing 
between exposure to the smallpox and the vaccination. The influence of a primary 
vaccination, which has been successful, upon the susceptibility of an individual 
to a second inoculation and indirectly as to his susceptibility to smallpox, is illus- 
trated by the results of Kitasato who analyzed 931 re vaccinations. His results 
were as follows: After one year, 14 per cent.; after two years, 33 per cent.; after 
three years, 47 per cent.; after four years, 57 per cent.; after five years, 51 per cent.; 
after six years, 64 per cent.; after seven years, 73 per cent.; after eight years, 80 per 
cent. ; after nine years, 85 per cent. ; after ten years, 89 per cent. 

Difference of opinion exists as to the scope of vaccine protection. Some hold 
that it protects against all the phases of smallpox; others that it protects against 
only one phase of the disease, that is the virus that produces the eruptive forms 
of the disease. One fact that supports this view is the development of variola sine 
eruptione in vaccinated persons. Ashburn, Vedder, and Gentry support this view 
but Ricketts and Bayles oppose it. It is well recognized that vaccinia is not a 
modified form of variola, since if the virus that causes all the symptoms of malig- 
nant smallpox in man be passed through monkeys or cattle for several generations 
it loses all its virulence as to local lesions, although it causes systemic illness. 
Unlike certain infectious agents, small-pox vaccine never regains its lost power for 
evil even when it is passed through human beings which are favorable fields for 
the growth of smallpox virus for 100 years (Immermann). If the views of Ash- 
burn, Vedder, and Gentry are correct we would expect variola sine eruptione to 
be a fatal disease without eruption, instead of the mild one which it is. (See 
Variola.) 

Method of Vaccination. — The skin on the arm or calf of the leg, having been 
cleansed by washing it with soap and water, is scarified or scratched by a needle 
or knife-blade in such a manner as to remove the epiderm and expose the true 
skin over an area of about an eighth of an inch in all directions. Care should be 
taken that the spot is not so deeply scratched as to cause free bleeding. Upon 
this area is now deposited the vaccine, which is then gently rubbed into the part 
and allowed to dry before any clothing comes in contact with it. Several forms of 
vaccine are used, but that most commonly employed at present is known as " glycer- 
inated vaccine lymph," prepared from the contents of the vaccine vesicles as they 
have developed on the belly of a heifer. This glycerinated lymph is put up in 



76 DISEASES DUE TO A SPECIFIC INFECTION 

small glass tubes, which are hermetically sealed at the ends, so that it may not be 
contaminated before it is used. Schamberg and Kolmer have shown that the 
application of a solution, made up of picric acid 4 grams, iodine 1 gram, alcohol 
100 c.c, forty-eight hours after vaccination prevents secondary inflammation. 
Another plan which has the advantage of avoiding a scab is to make two or three 
superficial incisions in the skin and to rub the vaccine into the cuts. 

Children should always be vaccinated during the first year of life, or immediately 
after birth, if exposed to smallpox. Vaccination should be repeated through life 
every five years, and oftener if smallpox is prevalent. If one inoculation fails it 
should be repeated at least three times, since sometimes primary failure is due to 
poor vaccine or to an error in technique. If after three attempts no "take" is 
produced the patient may be considered as immune, at least for a time. 

Primary Vaccinia in Man. — Three or four days after vaccination has been per- 
formed the infected area begins to be slightly reddened, and this reddening increases 
while at the same time a reddish papule develops which by the fifth day begins 
to look like a vesicle, particularly if the margin of the area inoculated be examined. 
This vesicle increases in size, becomes filled with thin, clear lymph, and by the 
eighth day reaches its greatest development. At this time the contained fluid 
begins to be more opaque and yellow and the top of the vesicle is seen to be slightly 
sunken — that is, the early stage of its umbilication has been reached. The skin 
surrounding the vesicle is now surrounded by a zone or areola of red which by the 
ninth or tenth day becomes very well developed, so that it extends for a consider- 
able distance in all directions; the spot inoculated is painful and the neighboring 
lymphatic glands may be swollen and tender. At this time, too — that is, about the 
tenth day — constitutional symptoms may come on and the patient suffer from mod- 
erate chills, a slight rise of temperature, and malaise. Sometimes roseola (roseola 
vaccinosa) may develop over the body. By the eleventh or twelfth day these symp- 
toms are modified, the vesicle begins to desiccate, and by the end of the fifteenth 
day it is completely dried up, although the scab may not fall off till the twenty-first 
or twenty-fifth day. The crust or scab is dark red in color and thin at its centre 
and at its edges, but there is a thickened area, or -ridge, between the centre and the 
periphery. After the crust falls off it leaves a pink spot which gradually fades 
and leaves, after some months, a foveated or pitted mark from which small scars 
may radiate. It is to be borne in mind that in some cases the constitutional 
symptoms are so mild as not to be worthy of note, while in others they may be 
quite severe. To be a true "take," the full development of the pock by the stages 
named is essential, but it is possible for the "take" not to ensue for a month after 
inoculation. (See Plate II.) If the vaccinated area becomes very much inflamed 
and painful the part should be put at rest and dressed with lead water and laudanum. 

Secondary Vaccinia in Man. — -Very few persons who have once been successfully 
vaccinated present the conditions just described when inoculated a second time. 

The difference, however, is one of degree, not one of kind, and vesiculation 
and umbilication should appear in all cases. The variations depend upon the 
degree of immunity induced and persisting from the first vaccination. If immunity 
is complete there is no "take." If not complete the primary papule may occur a 
day earlier than usual and a typical pustule may be reached as early as the end 
of the seventh day with the development of more or less severe systemic symp- 
toms as early as the fourth or sixth day. 

It is a point worthy of note that the so-called "raspberry excrescence" which 
sometimes follows vaccination on the fourth or fifth day, looking like a small nevus, 
is not a vaccine pock and confers upon the patient no immunity to smallpox — 
that is, it is not to be considered as a "take." Care must be taken, too, that the 
sore or mark produced by the injury of the operation be not taken for the specific 
lesion of vaccinia. 






>> 


s- 






73 


3 




d 


J3 


O 

'G 







00 


3 

a 




•i-H 




OQ 




a 








c 








•i-H 








o 








o 








05 






co 


> 






53 


as 

s 


>> 

13 


>> 


fe 

&H 


•r-t 


^3 

+3 


00 


s 


0. 


CD 


<h 

03 


5-1 


«M 




00 


Q 









5si 


c 






• ^ 









^ 


•i-H 






^ 


3 






g 


^H 






© 


o 






,5~ 


> 




>> 

03 


*<-» 


w 


J>> 


-d 


^ 
^ 




03 


-a 


© 




-a 


© 


g 




+3 


43 


cc 




"tf 


03 

3 








u 


"©" 






O 


© 
<3 



< 

PL, 




fe 



• 




• 




"©' 


c 




fl 




£ 












g 


•pH 










+J 




HJ 




©J 


o5 


>> 


05 




5* 


•I-H 


c3 
T3 


_g 




rO 


a 


J3 


o 




©> 


o 


43 


o 




rf» 


aJ 




05 




5J 


> 




t> 




SQ 


<D 









CO 


PC 




•i-H 


(X 




o 

HO 




05 


^ 




03 




g 


e3 




i~«s 




T3 




""o 




o 


J3 




O 






05 


1> 




© 




> 






•<o 




<D 






l»o> 

© 




ft 







p~o 

© 
© 


d 




CD 




Bs 







£ 






•i-i 




• i-H 






05 


>> 






>> 




G 

•i-H 


c3 


05 

> 


73 







J 


J 






05 




>> 


43 

oe 




> 






CO 






(X 




£ 

•fH 

Oh 







VARICELLA 



77 



VARICELLA. 

Definition. — Varicella is often called chicken-pox. It is an acute infectious 
disease which usually occurs in children under ten years of age, and rarely attacks 
individuals after puberty. In adults it is still more uncommon, although Tyzzer 
reports 38 cases occurring in adult male Filipinos and states that at the time of the 
last observation 300 cases had been recorded. The men were prisoners, and this, 
together with -race and climate, are considered possible factors in increasing suscep- 
tibility. In all probability one of the reasons for its rarity in those of mature 
years is that it affects so large a proportion of all children that most adults are 
rendered immune by an attack in childhood. The most marked characteristic 
of the disease is the appearance within the first twenty-four or forty-eight hours 
of fever and malaise and of papules, followed by vesicles, upon the skin of the fore- 
head and face, or upon the chest and back. (See Fig. 19.) 

Fig. 19 




Chicken-pox. (Schamberg.) 



Etiology. — Like all acute infectious diseases, chicken-pox is produced by a micro- 
organism, but as yet it has not been isolated. Tyzzer found specific nuclear and 
cytoplasmic inclusions in all the lesions, but obtained no evidence favoring the 
hypothesis that they are parasites. It also resembles the other acute infectious 



78 DISEASES DUE TO A SPECIFIC INFECTION 

eruptive diseases in that it occurs in epidemics, although at times isolated cases 
take place that cannot be traced to any source of contagion. While the eruption 
in its peculiarities resembles to some extent that caused by smallpox, chicken-pox 
bears absolutely no relation to that malady and in no way protects a patient from 
developing a typical attack of variola. (See Variola.) 

Symptoms. — At a time varying from ten to fifteen days after exposure to varicella 
the child usually manifests some evidence of a beginning illness. If very young it 
may be unusually restless and fretful, there may be some disorder of the digestive 
apparatus, and vomiting may occur. Fever is an early symptom and it may be 
moderately high — that is, about 103° or even 104°. Often, however, it fails to 
reach such a height. If the child is old enough to describe its sensations, some 
aching in the back or in the limbs may be complained of. 

After about twenty-four hours the eruption appears in the form of red papules, 
which speedily become vesicles containing clear or turbid serum. The vesicle 
is superficial, it is not surrounded by a zone of induration, as it is in smallpox, and 
it does not become umbilicated, although the top of the vesicle, when it is ripe, 
may be flattened. By the end of thirty-six to forty-eight hours the vesicle becomes 
a true pock, the previously clear serum becoming opaque but not purulent unless 
it is denuded by scratching, and then infected. These pocks speedily shrivel and 
by the fourth day form crusts, which readily fall off and rarely leave a scar unless 
the skin be scratched by the child so that the deeper layers become infected. Many 
individuals bear scars of this sort upon the face, and they are particularly well 
marked in women with a fair skin. 

The eruption of chicken-pox develops in a series of crops, or, to speak more accu- 
rately, it continues to develop in new areas as those which were affected first begin 
to pass into the stage of crusts. An examination of the patient on the third day 
may therefore reveal the eruption in all stages of development. 

It is a noteworthy fact that the eruption of varicella is always discrete and never 
confluent. It is never profuse as in smallpox. Rarely the vesicles appear on the 
mucous membranes. 

The severity of the fever and of the signs of general illness vary greatly in children 
affected by varicella. In some cases the disease runs so mild a course that the 
child is not kept in bed, in others it causes a considerable degree of illness; but in 
the majority of instances it is a very mild malady. In children who are weakened 
by previous disease it sometimes develops into a dangerous malady, in that the 
associated digestive disturbance still further impairs vitality, or because the lesions 
of the skin become infected and sloughing or gangrene appears. Sometimes 
erysipelas is developed in this manner in poorly nourished children. Rarely, if 
the child is exposed to cold, nephritis develops. Allaire reports peripheral neuritis 
of the left arm following an attack of varicella in a child aged eight years, the pocks 
having suppurated. 

Diagnosis. — The eruption of chicken-pox must be separated from that of modified 
or mild smallpox. The most important factors in this separation are the superficial 
character of the pock, the lack of the sense of induration when it is taken between 
the thumb and finger, the early appearance of the rash on the chest rather than 
on the forearms, as in smallpox, and the mild character of the general symptoms, 
combined with the brief course of the disease and the speedy completion of the 
illness. 

Additional diagnostic factors are the presence of a good vaccination mark which 
largely excludes variola. Again, the onset of varicella is usually devoid of pro- 
dromes, whereas smallpox presents for some days backache, vertigo, fever, nausea, 
and chills. The mere fact that the eruption is scanty does not, however, exclude 
smallpox. The vesicles of varicella do not become umbilicated as do those of 
variola, but they rapidly dry up and make a dark-colored scab. The eruption 



SCARLET FEVER 79 

of smallpox comes out in one crop, that of varicella in several crops; that of smallpox 
lasts from ten to twelve days in typical cases, never less than six days, whereas 
chicken-pox lasts but from two to four days. 

Prognosis. — The prognosis is always favorable unless the unfavorable preliminary 
states just noted are present. 

Treatment. — Medicinal treatment of varicella is usually unnecessary. Careful 
nursing that prevents exposure to cold and wet, regulation of the diet, and the use 
of a few drops of sweet spirit of nitre in a teaspoonful of liquor potassii citratis 
every four hours, to keep the kidneys active, are all that is needed in most cases. 
The fever runs so brief a course that antipyretic measures are not necessary. 

SCARLET FEVER. 

Definition. — Scarlet fever is an acute infectious disease which chiefly affects 
children under fifteen years of age. It is characterized by the development of 
an intensely scarlet, punctated rash on the second day of the illness, accompanied 
by a marked febrile movement. It is sometimes called "scarlatina," and it is 
to be clearly understood that this word is synonymous with scarlet fever and that 
it does not describe a modified or diminutive form of the malady, although the laity 
often employ the term in this manner. 

History. — Hirsch states that the oldest reference to an epidemic of scarlet fever 
dates from Sicily in 1543, but Sydenham, of London, first differentiated it from 
measles. Prior to his time it had been considered a form of measles. 

Distribution. — Like almost all of the acute infectious maladies, scarlet fever 
occurs in all parts of the world, although it seems to be much more prevalent in the 
temperate zone than elsewhere. In the United States it occurs less frequently 
in the Southern States than in the Northern States. It did not develop in the 
United States until 1735, nor in South America until 1830. In Australia and in 
Polynesia the disease first appeared in 1848, assuming a mild type, but a severe 
epidemic occurred in Melbourne in 1876. It is said that only imported cases are 
met in India, and only one case has been reported in Greenland. It does not 
occur nearly so frequently as does measles, and very many persons reach adult 
life without having suffered from it. This is in part due to the fact that it is not 
so readily transmitted as some of the other acute infectious fevers, and also because 
a large number of persons seem to be resistant to the disease. Johannessen states 
that of 185 children exposed only 28 per cent, developed scarlet fever, and out of 
314 adults exposed only 5 suffered from the malady. If the same number of 
cases had been exposed to the infection of measles, very few of the children would 
have escaped. 

Scarlet fever is more apt to occur in the winter months than at any other time, 
but statistics differ as to the winter months' frequency. Thus, Whitelegge from 
his statistics based upon cases occurring in nine English towns, found in the first 
quarter 219 cases; second quarter, 194; third quarter, 327; fourth quarter, 460; 
and Reece has supported his conclusions by the accompanying chart. (See Fig. 20.) 

On the other hand, Seibert, of New York, gives a statistical table which shows 
that the last winter months are those of greatest frequency. (See Fig. 21.) 

August Hirsch gives the following statistics based on an analysis of 435 epidemics 
occurring in all parts of Europe and North America: 178 epidemics occurred in 
winter; 157 in spring; 173 in summer; 213 in autumn. 

The frequency and mortality of scarlet fever have greatly decreased in the 
last sixty years. (See Fig. 22.) 

Etiology. — Scarlet fever does not disseminate itself through the air as does 
measles; direct contact or near association with the infected person, being needful 
for the transmission of the disease. The desquamated skin has been recently denied 



80 



DISEASES DUE TO A SPECIFIC INFECTION 

Fig. 20 



Per cent 
+ 70 

too 

+ 50 
+ 40 
+ 30 
+ 20 
+ 10 
MeanO 

- 10 

- 20 

- 30 

- 10 

- 50 

Showing seasonal mortality of scarlet fever in all ages and both sexes in England 

and Wales. (Reece.) 

Fig. 21 



Jan. 


Feb. 


Mar. 


Apr. 


May 


Jhine 


July 


Aug. 


Sej.t. 


Oct. 


Nov. 


Dec. 



































































































































































































































































































200 

'190 

'180 

170 

ISO 

150 

140 

130 

120 

110 

!00 

90 

80 

70 

-,60 

50 

40 

30 

20 

10 



JAN. PES. MAR. APRIL MAY 




JUNE JULY AUG. SEPT. OCT. NOV. DEC. 



CO ,T?- |lO |^b~T 1^- OOOl Orr(N TO -^j- , (b I (D N 1 00|0)OT-OjrQ'tiOCONCO OO t- - CM 

'OjIcvjItNlcvjtNcvJOJcococoTOcoco coco'roico^-^-^j-^j-Tfrj-Th'^-^- rj- in in io 





I 



I 



Frequency of scarlet fever, by weeks, throughout the year. A comparison of Charts 20 and 21 shows 
that although the greatest morbidity is in the first five months, the greatest mortality is in the last five 
months of the year. (Seibert.) 

Fig. 22 



r -° £ 


;isii 


77 


^ 'f — 




:ry|; 




o 


5 <* '■ 


Off C 


7 


j" - - 


- '■?- 


_- ■ 


: -i 


x X 




-ti-^r-Tr-Cr-iMn-f^ci-tD^OHii^-t.s^fxsb^J ec 
i- l- t- r- <- i- i-a> cocooo 30 oodb ooaooo c-. -. r r - r r * ~- r- o o o o 

X v. -,. x v. x x x 3D X X '. 3D XI X /„ C X X X X) x ' ' ■'- X X r. r -• :. 






































IdO D £ 


1 

ATHSREC 


I 

ISTE 


RED 1 


«<U 


DED 


Wl" 


i> 






















s 9 


*RUET 


FE'V^R 


'J-mZ 


NCH ( 6 


MAI 


!& 


MA 








II 1 














130 — - 




X 


o 


















\ 








I 








f 


Q 

O 

D 


1- r ' rl 
o 


/I 






















/ 








100 -■ 
90 -■ 
80 - 










\ 




I 




:i 




il 
















1 


f, 


l\ 


\r 


/ / 


I 






| IV 1 


\ 


/ ;' 






f i\' 








tr-*^ V \ 


Ii' ; i \ ' 


1 \ f\ 




■BfcM| Vi;:lfl| 


/ \/>k 




J 'w^^m^ 




rv 




\ 


2(1 | 

10 ! 


ill 




ii 


: ; 


Ii 


,i,j 


j 




1 1 


: ; 




1 .!. 


\ 


! 


i . 


! 


i 


i 1 i i ! I i ! i i i 1 i ; : : : 1 : 



Showing the decreasing mortality of scarlet fever in England and Wales. Deaths per 100,000 
population. (Modified from Wilson and Reece.) 



SCARLET FEVER 



81 



as a cause. The disease is usually transmitted by the nasal mucus as in sneezing, 
and by clothing, and other articles which have been in contact with the patient. 
Thus books, cards, letters, and pets, such as dogs and cats, and other means of 
conveyance may assist in spreading the infection. The clothing of the nurse and 
physician may convey the disease, and cases are very numerous in which physicians 
have so communicated scarlet fever to their own children after visiting patients 
ill with this malady. 

The persistence of the infection in articles of clothing is very remarkable. No 
other acute disease renders the surroundings of the patient a source of danger 
for so long a period. Instances in which clothing or upholstered goods have 
transmitted the disease to healthy children two years after recovery of the first 
patient are recorded. 

Articles of food may also convey the infection. Thus Ekholm has reported 
an instance in which six families who partook of milk from a dairy in which there 
was a milkmaid who had a phlegmonous pharyngitis, suffered from scarlet fever. 

Fig. 23 



111 
C3 
< 

Z 
HI 

o 
tr 
ui 

Q- 


DC CC 
UJ < 
Q UJ 

z >■ 

3 ,- 


5 CN 

UJ Q 

^ Z 
1- < 

1U 

CO 


uj w 

UJ Q 


5 * 

UJ Q 

£ z 

1- < 


UI Q 

M 

UJ <- 

m 


uj <o 

UJ Q 

5 z 
1- < 


UI Q 

£ z 

1- < 


5 » 

UJ Q 

5: z 

t- < 

UJ ^ 

00 


UJ °> 
UJ Q 

^ z 

1- < 

00 


z o 

UI i- 

UJ _ 
^ Q 

t- < 

UI 

oo en 


15 


























































































































































1 












































14 




































/ 
































































































1 


' 


































































13 






- 


- 




















































































































1 




































































12 
































, 


i 


































































































/ 






































































11 
































/ 


































































































/ 


f 






































































10 


































































































































/ 








































































9 




























J 


I 


































































































/ 








































































8 




























/ 












































\j 










1 














- 




























/ 












































\ 
























i 


























/ 
















































\ 










































































































J 
















6 










































































































































































































5 










































































































































































































4 










































































































































































































3 










































































































































































































2 









































































































































































































Showing age incidence of scarlet fever based on 7470 cases, and representing the combined 
statistics of Whitelegge, Ballard, and Keen. 



The breath of the patient and the air of the bed-room are probably incapable 
of transmitting the infection, unless the latter is laden with the dust containing 
the microorganism. It is noteworthy that nurslings are not as susceptible as 
children of from two to five years, at which period of life the disease most often 
occurs. The age incidence is well shown in Fig. 23. 

A patient who is a sufferer from the infection of scarlet fever is not capable 

of transmitting the disease until the rash develops. At the fourth or fifth day of 

the disease the infectiousness of the case is perhaps at its height, and the ability 

to transmit the malady exists as long as there is the slightest discharge from the 

6 



82 DISEASES DUE TO A SPECIFIC INFECTION 

nose, which is often for as long a period as six weeks. It is important to remember 
that not only the nasal mucus but the discharge from a purulent otitis media or 
from a chronic consecutive scarlatinal pharyngitis are also active sources of infec- 
tion, and until all these parts are entirely healthy the danger of spreading the 
disease exists. Indeed, numerous instances are recorded in which children with 
such mild consecutive pharyngitis as to escape notice have conveyed the disease 
several weeks after apparent complete recovery from scarlet fever. 

Many investigators have endeavored to isolate the specific microorganism 
of scarlet fever, but without success. Loeffler, Fraenkel, and other German 
physicians first demonstrated the presence of streptococci in cultures prepared 
from secretion taken from the throats of scarlet fever patients, but their observations 
were limited to a small number of cases and are of interest from an historical rather 
than a practical stand-point. The same statement may be made concerning the 
researches of Klein in connection with an epidemic of scarlet fever (1885) caused 
by contaminated milk from a farm at Hendon, in England, for although Klein 
cultivated a microorganism from lesions on the udders and teats of cows on this 
farm, which apparently was identical with one he found in the blood of scarlet 
fever patients, and although this latter organism when injected into calves produced 
a lesion resembling the one with which the Hendon cows were affected, the inquiry 
instituted by the Medical Society of Edinburgh and the investigation of Dr. Crook- 
shank, of London, proved that the disease from which the cows suffered was a 
modified form of cow-pox, and, moreover, that the persons who milked the cows 
did not contract scarlet fever. A similar history as to cows and patients has more 
recently been recorded in Lincoln, England. In 1891 Kurth found in the throats 
of scarlet fever patients, in pus from the cervical abscesses and in the viscera of 
persons who had died from scarlet fever, a streptococcus which formed a twisted, 
gelatinous mass when grown in broth. This organism, called by Kurth Strepto- 
coccus conglomeratus, was subsequently studied by Mervyn Gordon, who found it 
present in the throats of twenty out of twenty-seven scarlet fever patients, in the 
internal organs of most patients who died from the disease, and in the fluid of a 
scarlatinal pleural effusion. Baginsky and Sommerfield, who published the results 
of their investigations at about the same time as Gordon, found a streptococcus, 
having virulent properties and generating a toxin, in all cases of scarlatinal angina, 
and in cultures made from the viscera, bone-marrow, and blood of one hundred 
and forty-two children in whom the disease terminated fatally. This streptococcus 
they considered to be the specific organism of scarlet fever. 

Of the work done by American bacteriologists that of Class, of Chicago, should 
be mentioned. In 1899 Class noticed the frequent presence of a diplococcus in 
cultures made from the throats of patients having different forms of angina, and 
upon further investigation he found that the organism invariably occurred in 
cases of scarlatinal angina. He then made cultures from the blood of scarlet 
fever patients and from desquamated epidermal scales, and found the same diplo- 
coccus. Gradwohl, of St. Louis, and Calvin Page, of Boston, have also found an 
organism identical with the one described by Class, but their observations were 
confined to a small number of cases. 

From this brief resume of the bacteriology of scarlet fever, it is apparent that 
streptococci are generally present in the throat of scarlet fever patients, and that 
they are often found in the blood and internal organs; but when we come to consider 
that streptococci have been found in healthy throats, that cases of streptococci 
angina exist independent of scarlet fever, and that streptococci are found in the 
blood in other diseases, it is not justifiable to assume that any one of the forms 
thus far described is the specific organism of scarlet fever. Closely associated 
with the specific germ of scarlet fever, whatever it may be, we always find a variety 
of the streptococcus, and it has been claimed by some that this is the cause of the 



SCARLET FEVER 83 

disease. There can be no doubt that it is responsible for a large number of the 
symptoms and complications of the disease. 

Prevention or Prophylaxis. — Every case of scarlet fever should be promptly 
isolated and every attendant of the patient should also be prevented from mingling 
freely with the inmates of the house. The food should if possible be placed in an 
outer room and from there obtained by the nurse for the patient. If the nurse 
is to leave the room her clothes should be changed. Before she leaves the con- 
valescent patient to take care of other cases she should take a hot bath and have 
her hair shampooed. Her nasopharynx should be well cleansed by an antiseptic 
spray or douche. The clothing she has worn in the sick-room should be steril- 
ized by boiling. The physician should always change his clothes on entering and 
leaving the room, or at least wear over his street dress a long operating gown to 
protect him from the infection. If he is attending, or about to attend, a case of 
confinement he should refuse to take charge of a case of scarlet fever. The same 
rule holds true as to operative cases. 

All clothing and bedclothing should be immersed in boiling water, or in a disin- 
fectant solution, before they are taken from the sick-room, and books and cards 
which have been in the patient's room should be burned. If possible it is better to 
burn the pillows and mattress than to attempt to disinfect them. If they are 
disinfected, steam under pressure should be used for this purpose. The hanging of 
sheets saturated with disinfectant fluids over doorways and the placing of pans of dis- 
infectants about the house are utterly useless except that their presence constantly 
reminds the inmates or visitors that an infectious disease is present and so aids in the 
maintenance of caution. An amount of disinfectant in the air sufficient to destroy 
the contagion will destroy the patient and nurse. After the illness is over and the 
patient has left the room, it should be carefully disinfected by an adequate formal- 
dehyde generator, the floors and walls being first moistened with water to aid in 
the efficiency of this gas. Afterward the floors and walls should be scrubbed with 
1 to 2000 bichloride solution or one of chlorinated lime. 

No case should be isolated less than five weeks, and no case should be allowed 
to mingle with other persons as long as nasal, aural, or pharyngeal discharges 
exist even if they persist for months. There is no proof that infection is transmitted 
by scales. Before the patient is discharged he should receive at least three hot 
baths. Particular attention should be paid to the scalp and hair. Sleeping with 
other children is to be prohibited for several months. 

After exposure, a child should be placed in quarantine for at least a week to 
discover if the disease is to develop. When an epidemic is present all schools 
should be closed. 

Pathology and Morbid Anatomy. — A point of primary importance to be borne 
in mind in considering the pathology of scarlet fever is that the organs of the body 
suffer from a multiple, not a single infection. Whether a special form of strepto- 
coccus is the cause of the disease, or whether an entirely distinct organism is the 
cause, the fact is that the disease is accompanied by streptococcus infection in all 
cases and not rarely by other forms of infection as well. 

The organic changes produced in the body by an attack of scarlet fever are 
marked, but none of them can be said to be characteristic of the disease. Altera- 
tions in the skin and inflammation of the mucous membrane of the mouth and 
pharynx are the most constant changes, but even these may escape notice. The 
skin is the seat of a very acute inflammatory process involving to a varying degree 
all its layers and terminating, even in mild cases, in exfoliation of the superficial 
cells, often in large flakes. The pharyngeal mucosa is inflamed, the inflammation 
varying in degree from a mild acute pharyngitis to extensive necrosis involving 
the deeper strata of the uvula and tonsils. This inflammation in a modified form 
extends at times all the way down the esophagus and by way of the Eustachian 



84 DISEASES DUE TO A SPECIFIC INFECTION 

tube into the middle ear, where it not infrequently causes so destructive a change 
as to produce permanent deafness; or if the infection be severe and no vent for 
the pus is afforded the mastoid cells become involved and, finally, a secondary 
meningitis, or abscess of the brain, is produced. This is a rare sequel. In still 
other instances the inflammatory process extends into the nasal cavities and from 
them proceeds to an infection of the antrum of Highmore or even the frontal 
sinus. Extension of the pharyngeal lesions to the lymphatics of the submucosa 
may cause infection of the cervical and submaxillary lymph nodes, so that there 
is developed great swelling under the jaw, and in some instances suppuration, 
the so-called "collar of brawn." 

Equal in frequency with these changes, and of more importance, are those which 
take place in the kidneys. These changes not only endanger the life of the patient 
during the illness, but occasionally leave him with kidneys structurally so impaired 
that complete restoration to health may never take place. The renal changes 
are primarily those of an acute diffuse nephritis involving the whole texture of the 
kidney, particularly the cortex, and accompanied by marked albuminuria, inter- 
tubular cellular infiltration and necrosis, and desquamation of the epithelium lining 
the tubes. Areas of necrosis and infarction and even acute suppurative nephritis 
occur, although infrequently. 

When the infection with the streptococcus is particularly severe and the evidences 
of toxemia are profound the autopsy reveals degenerative changes in the heart 
muscle, areas of necrosis in the liver, and bronchopneumonia with swelling and 
softening of the bronchial nodes. Degenerative or necrotic changes in the myo- 
cardium and endocarditis, vegetative or ulcerative, may be present. Pericarditis 
may be marked. As in all septic infections arthritis may be found in numerous 
joints. Pleurisy, if present, often results in empyema. 

With the onset of scarlet fever there develops a hyperleukocytosis amounting, 
according to Tileston and Locke, to from 18,000, to 40,000. After the eighth 
day, if there are no complications of an inflammatory nature, there is a gradual 
decline to the normal, somewhere about 6000 to 8000. The increase is chiefly 
in the polymorphonuclear cells. 

Schick and von Pirquet have advanced the view that the eruptive stage of 
all the exanthematous fevers is a manifestation of anaphylaxis, the time between 
infection and the appearance of the rash being that required for anaphylactic 
bodies or ergins to develop. This view is not universally accepted, but both 
Schick and Cederberg have pretty clearly shown that the late symptoms or sequelae, 
particularly postscarlatinal nephritis are due to this cause, at least in part, in 
that a state of hypersensitiveness is developed as the result of the presence of 
reaction or anaphylactic bodies which, if the system has not succeeded in eliminating 
or destroying all the germs, sensitize it to the toxic substance which the germs 
develop. As the kidneys are the organs actively engaged in excreting germs and 
toxins, these germs or poisons are present in the renal tissues in great abundance 
and this, perhaps, explains the frequency with which postscarlatinal nephritis 
develops. In those cases which escape such complications, the germs are elimi- 
nated or destroyed before the reaction bodies develop. The primary rash is toxic 
while the secondary rashes and complications are probably anaphylactic. 

Incubation. — The period of incubation of scarlet fever is about two to six days, 
but cases are recorded in which it has been as brief as twenty-four hours and as 
long as twenty-one days. Reimer gives the following figures: 1 day, 379 cases; 
2 days, 928 cases; 3 days, 751 cases. The period of incubation is, therefore, the 
shortest of all the acute exanthematous fevers. 

Symptoms. — The symptoms of an ordinary case of scarlet fever consist chiefly 
in sore throat, a moderately high fever, a scarlet rash first appearing on the chest, 
albuminuria of moderate degree, and a tendency to middle-ear inflammation. 



SCARLET FEVER 85 

The onset of the symptoms in scarlet fever is usually abrupt and the severity 
and abruptness of these symptoms is often indicative of the severity of the attack 
which is to follow. A child apparently in good health in the evening passes a 
restless night, and in the morning suddenly, without apparent cause and perhaps 
without preliminary nausea, vomits actively as soon as its breakfast is swallowed. 
Often this vomiting is almost malignant in its severity. If the temperature is 
taken, it will usually be found to be 101° or 103°, the skin feels hot and dry, the 
pulse is quick, the eyes bright, the expression listless, and the tongue and mucous 
membrane of the mouth distinctly reddened. Sometimes the first complaint 
on the part of the patient is one of sore throat, in other cases no such discomfort 
is mentioned; but if the mouth be opened the pharyngeal mucous membrane 
is seen to be angry and inflamed, and perhaps unduly dry. The child is manifestly 
ailing, is peevish, and is anxious to lie down. In from twelve to twenty-four 
hours from the manifestation of the preliminary symptoms just detailed, and in 
some cases in even less time than this, the eruption, or rash, develops, beginning 
on the neck and upper part of the chest, as a rule. 

No one of the eruptive diseases is so characteristic in its appearance as is scarlet 
fever, the skin of the patient being, as the name of the disease indicates, actually 
scarlet or as bright a red as is the shell of a boiled lobster. Again, in no other 
one of the eruptive diseases does the rash appear over so wide a surface in the 
first hours of its appearance as in scarlet fever. Not rarely the entire body and 
extremities are involved in four or five hours. 

There are four peculiarities about this rash which are worthy of note: first, 
it is punctate — that is, about each hair follicle in the skin the color is slightly 
deeper than elsewhere; second, the rash is often most marked in the folds of the 
joints, as about the groins; third, the skin of the face about the mouth or in the 
nasolabial line is pallid, forming a marked contrast to the scarlet hue elsewhere; 
and fourth, the rash on the upper part of the thorax is often very profuse. 

When the rash is developed, the sense of heat conveyed to the hand and com- 
plained of by the child is notable. The eruption persists from three to seven 
days in the majority of cases. Desquamation of the epiderm, which comes away 
in large flakes, rather than in fine bran-like scales, begins at the twelfth day but 
sometimes not until the twentieth day. The skin may literally peel off the hands 
and feet. In rare instances it may be shed from the hand in the shape of an old 
glove. This desquamation lasts from a week to three weeks, beginning about 
the neck and continuing longest on the palmar and plantar surfaces, where the 
skin is thick. Indeed, I have seen it continue between the toes for six or eight 
weeks. The period of desquamation is, however, greatly shortened, as a rule, 
if during the illness the child has been anointed by some oily substance to allay 
dermal irritation, or if during convalescence it is frequently bathed. 

The stage of invasion, already described, varies in certain cases to a considerable 
degree. It may be so mild as to lead to a belief that the rash is due to indigestion, 
and it may be so severe that the patient is first convulsed, and then speedily over- 
whelmed by toxemia. The eruption may not be widely diffused, but appear for 
a short time on the chest and abdomen, in the groin, or about the buttocks before 
it spreads elsewhere. It- may not spread farther than these areas, and may last 
only one day. Such cases are often given the unfortunate name of "scarlet rash." 
They are just as capable of giving scarlet fever to another child as a more severe 
attack. In other cases, of a malignant type, the rash seems to be suppressed, 
the skin is mottled, but the true rash fails to appear, or it may appear in blotches, 
which may seem to be macular, as in measles. When doubt exists in such cases, 
the patient will be benefited and the diagnosis cleared by a warm bath or warm 
pack to stimulate the peripheral circulation and bring out the rash. 

The temperature in scarlet fever runs its course side by side with the severity 



86 



DISEASES DUE TO A SPECIFIC INFECTION 



of the disease. It reaches its acme within a few hours from the onset, and is often 
as high as 105° within twelve hours. As a rule, this height is not maintained, 
but after twenty-four hours to three days it falls gradually to about 103°, and then 
gradually decreases daily by lysis, reaching normal, as desquamation begins, 
about the eighth or ninth day (Fig. 24). If it remains high or if a recrudescence 
occurs, some secondary trouble, such as middle-ear disease or bronchopneumonia, 
is to be sought for. 















Fig. 


24 
















DAY OF 
DISEASE 


1 


2 


3 


4 


a 





7 


s 


9 


10 


11 


12 


13 


14 


15 


io5 C 
io4 c 
™f 

102° 

ioi c 

IOO° 

99° 

NORM'L 
TEMP. 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 


M E 




A 


i/\ 


























/ 


/ 


V\ 


A 






























V 




/I 




























V 


/ 






























1/ 


i/l 






























V 


l^ 


/ 


/ 


A 










/ 


— - 












V- 


V 


/■ 


Ay 






— - 






9« 

































Chart of scarlet fever. 



In the stage in which the disease is fully developed the clinical picture presents 
very great variations in different cases. In some children with a well-developed 
rash, the systemic symptoms are so mild that it is difficult to keep the patient 
in bed, and all the manifestations seem of little moment. In others the general 
symptoms are sufficient to show that the child is seriously ill, and in still others 
of a severe type the systemic state may be one of deep toxemia, so that the child 
seems overwhelmed by the infection. The cases in which toxemia is marked are 
not necessarily those in which great glandular involvement is present, although 
both sets of symptoms may occur simultaneously. 

Sometimes the throat symptoms by their severity mask all others. Not only 
may the pharyngeal and tonsillar surfaces be ulcerated, but they may be covered 
by a false membrane, which, in some cases, is due to a concurrent diphtheria, but 
which may also be due to the streptococcus, and is always polymicrobic in nature. 
Such cases often present a horrid type of the disease, for the lips and teeth are 
covered with sordes, the tissues of the neck are infiltrated and swollen, and the 
head thrown far back to diminish pressure on the air-passages produced by the 
swelling. In such cases the general infection extends rapidly into the chest, and 
bronchial or pulmonary symptoms develop with great rapidity, thereby causing a 
fatal issue, although even with these grave complications recovery sometimes 
takes place. (See Complications.) 

If to these malignant manifestations are added a tendency to suppression of 
urine, because of the intense nephritis which has been produced, the signs of toxemia 
deepen into stupor and death ensues. Cases of this type rarely die before the 
sixth day, since this time is required to develop the condition described. There 
is, however, a fulminant form of the disease in which the malady, after being ushered 
in by severe convulsions, speedily develops into deep stupor, with hyperpyrexia 
and death. In some of these cases, however, the infection is so profound that a 
high temperature does not occur, the temperature never rising above 101°. These 
cases are very rare and are described more frequently by French clinicians than 
they are seen by Anglo-Saxon practitioners. 

A few cases are on record in which no fever has developed, and others in which 
no rash has been seen. 

Under the name "surgical scarlet fever" is described a febrile affection which 
attacks persons, usually children, after surgical operations or injuries. The term 



SCARLET FEVER 87 

is an unfortunate one, for no such malady exists as a distinct disease. The con- 
dition is an erythema due to sepsis or else it is an attack of scarlet fever coming 
on during convalescence from the operation. 

Complications and Sequelae. — Scarlet fever depends very largely for its gravity 
upon its complications and sequelse, which are not rarely met with. The most 
constant of these is a certain degree of renal irritation or inflammation. The con- 
dition of the kidneys from a time very early in the attack is such that slight albumin- 
uria may be considered a fairly constant symptom. In some instances this febrile 
albuminuria is the only evidence that the kidneys are affected, but in others the 
character of the urine and the general systemic condition render it very plain that 
a true nephritis is present. Not only does the urine of such patients show consider- 
able quantities of albumin and casts, but there is distinct puffiness of the eyelids 
and edema of the ankles, or even a generalized anasarca. In such patients, if 
this state persists, transudation may take place into the serous cavities of the 
body, and the patient suffers from the pressure produced by the fluid upon the 
heart and lungs. He may develop uremic symptoms, and these in turn may cause 
death. In many of these cases, however, the acute nephritis, responsible for 
these manifestations, speedily diminishes with the subsidence of the disease itself, 
and recovery follows with a rapidity which is extraordinary. I have seen recovery 
take place, even after the anasarca was so marked as to almost close the eyes and 
after repeated severe uremic convulsions. 

There is still another type of renal disorder met with in a few cases of scarlet 
fever in which the infection seems so intense that the kidneys are completely sup- 
pressed in their functional power very early in the attack, and in which we find 
great diminution of urinary flow, hematuria, and copious amounts of albumin 
and casts. In these cases the toxemia of the disease and that resulting from the 
renal lesions produces death in a very short time. 

Suppression of urine may be the first symptom. 

The renal changes of scarlet fever are, therefore, to be carefully watched, and 
the greatest care must be taken that the kidneys are not permitted to be additionally 
congested by the patient being chilled. Exposure during and soon after scarlet 
fever may change a mild renal state into a most desperate condition. 

A very considerable number of cases of scarlet fever give positive cultures of 
the Bacillus diphtheria? during convalescence as well as during the attack. Higgins 
states he found this organism in the nose and pharynx of no less than 25 per cent, 
of the children sent home as cured of scarlet fever. As long ago as 1898 Todd 
reported such a result in Rve cases out of 365 patients suffering from this disease. 
This is far in excess of the percentage of positive cultures in supposedly healthy 
persons. Thus in 3096 persons in communities in Massachusetts, practically free 
of the disease, the bacillus was found in only 1.4 per cent. 

As a sequel, rather than a complication of scarlet fever, inflammations of the 
joints sometimes occur. This is not acute rheumatism, but of the nature of a 
septic arthritis. Rarely the joint suppurates. The swelling does not persist, as 
a rule, if the effusion be simply serous. Another very rare sequel of scarlet fever 
is dislocation of the hip-joint. In 1804 J. Franck reported a case of dislocation of 
the hip occurring in an attack of scarlet fever. In 1894 Champenois published 
an account of three other cases, which were all he could collect from the literature. 
Since 1894 H. Stanfield Collier has reported two cases. Robert Jones, of Liverpool, 
states that one such case has come under his observation. 

Much more common that arthritic changes during or after scarlet fever are 
those which are met with in the ears, due to an extension of the septic inflammation 
from the throat through the Eustachian tube to the middle ear. These have 
already been referred to when considering the pathology of the disease. The 
physician should always be on his guard for aural inflammation in the course of 



88 DISEASES DUE TO A SPECIFIC INFECTION 

this malady and after it has run its course. Permanent deafness not rarely results 
from the otitis media due to this cause. 

Parotitis sometimes occurs as a complication. 

Next to acute articular rheumatism, scarlet fever stands as the most common 
of all the acute infections in producing valvular disease of the heart. These changes 
are in the endocardium and myocardium, and may be acute and transient or become 
permanent. Very rarely does the endocarditis become severe enough to be called 
ulcerative. Great responsibility rests upon the physician in regard to the cardiac 
changes in this disease, because, while it is true that he cannot prevent them, he 
can often, by insisting on rest during the attack and during convalescence, to a large 
extent, limit their severity, both as to their temporary and permanent character. 
This is the more important, since, as in all acute infections, the heart is often the 
seat of a myocardial change. 

Bronchopneumonia develops in a small proportion of cases. Empyema may be 
a sequel to scarlet fever, and is usually insidious in onset. 

The induration of the cervical glands, which may suppurate, has already been 
referred to. 

Nervous complications of scarlet fever, aside from delirium and convulsions 
due to the toxemia, are rare. As a sequel, chorea may develop, or hemiplegia 
arise, caused by an embolus lodging in a cerebral vessel. Very rarely an acute 
ascending paralysis, which is the result of neuritis, may develop in the lower 
limbs. 

An exceedingly rare complication of scarlet fever is peritonitis, due in all proba- 
bility to a streptococcus infection of the peritoneum. McCollom and Blake, of 
Boston, have reported two such cases in the Boston City Hospital Reports. 

Diagnosis. — While scarlet fever in its typical development is not difficult of 
diagnosis, it not infrequently happens that mild attacks render a decision as to the 
exact nature of the illness most difficult to determine. The chief reason for this 
is that children very commonly, and adults more rarely, develop a roseola or rose 
rash as a result of many different causes, and if the manifestation of scarlet fever 
be mild, or the rose rash be severe, the skin lesions may not only not aid in diagnosis, 
but greatly impede the physician in reaching a decision. The most common of 
these rose rashes is that produced by certain types of indigestion, and particularly 
that which follows eating fish, shell-fish seeming especially prone to cause it. As 
active vomiting and diarrhea and even fever may be present in such cases, the 
patient at first sight quite markedly resembles one suffering from scarlet fever; 
but the absence of sore throat, of enlarged tonsils, of enlarged cervical glands, and 
a history of no exposure to the specific fever, all aid in excluding scarlatina, 
particularly if it can be discovered that indigestible food has been ingested. Then, 
too, the rose rash of indigestion does not, as a rule, appear first on the chest. In 
some persons, with a very sensitive skin, contact with nettles or other irritants 
may cause a roseola. In all such cases the physician should not be hasty in making 
a diagnosis, but insist that enough time be given to permit him to make a careful 
study of the case for several days before expressing an opinion. In such instances 
the patient should be isolated until the diagnosis is decided. 

The rose rash sometimes met with in German measles is never as scarlet as it 
is in true scarlet fever and is distinctly maculated. Further, it appears on the 
face before it is seen on the chest, the punctation of the rash of scarlet fever is 
absent, the fever is slight and lasts but two or three days, and flaky desquamation 
does not occur. 

Roseola due to vaccination and that due to the use of diphtheria antitoxin are 
easily diagnosticated by the history of the patient. 

Should a rose rash with fever develop in an adult there is much more likelihood 
of its being due to early secondary syphilis than to scarlet fever. The rose rash 



SCARLET FEVER 89 

of syphilis is not, however, so bright a red as that of scarlatina. Such a rash, 
when due to syphilis, disappears and reappears, becomes dusky, and, finally, it is 
apt to be circinate. 

Sometimes in acute and chronic nephritis not due to scarlet fever a rose rash 
develops. The absence of throat symptoms and the signs of nephritis revealed 
by the urine aid in the differentiation. 

A condition called "erythema scarlatiniform" has a sudden onset with fever, 
and is characterized by a rash which develops rapidly over the whole body, lasts 
for several days, and ends in desquamation. The absence of throat symptoms 
in these cases is once more an important differential point. Further, the other 
symptoms are by no means so severe as the rash would lead one to expect. Such 
patients, too, usually have a history of repeated attacks. 

A factor of very great value in diagnosis is the peculiar appearance of the tongue 
in many cases of scarlet fever. At the time of onset it may have a heavy white 
coating, which soon diminishes in degree and becomes dotted with red and enlarged 
papillae. This has been called the "strawberry tongue" of scarlet fever. 

Another point of some importance is the time at which desquamation appears, 
for the mere occurrence of desquamation is by no means peculiar to scarlet fever. 
In this disease this symptom usually develops about the sixth day on the face and 
neck, and about the eighth day on the chest and back. The hands do not begin to 
desquamate until as late as the twelfth day, and the feet some days later than this. 
Other eruptions which resemble scarlet fever and desquamate, usually begin to 
shed the skin in these areas earlier than the days just named. 

In the cases of scarlet rash due to sepsis it is noteworthy that the progress of 
the malady is always aberrant or irregular, for the throat symptoms are often 
absent, the temperature is rather that of sepsis than scarlatina, and the septic 
symptoms may be severe. These cases are particularly interesting and worthy 
of the most careful, study, because antiseptics, when absorbed, sometimes produce 
a scarlatiniform rash, and because if the case be one of true scarlet fever it is a 
menace to all other children, sick or well. As the differential diagnosis of such 
cases cannot be made in some instances till the disease has lasted for some days, 
or until desquamation has begun, all patients with such symptoms should be 
promptly isolated. A focus of septic infection is to be carefully sought for. 

Under the name of the Rumpel-Leede test the following test to determine that 
scarlet fever is the cause of an illness may be resorted to, particularly in the period 
between the fading of the eruption and the beginning of desquamation, when the 
case is very infectious. A bandage like that used as a cuff in the Tycos sphygmo- 
manometer is placed around the arm and pressure is applied to the point of 
extinguishing the radial pulse. When it is removed there may be found in scarlet 
fever on the flexor surface just above the elbow several well-marked petechia? not 
there before. 

Dohle found in the polymorphonuclear leukocytes of scarlet fever certain so-called 
"inclusion bodies" which have been proved not to be pathognomonic of the disease 
although they occur with great constancy during the first five or six days of its 
onset. In some cases they fail to appear at any time. If antitoxic serum has 
been used or sepsis or streptococcic sore throat is present, their presence possesses 
no special diagnostic value as to scarlet fever. They occur in a small proportion 
of cases of measles. Boltenstern, who has exhaustively considered their value 
in diagnosis believes that they are a distinct aid, but Ker, who is a Medical Superin- 
tendent of the Edinburgh City Hospital, believes that this aid to diagnosis "is 
hardly worth the trouble entailed." He believes that it is of most value in separat- 
ing serum rashes from true scarlet fever. These "inclusion bodies" occur as 
round or oval granules, of which one or two may be found in the protoplasm of 
the cell. They stain well with Manson's stain or with carbol-methyl blue. In 



90 DISEASES DUE TO A SPECIFIC INFECTION 

addition to these granules other shapes which are spiral or rod-like in appearance 
also occur. 

Prognosis. — This varies greatly in different epidemics and depends largely upon 
the severity of the symptoms in a given case. The malady is always to be con- 
sidered a grave one. The actual mortality is shown in the following statistics. 
Of 26,921 cases of scarlet fever, 3216, or 11.9 per cent., were fatal. Holt states 
that the average mortality is from 10 to 14 per cent., but for children under five 
years of age the mortality varies from 20 to 30 per cent. (See Fig. 25.) The 
diminution of mortality after the first decade of life is noteworthy. 

Treatment. — In the treatment of scarlet fever the fact must never be lost sight 
of that the disease is self-limited, that it is bound to run its course, and the most 
the physician can do is to guide his patient through the illness with the hope that 
complications may be avoided and that severe symptoms may be modified. 

First and foremost in the treatment of this malady, it is essential that the patient 
have hygienic surroundings, with plenty of fresh air and careful avoidance of 
draughts and exposure to sudden changes of temperature, since such exposures 
by chilling the surface of the body are almost certain to exaggerate the renal con- 
gestion or inflammation which is practically always present during the acute 
stages of this disease. Indeed, it may be said that the prime object of the physician 
and nurse, from the beginning to the end of the attack, is to use every effort to 
avoid sources of irritation to the kidneys, for it cannot be doubted that many 
cases of serious renal difficulty which arise in connection with scarlet fever depend 
upon carelessness in this respect. It is also important to remember that these 
precautions in regard to exposure are not only necessary during the acute attack, 
but until convalescence has been thoroughly completed and until the urine no 
longer shows any evidence whatever of renal irritation. As these lines are written 
I have seen in consultation a boy, aged fourteen years, who apparently had recovered 
entirely from an attack of scarlet fever, except that there was still some desquama- 
tion in the palms of his hands. He was allowed to play ball out-of-doors, became 
overheated and then chilled, and within forty-eight hours suffered violent uremic 
convulsions, which nearly cost him his life. 

Medicinally, it is usually well in cases of scarlet fever to prescribe from the first 
a mild alkaline diuretic, of which, perhaps, the best is 5 grains of citrate of potassium 
with 20 drops of sweet spirit of nitre in water three or four times a day to a child 
of eight years, giving at the same time copious quantities of such pure water as 
the non-sparkling water from Poland Springs, or any other spring-water which 
contains a very small amount of organic and inorganic matter. By these means 
we flush the kidneys of toxic substances which in a concentrated form might produce 
serious renal irritation. 

The second point of therapeutic importance is the condition of the throat. If 
the child is old enough to gargle its throat with a weak solution of chlorate of 
potash (3 or 5 grains to the ounce) four or five times a day, such a gargle is useful 
from the very beginning to the end of the attack. When the inflammatory changes 
in the pharynx are severe, the part may be cleansed with a spray of peroxide of 
hydrogen, or this drug may be applied by means of a cotton applicator, the throat 
being afterward cleansed by a spray of Dobell's solution. For the pseudomem- 
branous pharyngitis which sometimes develops, a similar local treatment is advisable, 
and, combined with this, both diphtheria antitoxin and antistreptococcic serum 
should be given. If the false membrane be due to the Klebs-Loeffler bacillus, 
diphtheria antitoxin is certainly indicated, and, as the streptococcus is always 
present in scarlet fever, and is probably responsible for the formation of false 
membranes in some cases, the use of serums designed to antagonize both of these 
poisons is manifestly rational. 

For the relief of the intense burning and itching of the skin which is present in 



SCARLET FEVER 



91 



some cases, the child may be anointed with olive oil containing 0.5 to 1 per cent, 
of carbolic acid, or weak carbolized vaselin may be used. Sometimes a very 
distinct fall in temperature can be produced by 
allaying irritation of the skin in this manner. 

Should the fever become high enough to deserve 
attention — that is, if it persistently remains above 
103° or if it occasionally rises as high as 105° — 
the patient should be sponged with tepid water 
and alcohol, a small ice-bag being simultaneously 
applied to the head. Such a sponging, given early 
in the evening, will, by diminishing the irritation 
of the skin and quieting the peripheral sensory 
nerves, often cause the child to pass a comfortable 
night. The antipyretic coal-tar drugs are contra- 
indicated in these cases, except under extraordin- 
ary circumstances. 

If intense nervous irritation is present, 5 or 10 
grains of the bromide of strontium or sodium may 
be given several times a day. Full doses of chloral 
have been highly recommended, but they are often 
contra-indicated because of the irritant effects 
upon the kidneys and the depressant influence 
upon the heart. Should evidence of circulatory 
failure develop, small doses of an old brandy 
poured over shaved ice, or given in cool water, 
may be administered every two or three hours 
with advantage. Or, small doses, frequently re- 
peated, of aromatic spirit of ammonia may be 
used in the same manner. If the circulatory 
failure is acute or sudden, either the aromatic 
spirit of ammonia or Hoffmann's anodyne should 
be used as rapidly acting diffusible stimulants. 

Pain in the ear should be relieved by irriga- 
ting the external auditory canal with normal 
salt solution as hot as the child can bear it. In 
all these cases a careful examination of the ear- 
drum should be made twice a day to see whether 
there is any bulging due to accumulated secretion 
or suppuration in the middle ear, and if this is 
present paracentesis of the tympanum should be 
performed at once to relieve the pain and avoid 
danger of infection of the mastoid cells. 

If evidences of septicemia are present and the 
patient seems anemic, either during the later stages 
of the attack or during convalescence, the tincture 
of the chloride of iron, in the dose of 5 drops three 
or four times a day, is advantageous, since it tends 
to combat the anemia and the infection and also 
exercises a slight stimulant influence upon the 
kidneys. For the relief of persistent albuminuria 
after the attack is passed, the child should be 
prevented from taking excessive exercise, but, 
nevertheless, should live in the sunshine as much as possible, and may take 
either small doses of the tincture of chloride of iron or a very minute dose of 





















Fig. 


25 






















LU < 

D LU 

z >- 

3 r- 


5 ° 

UJ Q 

5 Z 

1- < 

LU r- 
DQ 


z o 

i * 
<~ < 

LU 

DQ If) 


z 2 

LU 

LU Q 

i 5 

LU O 

LTQ ,_ 


z ° 

LU <M 
LU Q 

^ z 

1- < 


58 












































57 












































50 














f 






























55 










































- 


51 










































53 












































52 












































51 












































50 












































19 












































18 












































17 








































lb 












































15 












j 
































11 












J 




























13 












_[ 
































12 












| 
































11 












1 






























- 


10 












7 


























39 












T 






























38 












T 
































37 












1 
































36 












j 








. _ 
























35 












7 








. 
























31 












































33 




















' 
























32 












































31 












































30 




















| 
























29 












































28 












































27 












































20 




















1 






1 


















25 












































21 












































23 












































22 




















1 
























21 




















l 
























20 






















\ 






















18 






















\ 






















18 












































17 












































10 












































15 
























I 




















11 
























\ 




















13 
























\ 




















12 






1 






































11 






j 


















\ 




















10 






l 




















I 


















9 












































8 


























\ 


















7 


























\ 


















6 


























\ 


















5 












































1 












































3 












































2 












































1 











































Showing the mortality of scarlet 
fever according to age, based on Johan- 
nessen's 9855 cases. 



92 DISEASES DUE TO A SPECIFIC INFECTION 

the tincture of cantharides — say, \ to 1 drop twice or thrice a day, well diluted; 
but the cantharides is contra-indicated if the microscope shows in the urine the 
presence of red blood cells, indicating that the kidneys are still acutely inflamed. 

In those cases of scarlet fever in which the rash fails to develop its full efflorescence 
promptly, and particularly in those cases in which the skin is mottled and marbled, 
indicating poor capillary circulation, it is exceedingly useful to immerse the child 
in a hot bath. In other cases the cool-warm pack may be used. This consists 
in stripping the child of its night-clothing and rolling it in a sheet which has been 
dipped in warm water, which, by the time it is wrapped around the child, has 
become considerably cooled by evaporation. As soon as the sheet is wrapped about 
the child, an ice-bag being in the meantime applied to the head, it is wrapped in a 
blanket, and in a few moments the heat of the child's body transforms the cool 
sheet into a warm pack. The primary effect of the cool sheet is to drive the stagnant 
blood out of the peripheral capillaries, and the effect of the warm sheet is to bring 
new blood into these vessels. By these means we are very frequently enabled 
not only to improve the circulation and develop the rash, but to diminish the toxic 
symptoms and relieve nervous stress. It is hardly necessary to add that exposure 
for any length of time to the cool sheet is to be avoided. The blanket is to be 
placed tightly about the child at the earliest possible moment after the cool sheet 
comes in contact with its body, so that the chilling of the surface will be only 
instantaneous. French therapeutists, and some other practitioners, have advised 
that in those cases in which cerebral symptoms are very marked and toxemia 
is evidently profound, the child should be placed in a warm bath, and that cool 
water should be poured over its head,- neck, and chest for a moment, in order to 
produce a certain amount of shock and rouse the flagging powers of the body. 
This method has been so highly endorsed by excellent practitioners that it cannot 
be condemned for theoretical reasons, but the author has never been brave enough 
to employ it. 

Within the last few years several attempts have been made to produce an anti- 
scarlatinal serum without very satisfactory therapeutic results. In the cases 
in which the author has directed its use, it has seemed to modify the throat symp- 
toms, but otherwise it has not affected the progress of the disease. 

MEASLES. 

Definition. — Measles is an acute infectious disease, usually epidemic, which 
most commonly attacks children and rarely occurs after the second decade of 
life. The skin during an attack is covered more or less profusely by a dusky red 
eruption of a maculopapular type. The eyes are congested and lachrymose, and 
the nasal and pharyngeal mucous membranes swollen and red. One attack usually 
confers immunity. Measles is sometimes called " Morbilli" 

Distribution. — Measles is met with in all parts of the civilized world. If by 
chance it is carried to a people who, by reason of isolation, have not been exposed 
in previous generations to its effects, it often develops a malignant form and 
causes a great mortality. Perhaps the most noteworthy example of this is the 
case of the inhabitants of certain of the Fiji Islands, who, being exposed to the 
infection, fell ill and died by thousands, so that it is estimated that 20,000 deaths 
occurred in four months. The epidemic ceased only after every person on the 
islands had been infected. 

The susceptibility of children in the first ten years of life to the infection is 
quite remarkable. If a large number who have not been rendered immune by a 
previous attack are exposed to the infection, nearly all fall sick. Smith and Dabney 
report an instance in which 110 children between eight and eighteen years of age 
were exposed, and only 2 were not taken ill. 






MEASLES 93 

Measles is much more prevalent in the spring and winter months than in the 
summer months, probably because the open-air life and free ventilation of the 
warmer season aids in preventing the exposure of susceptible persons to a concen- 
trated form of the contagion. 

Etiology. — Measles is in all probability due to a distinct microorganism but 
so far it has not been isolated. It belongs to the ultramicroscopic group and passes 
through a Berkefeld filter. It resists freezing twenty-four hours. 

Hektoen first transmitted the disease from man to man by means of the blood 
in 1905, and Anderson and Goldberger have produced the disease in monkeys 
when using blood obtained less than fourteen hours after the onset of the eruption. 
They also showed that discharges from the mouth and nose in the first twenty- 
four hours transmitted the disease. The desquamated skin failed to transmit the 
malady. 

The disease spreads with great readiness through the air and contact with the 
patient or his garments is not necessary for its transmission, although such contact, 
of course, provides the infection in more concentrated form. There is no doubt 
that the breath of a patient suffering from measles carries the infection, and so 
does the nasal and pharyngeal mucus, so that the expulsion of these secretions 
by coughing or sneezing may result in nurses or visitors becoming a means of 
transmitting the disease by their garments becoming contaminated in this manner. 

Very short exposure to infected air is sufficient for infection, and even when 
careful precautions are taken to prevent the spread of the disease it not infrequently 
happens that all the other children in a house develop the malady, partly because 
it is infectious from the earliest period of invasion before its presence is recognized, 
but largely because of the ease with which it is conveyed by the air. This great 
diffusibility of the virus of measles is quite in contrast with the limited diffusibility 
of the poison of scarlet fever. 

Although it is true that the diffusibility and activity of the infection of measles 
is exceedingly active while the disease lasts, it is also a fact that it speedily disappears 
after convalescence is established. Three weeks after the attack begins, the patient 
rarely transmits the disease, and by this time, with ordinary ventilation, the room 
and surroundings of the patient are usually innocuous. Any condition of ill-health 
which diminishes vital resistance very distinctly increases the susceptibility of an 
individual to infection, and in these instances the disease is prone to be severe. 

The period of incubation of measles is usually from eleven to fifteen days but 
cases are recorded in which the disease began one week after exposure. 

Prevention. — Measles is to be prevented by complete isolation of the patient, 
by the disinfection of all garments of the patient and nurse before they leave the 
sick-room, and by free ventilation, so arranged that the other, rooms in the house 
are not exposed to a draught from the sick-room. After the attack has passed 
the patient should be given several hot baths to rid the body of all desquamating 
skin, and the scalp should be cleansed with special care. The period of isolation 
should be 15 days. 

Frequency. — Measles is one of the most common of the acute exanthemata 
and affects nearly all persons living in cities before they reach adult life. Indeed, 
it may be said to be the most common of all diseases in childhood. 

Pathology and Morbid Anatomy. — There are no noteworthy changes produced 
in the various viscera by measles, if we exclude those ordinarily considered as 
complications and the changes in the mucous membranes of the respiratory and 
digestive tract, consisting of acute irritation and catarrh. With the onset of the 
disease these membranes become hyperemic, and, it may be, dotted with an eruption 
much like that which is seen on the skin. 

The pathological changes due to complications are chiefly those of bronchitis 
and bronchopneumonia, conditions which are exceedingly common in young 



94 



DISEASES DUE TO A SPECIFIC INFECTION 



children, and in patients who are poorly nursed and badly nourished, when suffering 
from acute infectious diseases. 

Symptoms. — Measles is usually ushered in by the symptoms of an ordinary 
cold or attack of coryza. There may be an initial chill, but this is often absent, 
the fever being the first additional symptom which becomes manifest. The patient's 
face looks flushed and, it may be slightly swollen about the eyes and nose, and the 
conjunctivae are injected, the general expression of the face being tearful. At 
this time, and later, in the disease photophobia may be marked. Sneezing may 
be noticeably frequent, and an examination of the pharynx will reveal the fact 
that its mucous membrane is reddened and the hard palate dotted with a measles- 
like rash, which often appears here before it develops on the skin. Some cough 
may be present in the stage of onset as the result of the pharyngeal and laryngeal 
irritation, and headache may be complained of. 

Fig. 26 



3 2 

D 102 

8 

: o 



t 4 
L 1! 
.100 



N0RMAL4 

98 

































































































































H 






































+ 1 






































X t 






































4t t 


1 




































H r 


1 


































_ 


n 




































\ 


P— J 




































l- A 


F3 




































. ft 


U 




































u 


tf 




































-. 


► At 


























,-i 










L4 4 


I 4- 


























1 








A 


/ 1 


V 
































A 


/\ 


Q t 


































A 


/ > 


A t 


1 
































\ 




u " 


z\ 


























1 






1 ' 


, 


IE 


J 






























-j 


- f 


t 


* \- 


M - 


-\ 


1 


























i 




j 


_ \- 


=5 = 


-\ 


\- 
























1 


/ 


1 




A- 


_ \r __ 


/ 


1 
























1 


1 






4. 


x 


IT 


























1 


/ 










-»- 




A 






















/ 










_ 1 






l\ 






















I / 














\ ; 


1 \ 






















v 














\y 




\ 


































1/ 




\ 


A 




K 




























J 




^ 


\ 


, 1 


' \ 




































v 




\> 


A 




































V 


V ,• 
































\S 





































Showing initial fever with the subsequent fall and then a rise when the rash is well developed 
in a case of measles. Also shows an ending of the fever by crisis. 



There are present in many cases upon the buccal mucous membrane before the 
rash develops a. number of small, white-tipped, reddish spots first described by 
Filaton, but more commonly called "Koplik's spots." (See Plate III.) When 
present they are pathognomonic of measles, but their absence does not negative 
the diagnosis of the presence of this disease. 

The fever usually begins to rise with the onset of the catarrhal symptoms, increas- 
ing day by day till it reaches its acme of 103° to 105° on the fourth or fifth day 
from invasion, and remains fairly constant at about this level until the rash begins 
to fade, on the fifth to the seventh day, when the fever ceases abruptly or by lysis, 
reaching normal in a few hours or by the end of two or three days (Fig. 26). 

The eruption of measles develops on the third or fourth day of the disease, and 
at first is most marked back of the ears and about the roots of the hair or on the 
forehead. The individual spots look like a flea-bite and are rather dusky red in 
appearance. By the end of twenty-four hours or at the expiration of the fifth 
day this rash is usually pretty well diffused all over the body, and the macular 
appearance of the eruption begins to become papular, so that it can be distinctly 
felt by the finger-tip of the physician. This rash varies greatly in its degree. 
Sometimes it is so profuse that every part of the body is covered; in other instances 
very considerable spaces of unaffected skin can be found between the groups of 
papules. It has been generally stated that the crescentic arrangement or grouping 



PLATE III 



Fig. 1 



Fig, 2 





Fig. 4 



Fig. 3 





The Pathognomonic Sign of Measles (Koplik's Spots). 



Fig. 1. — The discrete measles spots on the buccal or labial mucous membrane, showing the isolated 
rose-red spot, with the minute bluish-white centre, on the normally colored mucous membrane. 

Fig. 2. — Shows the partially diffuse eruption on the mucous membrane of the cheeks and lips; patches 
of pale pink interspersed among rose-red patches, the latter showing numerous pale bluish-white spots. 

Fig. 3. — The appearance of the buccal or labial mucous membrane when the measles spots completely 
coalesce and give a diffuse redness, with the myriads of bluish-white specks. The exanthema on the skin 
is at this time generally fully developed. 



Fig. 4. — Aphthous stomatitis apt to be mistaken for measles spots. 
Minute yellow points are surrounded by a red area. Always discrete. 



Mucous membrane normal in hue. 



MEASLES 95 

of the rash is diagnostic of measles. That this is erroneous the author is convinced, 
as he has frequently seen it occur in other morbilliform eruptions. When the 
disease is in its fully developed stage the skin of the face may be quite swollen 
and that of the neck and chest well covered by the eruption ; but as the lower part 
of the trunk and the lower limbs become involved the rash on the face usually 
begins to diminish and slowly fades, leaving for several days after it has entirely 
disappeared, a faint mottling of the skin with the desquamation of branny scales, 
which is scanty in some cases, but profuse in those who have had an intense 
eruption. The entire duration of the rash is from five days to one week, and the 
period of desquamation lasts for about the same length of time. Occasionally the 
patient suffers from prodromal rashes such as a punctate erythema which begins 
on the trunk instead of the face. Sometimes it develops on the limbs. Such a 
rash may at first be thought due to scarlet fever. In other cases a papular 
erythema may be present. 

Hecker and others have proved that during the last few days of incubation and 
during the course of the eruption in measles there is constantly present a distinct 
leukopenia. It is so constant that he proposes to use it as a diagnostic aid, asserting 
that the leukopenia is present four and a half days before the outbreak, and three 
and a half days before the appearance of Koplik's spots. Two or three days before 
the eruption there may be a temporary increase in leukocytes. The decrease 
is almost solely in lymphocytes, the neutrophiles being relatively in excess. Indeed 
a diminution of lymphocytes may be present six days before the eruption. 

During the well-developed stage of the disease the patient nearly always presents 
some symptoms of bronchitis. These may be so mild as to be undemonstrable, 
or so severe as to threaten life. The thorax should be frequently examined, in 
order that the development of this complication may be recognized and its severe 
effects, as far as possible, avoided. 

Variations. — It must not be thought, however, that measles always follows the 
course just described. All the acute infections present widely different symptoms 
in different epidemics and in different persons, and measles is no exception to 
this rule, for in some cases the systemic or constitutional disturbance is so slight 
as to be of no importance, whereas in others it is exceedingly severe. In strong, 
hearty children the course of measles is rarely grave if they are protected from cold 
and exposure, whereas in puny, badly nourished infants it is one of the most fatal 
maladies. 

The following variations from the ordinary course of measles are met with: 

A mild type, with a scanty rash and almost no constitutional disturbance, 
which runs its course without complications if ordinary care is exercised. 

A severe type, in which nervous and constitutional symptoms predominate, 
in which the eruption may be exceedingly profuse, but is more commonly indistinct 
or poorly developed, perhaps because of poor circulation in the skin by reason of 
toxemia. 

Another severe type is known as hemorrhagic or "black" measles, because 
of the tendency to the occurrence of hemorrhages in the skin. Still another form 
is a respiratory type, in which the patient may suffer from great laryngeal and 
tracheal distress or from a serious bronchopneumonia. It is often said of these 
cases by the laity that the rash has been driven in by exposure to cold and is exerting 
its deleterious influence on the lungs. This is not exactly true, but it is, neverthe- 
less, a fact that when we can, by means of a hot pack, restore the peripheral circula- 
tion and so indirectly cause the rash to be manifest, the symptoms of toxemia 
and respiratory disorder often become decidedly less. 

Rare cases are met with in which, after vomiting, purging, convulsions, and 
coma, death speedily occurs, even before the rash has had time to become well 
marked. 



96 DISEASES DUE TO A SPECIFIC INFECTION 

Complications and Sequelae. — It has already been intimated that measles in 
itself is a disease which, in most individuals, with ordinary care, pursues a safe 
course and ends in recovery. While this is undoubtedly true, it is also a fact that 
it takes high rank among the acute infectious diseases which produce death, by 
reason of the complications which are prone to occur. 

Of all these by far the most frequent and deadly is bronchopneumonia, a complica- 
tion which is often severe in its course and which causes a great number of deaths 
when measles attacks young infants. The physical signs and symptoms are 
described in full in the article on that disease, but it is important to remember 
that in measles the disease is insidious and speedy in its onset, so that a pneumonia 
may be developed before the physician discovers it, unless he be on his guard and 
resorts to frequent examinations of the chest. Bronchopneumonia during an 
attack of measles in a child under one year of age is an exceedingly common and 
very grave complication of the disease. In children of five years or more this 
complication usually does not occur if the primary state of the health is fairly good 
and if careful nursing prevents exposure to "catching cold." 

A second complication of far less importance than bronchopneumonia, both 
as to frequency and results, is diarrhea and vomiting due to a catarrhal state of 
the bowels and stomach. It also is a complication which is due in a considerable 
proportion of cases to bad nursing and can generally be avoided by proper feeding 
and the avoidance of draughts. It not infrequently happens that these digestive 
disturbances are mild during the acute illness, while the patient is required to be 
prudent and quiet, and become pronounced when the acute illness is past and the 
attendants become careless as to exposure and feeding. This gastro-intestinal 
disorder varies from a mild catarrh to a severe enterocolitis. 

Another complication seen in many cases is a mild degree of stomatitis, which 
in poorly nourished children may become ulcerative. Even so severe and fatal 
a lesion as noma may develop in cases with very low vitality. Very rarely gangren- 
ous ulceration of the ear, the labiae, or the prepuce takes place. 

So far as the nervous system is concerned, it may be said that it is rarely affected. 
In the stage of onset in very young children with poor resistance and an unstable 
nervous system there may be convulsions, but they are exceedingly rare. Meningi- 
tis as a sequel to measles is also very rare. Even meningitis due to middle-ear 
disease is rarely met with, for the otitis of measles, while not uncommon, is usually 
mild and rarely causes secondary lesions. 

The eyes are usually inflamed and there may be a mucopurulent conjunctivitis, 
or, if the general health be poor, keratitis may prove troublesome. So rarely are 
the heart and kidneys affected to any serious degree that these organs may be 
considered almost immune. A feebleness of the heart due to the infection and 
fever may be present for a time, and a transient albuminuria is often manifested, 
but both of these symptoms usually rapidly disappear if the patient is kept at rest. 

Measles is an infection which is not rarely complicated by other acute infections. 
Diphtheria may develop during its course, and whooping-cough is so exceedingly 
frequent that some relation between the two diseases has been thought to exist. 
When whooping-cough does occur as a complication the danger of brochopneu- 
monia is greatly increased. Still another sequel of measles is tuberculosis, probably 
because the catarrhal state of the mucous membranes offers a path for infection 
by the tubercle bacillus or because the devitalizing influence of measles permits 
an old focus of tuberculous infection to become active. 

The persistence of a febrile movement in a case of measles after seven days 
should always arouse the suspicion of some inflammatory complication which 
should be most carefully searched for. Neumark calls attention to the value of 
leukocytosis as indicating a complication, the leukocytes being about in number 
normal in uncomplicated measles. 



MEASLES 



97 



Fig. 27 



Diagnosis.— Measles must be carefully separated from a large number of con- 
ditions which somewhat resemble it. Many kinds of food, particularly shell-fish, 
produce a rash which looks remarkably like measles, but which usually lasts only 
a few hours, but the watering and hyperemic eyes and swollen visage of measles 
are not present. Antipyretic or other coal-tar products do likewise in some persons, 
and the physician should always inquire as to the use of these foods or drugs 
before stating that measles is present. Sometimes a morbilliform rash follows 
vaccination or precedes smallpox. The use of antidiphtheritic serum may also 
cause such an eruption. The contact of a cater- 
pillar with the skin in some persons may cause 
a measles-like eruption which lasts only a few 
hours. None of these states, however, are ac- 
companied by the appearance of Koplik's spots, 
by marked coryza, nor by the appearance of 
the rash on the mucous membrane of the soft 
palate. Fever, too, is usually absent. (For 
the diagnosis from Rotheln, see Rubella.) 

Prognosis. — From what has already been 
said it is evident that the prognosis in a case 
of measles is dependent not on the fact that 
measles has developed, but rather upon the 
age of the patient, the vital resistance or the 
general condition of the system, and the sur- 
roundings as to sanitation and nursing. Given 
a poorly nourished infant in bad surroundings 
and with inefficient care, measles becomes one 
of the most fatal diseases to be met with, 
whereas in a case where these conditions are 
good the prognosis is fairly favorable. We 
find, too, that the danger of the disease de- 
creases greatly with each year of life; so that 
children near puberty rarely die from this 
malady unless poorly nourished or badly ne- 
glected (Fig. 27). If bronchopneumonia de- 
velops, the prognosis must be guarded in direct 
proportion to the youth of the child. Thus, 
out of a series of 408 cases of measles complica- 
ted in this manner, 290, or 71 per cent., died. 
This, however, is an exceedingly high figure 
and by no means represents the death rate in a 
general run of cases in which all ages and 
conditions of patients are considered. Under 
these conditions the death rate for all cases 
is probably about 35 per cent. Thus, Holt 
speaks of an epidemic in the Nursery and 
Child's Hospital in New York in 1892, in which 

the mortality was 35 per cent., and in 9239 cases of measles occurring in France, 
principally in hospitals of Paris, there were 3096 deaths, or a mortality of 33.5 
per cent. It is, moreover, to be carefully borne in mind that hospital or asylum 
statistics are utterly worthless in determining the death rate for ordinary private 
practice, because most of these hospital cases are primarily in bad health or are 
brought to the hospital desperately ill from neglect. Including all cases in private 
practice the mortality should not be over 5 to 10 per cent., and in many epi- 
demics it is much lower, even in institutions and where good nursing is not to be 



UJ 

(3 

< 

H 
Z 

UJ 

O 

<r 

UJ 
Q- 


cc en 

UJ < 

Q UJ 

z > 


z 

UJ CM 

UJ Q 

$ z 

1- < 

UJ .- 

CO 


z 

UJ "> 
UJ Q 

M 

UJ OJ 

CO 


z 

UJ <*■ 
UJ Q 

£ z 

1- < 

UJ en 
CO 


z 

uj m 

UJ Q 

<: z 

1- < 

UJ <4- 
CQ 


40 














































39 










A 




































38 










\ 




































37 














































36 








J 


1 


\ 


































35 














































34 








_]_ 






\ 
































33 














\ 
































32 








/ 






\ 
































31 














































30 














































29 








_J . 








\ 






























28 








/ 






































27 








/ 








] 






























26 








H 






































25 






1 












\ 




























24 


















\ 




























23 












































22 






! 














\ 


























21 




















\ 


i 
























20 






| 
















\ 
























19 






[ 
















\ 
























18 
























V 






















17 
























\ 






















16 














































15 














































14 














































13 














































12 














































11 














































10 














































9 














































8 














































7 














































6 














































5 














































4 














































3 















































Showing the mortality of measles 
according to age, based on 29,464 cases 
collected by H. Courtenay Fox. 



98 DISEASES DUE TO A SPECIFIC INFECTION 

had. Thus, in an epidemic in the Faroe Islands only 8 cases out of 1123 cases 
died, and at the Boston City Hospital only 5 were fatal out of 366. 

Treatment. — When measles runs a natural course, little or no medication is 
required; for, as it is a self-limited disease, it cannot be jugulated. The therapeutics 
of an attack of measles, therefore, consists in the prevention of complications and 
the relief of symptoms which are so prominent as to be distressing or perhaps even 
dangerous. In order to avoid irritation of the eyes and to lessen the suffering 
due to photophobia the sick-room should be kept dark. Light bed-covering should 
be employed, and heavy quilts which cause the child to perspire unnecessarily 
are to be tabooed. As a mild gastro-intestinal catarrh is often present with the 
fever, food should be light, given at frequent intervals, and should consist chiefly 
of nutritious fluids, such as the various broths, milk, an egg boiled only one minute, 
and similar substances. 

If the irritation of the conjunctivae is marked, eye drops, composed of 4 grains 
of common salt and 4 grains of boric acid to an ounce of water, may be used several 
times a day; and if the cough is sufficiently constant to prevent sleep, it may be 
controlled by small doses of codeine, •£$ of a grain once, twice, or thrice in twenty- 
four hours, to a child of two years, or heroin may be used. Should the fever reach 
105° there is usually no necessity of reducing it owing to its short duration, but the 
child's comfort can be much increased by sponging it with tepid water and alcohol, 
or even with water at 70°, using active friction at the same time. These cases do 
not need an immersion bath and it is not wise to give it to them. If the circulation 
has a tendency to fail, carbonate of ammonium in the dose of 2 grains four or 
five times a day may be given in syrup of acacia. For the relief of headache a 
small ice-bag may be applied to the head, provided that a nurse is at hand to 
prevent it from slipping down upon the neck, or about the ears, and also to prevent 
it from wetting the pillow. It should usually be wrapped in a towel to prevent 
the accumulation of moisture, and also to protect the head from too great cold. 

In cases in which the rash is not well developed and the skin is dusky in hue, 
the brief use of a hot pack is very useful. 

Should diphtheria arise as a complication antitoxin should be given. 

After the disease has run its course, convalescence should be aided by the use 
of simple bitter tonics, the hypophosphites, iron, and arsenic, and, if malnutrition 
is present, cod-liver oil proves itself an exceedingly valuable remedy, since it im- 
proves the nutrition of the patient and exercises a most beneficial effect upon the 
mucous membranes. If the bronchitis is persistent and a considerable quantity 
of mucus is in the bronchial tubes, 3 grains of chloride of ammonium may be given 
in a teaspoonful of fluid extract of liquorice and a teaspoonful of water three or 
four times a day, and gentle counter-irritation in the form of chloroform liniment 
or ammonia liniment may be applied to the chest. After the eruption has dis- 
appeared and desquamation has begun, the child should be bathed daily in order 
that the skin may be thoroughly rid of dead epithelium; and before the patient 
plays with other children the scalp should be shampooed several times, since not 
infrequently desquamation continues upon the head long after it has ceased upon 
the trunk. 

For a long time after the rash of measles has disappeared the greatest care should 
be exercised that the patient is protected from exposure, as acute and chronic 
catarrhs of any or all the mucous membranes are very prone to develop under very 
slight provocation. 

RUBELLA. 

Definition. — Rubella is sometimes called " Rotheln" or "German measles, ""Rubeola 
notha," "Epidemic Roseola," and "Hybrid Scarlet Fever." It is a disease distinct 
from measles and scarlet fever, and is one of the mild acute infectious eruptive 



MUMPS t 99 

diseases of childhood. It rarely affects adults. Johann Seitz studied an epidemic 
involving 21 families and comprising 111 cases, and found that 4 per cent, of all 
adults were attacked. The ratio for children was much higher, being 64 per cent. 
Rubella occurs as a rule in epidemics, but sporadic cases are met with. 

Etiology. — The microorganism of this affection has not been isolated, but the 
disease is distinctly infectious and is contracted by one patient from another, not 
only by contact, but also by clothing and through the air. 

Symptoms. — After a period of incubation lasting from ten to twelve days the 
stage of onset manifests itself by chilliness, general malaise, some running of the 
eyes and nose, but there is not marked reddening of the conjunctiva. As early 
as the first day of the illness the rash appears as a macular eruption which is red 
in hue, but is not scarlet. This is a so-called "rose rash." In some cases, however, 
this rash does not develop till the third day. The rash shows itself first on the 
face, then on the anterior surface of the thorax, and speedily covers the entire 
body. It is not as scarlet as in scarlet fever nor so dusky as in measles. It can 
often be seen on the soft palate before it appears on the skin, in the form of bright 
rosy-red spots (Forchheimer's spots) . The individual macules may remain separate 
or coalesce. In some instances, however, the skin has a diffuse redness like that of 
scarlet fever, but it is less scarlet. The macules last about three days and then 
fade gradually, being usually, but not always, followed by slight scaly desquamation. 
As a rule the rash on the face fades at about the time it becomes well developed 
on the lower part of the trunk. The skin is rarely as much stained after the rash 
disappears as it is after measles. 

A noteworthy sign to be sought for is the enlargement of the lymph nodes. They 
feel like a string of beads below the ears, in the lateral cervical region, and at the 
back of the neck. Sometimes the inguinal glands are also affected. 

The febrile movement is usually very moderate, the temperature often not rising 
above 100°. The general symptoms may be so mild that the attention of the 
nurse is first called to the illness by the rash. 

If the child is carefully nursed and clothed and properly fed, the malady pursues 
a rapid course of recovery. If, on the other hand, the child be feeble and exhausted, 
this disease may be severe in its manifestation and be accompanied by otitis media, 
catarrhal pneumonia, or even albuminuria and jaundice. Isolation should be 
kept up for ten days. 

Diagnosis. — Rubella is to be separated from true measles by the moderate 
character of the coryza, by the absence of Koplik's spots, the early swelling of 
the glands in the neck, and by the absence of bronchial irritation. From scarlet 
fever it is separated by the absence of high fever and of the well-diffused scarlet 
rash, which is not macular, and by the absence of the sore throat of that affection. 
Vomiting in onset is rare in rubella but very common in scarlet fever. While 
these differential points are of value in many cases, it is a fact that in some instances 
a diagnosis is most difficult until the case has been studied for some days, when the 
mildness of the symptoms and the brevity of the attack aid in deciding that neither 
measles nor scarlatina are present. For this reason careful isolation should be 
practised. If the rash lasts more than three days it is probably not German 
measles. The presence of albuminuria and nephritis points to scarlet fever. 

Treatment. — The treatment of rotheln consists in rest in bed and the use of 
spirit of nitrous ether and citrate of potash as diuretics, and in attention to the 
bowels and kidneys. Exposure to cold should, of course, be avoided. 

MUMPS. 

Definition. — Mumps, or epidemic parotitis, is an acute infectious disease affecting 
the parotid gland and accompanied by mild systemic symptoms which may not 



100 DISEASES DUE TO A SPECIFIC INFECTION 

be severe enough to demand notice. It occurs in the great majority of instances 
during childhood, between the fourth year and puberty, and one attack protects 
the patient from a second. 

Etiology. — Mumps is usually conveyed by contact from one patient to another, 
but it may be carried by a third person or by garments to a susceptible individual. 
It is contagious from the beginning to the end of the attack, and it is probable 
that persons who have so far recovered as to have no visible swelling of the parotids 
can still transmit the disease. For this reason the patient should be kept separate 
from other children for a period of three weeks after the swelling disappears. It 
is, however, a noteworthy fact that mumps is by no means so infectious as are the 
eruptive fevers, and many children escape the disease even when thoroughly 
exposed to it. 

The period of incubation is uncertain. Sometimes it is brief, in other cases 
surprisingly prolonged. Holt, in 42 cases collected from literature, found it varied 
from three to twenty-five days. In all probability it is about fifteen days in the 
average case. 

Pathology. — The chief change in mumps, and, indeed, the only one which is 
characteristic, is the swelling of one or both parotid glands. The swelling is due 
to a primary parenchymatous inflammation, followed by involvement of the 
connective tissue of the gland as well. Rarely the other salivary glands become 
swollen, and still more rarely the parotids suppurate. This result occurs only 
in children who are impoverished by other diseases, and is due to an invasion of the 
gland, through the duct of Steno, by pyogenic organisms. 

Symptoms. — The chief symptoms of mumps, aside from the swelling of the glands, 
is pain in the parotid region, which is greatly increased by moving the jaw or by 
taking any sour material into the mouth. In susceptible persons there may be 
some feeling of malaise or wretchedness and the fever may reach 103° or 104° 
on the first day, although a temperature of 102° is more commonly met with. 

The swelling of the gland is usually at its height by the third day and remains 
at this stage for two or three days more, when it begins to decrease and then grad- 
ually disappears. In some cases the degree of swelling is so marked that the tissues 
of the face and neck share in it to such an extent that the patient is unrecognizable. 
The swelling is bilateral in the vast majority of instances, but it often begins in a 
single gland. 

Complications and Sequelae. — While mumps is a very mild disease in many cases, 
it at times becomes severe, chiefly because of the complications which arise. These 
are more frequently met with in adults than in children. The most common of 
them is orchitis, which may be bilateral and severe enough to cause the patient 
intense suffering and force him to remain in bed. 

Before the age of puberty the testicles are rarely involved, but after puberty 
orchitis is a frequent complication. Bich collected statistics on 862 cases of mumps 
occurring in young men between the ages of eighteen and twenty-five years, and 
found that 29 per cent, of the number were affected with orchitis. Granvier's 
record of cases occurring in the French army gives a percentage of 23. Usually 
only one testicle is involved. Thus, of 159 cases collected from various sources 
152 were unilateral. The combined statistics of Granvier and Bich, based on 
309 cases of orchitis, showed that atrophy of the testicle resulted in 176 cases, or 
57 per cent. Active exercise seems to predispose to this complication, and it 
is much more frequent in some epidemics than in others. Some years ago 
mumps appeared in an epidemic among the students of the Jefferson Medical 
College, and a very large proportion of those attacked developed metastasis to a 
testicle. The development of the orchitis is usually associated with a second 
rise of temperature and a general sense of illness which is in excess of that present 
at the onset of the primary illness. The swelling of the testicle lasts about a 



WHOOPING-COUGH 101 

week, and after the acute inflammation has passed the gland may be enlarged for a 
long period of time. 

Cases have been recorded in which convulsions, meningitis, and arthritis have 
developed as complications of mumps. 

In young girls who have mumps, secondary swelling of the mammary glands, 
of the ovaries, or of the labise may develop, but secondary changes are far more 
rare among females than are those detailed as occurring in males. 

Simonin, a French surgeon, has reported 10 cases of pancreatitis which occurred 
among 652 cases of mumps. The symptoms of pancreatitis appeared from the 
first to the twelfth day of the disease, but usually from the third to the sixth day, 
and lasted from two to seven days. The chief symptoms were epigastric pain 
and vomiting, but no glycosuria. Cuche has stated that he found epigastric 
tenderness present in 20 out of 26 cases of mumps. 

Treatment. — The treatment of mumps consists in the use of mild alkaline diuretics 
and rest, for if the patient can be persuaded to avoid exercise and to use a light 
diet active medication is never needed. Sour foods and acid drinks are to be 
avoided, for when they are taken into the mouth they cause severe pain. If the 
febrile movement is marked and the pulse is quick 3 minims of tincture of aconite 
every two hours is useful for the first twenty-four hours of the malady. By decreas- 
ing the congestion in the gland the aconite not only moderates the inflammation, 
but also diminishes the pain. Local applications to the swollen parotids are usually 
not needful, but if any are employed they should be hot rather than cold. Should 
metastasis to the testicle occur, rest in bed is imperative, since taking exercise 
at such a time causes great increase in the swelling and pain. The scrotum should 
be supported by a bandage. Aconite in full doses and citrate of potassium are 
useful remedies when the swelling of the scrotal contents is severe. 



WHOOPING-COUGH. 

Definition. — Whooping-cough is sometimes called Pertussis, and is an infectious 
disease chiefly met with in childhood. It consists, as its name implies, in a respira- 
tory disorder which is peculiar in two particulars. The patient in the well-developed 
stage of the disease is seized at varying intervals by a paroxysm of coughing which 
is so constant and violent that in a few seconds the quantity of residual air in the 
thorax is greatly decreased below the normal amount, producing in this way a 
sense of suffocation and flushing of the face or cyanosis. Immediately after the 
cough ceases the patient endeavors to take a deep inspiration to compensate for 
the excessive expiratory effort, when there is developed a narrowing of the glottic 
opening so that it is very difficult for the air to enter the larynx. This violent 
effort to draw air through a narrow opening produces a peculiar "whoop," which 
gives the disease its name. The name "whooping-cough" does not signify that 
the cough is whooping in character, but that there is a cough followed by a whooping 
sound. 

History. — The first recorded epidemic of whooping-cough appeared in Paris 
in 1573. 

Distribution and Frequency. — Whooping-cough is a disease which is found in 
all parts of the world, and is apt to occur in epidemic form, particularly during the 
months of March and April. It is least prevalent in September and October. It 
is rare and mild in the Tropics, severe in colder climates. Ceylon has 17 cases 
per 1000, England 347 per 1000 population. As already stated, it is particularly 
prone to attack children; so that few persons reach adult years without suffering 
from an attack. If they do escape during childhood, they may suffer from it 
even in advanced old age. Even sucklings are attacked by it, and in this class 



102 DISEASES DUE TO A SPECIFIC INFECTION 

of cases it is an exceedingly fatal malady. Two-thirds of its deaths occur in patients 
under one year of age. It is also a grave disease in old age. 

Whooping-cough attacks both sexes with about equal frequency. Rosen col- 
lected 43,393 cases, of which 21,850 occurred in boys and 21,543 in girls. If the 
statistics of Goodhart, Comly, and Rilliet and Barthez are combined, it is found 
that in 4157 cases 1868 occurred in boys and 2289 in girls. 

Etiology. — The baccillus of pertussis was discovered by Bordet and Gengou in 
1900 and obtained in pure culture in 1906. It is a minute ovoid Gram-negative 
cocco-bacillus about the size of the influenza bacillus. 

Whooping-cough so often occurs in close connection with an attack of measles 
that the two diseases must be regarded as nearly related. 

The exact period of incubation is unknown. It probably varies greatly in 
different persons and in different epidemics. Sometimes it seems to be as short 
as two days; in others it apparently takes ten days, or even longer than this. The 
infection is perhaps conveyed by the air and certainly is transmitted by the sputum, 
either by the direct expulsion of particles of it into the face and air-passages of the 
child not as yet affected, or upon clothing or the food, so that it gains access to the 
respiratory tract. The infection is most marked during the acme of the malady, 
but is active at all times during the attack, and probably for a week or more after 
the cough has lost all characteristics of the disease. Children who have suffered 
from this disease should not come in contact with those who have not had it, for 
three or four weeks after the last whoop is heard. 

Pathology and Morbid Anatomy. — Mallory, of Boston, has shown that in pertussis 
the bacillus pertussis is found packed in large numbers about the cilia of the epithe- 
lial cells lining the trachea and bronchi. The organisms interfere mechanically 
with the movements of the cilia. This condition is peculiar to this malady. Pri- 
marily the only noteworthy change present in the thoracic organs during whooping- 
cough is a mild catarrhal state of the mucous membranes of the whole respiratory 
tract. Secondarily, the pathological results are far more serious in that the bron- 
chitis and the great strain thrown upon the heart by asphyxia result in conditions 
which may destroy the patient, death usually ensuing in fatal cases from exhaustion 
due to excessive cough, lack of food, and lack of rest combined with bronchopneu- 
monia, which in turn is also due to several causes, of which lowered vital resistance 
and a feeble heart are important factors. Then, too, in the violent inspiratory 
efforts of the patient small particles of food or infected mucus may be drawn into 
the smaller bronchi and so produce local infection. As stated in the article on 
Bronchiectasis, this condition in its cylindrical form may be caused by pertussis. 
(For further pathological changes see Complications.) 

Symptoms. — The symptoms of whooping-cough have already been described 
to some extent. Usually the patient develops what is apparently a slight cold 
in the head and thorax, followed by a cough, which may be described as nervous 
or spasmodic. Perhaps the word "sudden" can best be applied to it in the sense 
that each coughing spell is sudden in onset. At first there may be only one or 
two coughs, but soon they come in series, which day by day increase in frequency 
and violence. Sometimes the whoop, which occurs at the end of the series of short, 
sharp coughs, does not appear for several days. It may never appear in the mild 
type of case, the patient suffering only from the paroxysms of cough which exhaust 
the chest of air to a considerable degree. When the whoop does come on it appears 
at the end of the repeated coughs, and is caused by the attempt to inspire air 
suddenly and forcibly through the narrowed glottis. The whole paroxysm, there- 
fore, consists, first, of a series of coughs which increase in rapidity as one would 
count 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12 with increasing speed, and, secondly, in 
the long-drawn inspiratory whoop. Owing to the violence of the cough the face 
becomes suffused, the tears run, and the patient may even seem more or less con- 



WHOOPING-COUGH 103 

vulsed. The frequency of the paroxysms varies very greatly in different cases 
and at different times in the twenty-four hours. Some patients cough but once 
or twice a day, while others are seized every few minutes. Usually the child is 
greatly frightened if the attack is severe, and often it soon learns to recognize the 
early signs of an approaching seizure and runs to its mother or nurse for help. 
The attacks are provoked by crying, laughing, eating or drinking, and by inhalation 
of dust-laden air. Between the paroxysms perfect quiet and respiratory comfort 
may be present unless complications arise. In the severe cases nose-bleed and 
ecchymoses of the conjunctiva may occur and blood may come from the ears and 
mouth. The convulsive efforts during the cough very frequently cause vomiting, 
and at times the urine or feces may be forcibly expelled, or they escape after an 
attack because of profound exhaustion and the relaxation produced by the asphyxia. 
A nodular infiltration, or an ulcer, at the frenum of the tongue is often produced 
by irritation of the projecting organ upon the lower incisor teeth. The circulation 
is usually not much affected save during the paroxysm, when it is labored, owing 
to the asphyxia. Between the paroxysms it may be rapid and feeble if the attacks 
are frequent and severe enough to strain and dilate the heart. Some clinicians assert 
that permanent cardiac feebleness and dilatation may result from this disease. 

In severe cases in young children and in feeble individuals great asthenia may be 
produced by the violence of the spasm, the loss of sleep, and the loss of food from 
vomiting, which may occur at every paroxysm. 

Inspection of the bared chest during the inspiratory part of each attack reveals 
in the stage of inspiration deep retraction of the intercostal spaces, of the episternal 
notch, and of the epiclavicular areas. The epigastrium is also retracted, for all 
the auxiliary muscles of respiration endeavor to aid in the drawing in of air. Auscul- 
tation of the chest, particularly over the posterior surface, almost always reveals 
bronchial rales, due to the bronchitis which is present in all cases, even if they be 
mild. Care should always be exercised that this bronchitis is not increased by 
exposure to cold and dampness, since it is exceedingly prone to develop into broncho- 
pneumonia, particularly in young children and old persons. Indeed, it may be 
said that the high mortality of the disease is due almost entirely to this complication. 

A number of clinicians, particularly Cima and Meunier, have shown that even 
in the very early stages of pertussis there is present a very extraordinary leukocy- 
tosis. This is accompanied by an increase in the percentage of large and small 
lymphocytes, both increasing until the height of the disease is reached. Eosinophiles 
are found during convalescence. The lymphocytosis is of distinct diagnostic value 
in uncomplicated cases, Kolmer diagnosing 81 per cent, of a series of cases by 
the blood examination alone. As in most infectious diseases, a small amount of 
albumin is found in the urine in the majority of cases. 

The duration of whooping-cough varies from six to eight weeks, more commonly 
the latter than the former. 

Complications. — The complications of whooping-cough are chiefly connected 
with the respiratory tract. Bronchopneumonia, as just stated, is very common, 
and follows the bronchitis which usually is developed in the earlier stages of the 
disease. It is particularly apt to attack young children and to occur in the winter 
months. Somtimes a true lobar pneumonia develops. 

In nearly all cases of whooping-cough a moderate degree of compensatory emphy- 
sema comes on because of the violent respiratory efforts of the patient, and rarely 
this strain on the tissues of the lungs results in the rupture of an air vesicle and the 
development of interstitial or interlobular emphysema. In other instances the 
quantity of air which escapes in this way is very large and infiltrates the tissues 
of the mediastinum, the subcutaneous tissues of the chest, and in extreme cases 
those of the entire body. Instances of this condition have been reported by Gelmo, 
Ferrell, and Bierbaum, and have usually proved fatal. Cases are also recorded in 



104 DISEASES DUE TO A SPECIFIC INFECTION 

which pneumothorax has been produced. Another complication of importance, 
although it has been described as a symptom, is vomiting, which if it becomes 
constant is a serious condition, particularly in infants, since it may cause death 
from asthenia. 

The bronchial glands are nearly always enlarged and may be so much increased 
in size as to cause dulness on percussion over the sternum. The area of cardiac 
dulness is increased by reason of the dilatation of the heart due to the strain thrown 
upon it in the attack of coughing. Brick found changes in the hearts of all of 
14 cases coming to autopsy. There was in most instances an excentric hypertrophy 
of the right ventricle, less often simple hypertrophy or dilatation. The heart 
muscle was often fatty, particularly on the right side. 

Measles and whooping-cough are, as already stated, very commonly associated, 
but the whooping-cough complicates the measles more frequently than the measles 
complicates the pertussis. Sometimes in very young children the disease becomes 
so severe that the spasm of the cough seems to spread to all the muscles of the body 
and produce general convulsions. These cases are nearly always fatal. 

Paralysis complicating whooping-cough is not common. It is usually in the 
form of a hemiplegia, and occurs either during the acute period of the disease or 
as a sequel. When it takes place during the paroxysmal period it is due in the 
majority of instances to meningeal or cerebral hemorrhage in all probability, 
although statistics as to this question are scanty. Twelve cases of cerebral hemor- 
rhage due to whooping-cough have been collected by Townsend, of which seven 
recovered, and Brown has reported a case in which he operated for the relief of 
cerebral compression due to this cause, with excellent results to the patient. The 
literature of this subject has recently been analyzed by W. G. A. Robertson. Some- 
times paraplegia or monoplegia has occurred during the stage of convalescence. 
The prognosis seems to be fairly favorable, indicating that the lesion producing 
these conditions cannot be permanent. Small conjunctival hemorrhages are not 
infrequent, and more rarely large extravasations of blood into the conjunctival 
tissues take place, amounting to ecchymoses. Still more rarely temporary amblyopia 
develops as a result of disordered circulation in the retina or possibly of an actual 
retinal hemorrhage. 

Diagnosis. — The important points in the diagnosis of whooping-cough are the 
repeated and rapid coughs in series until the chest is almost emptied of air, followed 
by a sudden inspiration through the narrowed glottic opening. Some cases develop 
only the series of short coughs, and present no whoop afterward. The only cough 
resembling it is one due to enlarged bronchial lymph nodes, and in adults that due 
to a laryngeal crisis in ataxia. 

Prognosis and Mortality. — The prognosis in whooping-cough, as in most infectious 
diseases, depends upon the age of the child, its general nutrition and vital resistance, 
and upon the care the child can receive. In general terms it may also be stated that 
the prognosis is not so good in winter as in summer, as fresh air is not so readily 
obtained and there is greater danger of exposure to cold in the winter months. 
In itself whooping-cough is not a fatal disease. Death is due to the complications 
which ensue, and if these can be prevented the patient always gets well. In very 
young children, however, it is almost impossible to prevent the development of 
bronchopneumonia, and this is a dangerous condition in proportion to the youth 
of the child. In London whooping-cough stands second as a cause of death from 
the infectious diseases in children under two years of age. 

Hagenbach, of Basle, gives the following mortality statistics, which are based 
on the cases that came under his observation during a period of eleven years: 
Under one year, 26.8 per cent.; between one and two years, 13.8 per cent.; between 
two and five years, 3 per cent.; between five and fifteen years, 1.8 per cent. 

Holt states that the mortality for children under one year of age is 25 per cent. 



WHOOPING-COUGH 105 

Treatment. — It is vitally important that children who have whooping-cough 
should be put under the most favorable hygienic conditions as to sunlight, fresh 
air, and equable temperature. In the summer they do best out-of-doors when 
the weather is not too cool, if they are prevented from acting imprudently, as, for 
example, getting the feet wet. In winter they should be kept in a warm room, 
the temperature of which should be 70° night and day. The air of this room should 
also be moistened by liberating in it small quantities of steam obtained from a 
kettle of boiling water, from a croup kettle, or by dropping pieces of unslaked lime 
in a bucket of water. This is an exceedingly important measure if the room is 
heated by a furnace, since the air from the ordinary furnace is exceptionally dry 
and often laden with dust, and these two causes act as an irritant to the already 
irritated respiratory tract. When it is not possible to confine the child to a room 
which is heated evenly, a most excellent method of treatment, particularly in 
those cases where the paroxysms are frequent at night, is to place the child in a 
bronchitis tent. A bronchitis tent consists in throwing over a bed a large sheet 
which is supported several feet above the head of the child by means of broom- 
sticks or poles, which are tied at each corner of the bed. This tent can be made 
quite attractive for children by decorating it. Into, this tent, at the foot of the 
bed, may be discharged a small quantity of steam such as is given off from an 
ordinary kettle of water when it is kept constantly boiling. In this way the child's 
mucous membranes are not irritated by dry or cold air, but on the contrary are 
greatly soothed, and I have frequently diminished the number of paroxysms per 
day at least one-half by the institution of this plan of treatment, which has the 
additional advantage that it is prophylactic, and prevents the development of 
those serious complications like vomiting and bronchopneumonia, which are 
much aided in their development by repeated and violent paroxysms of cough. 
With a little attention a child may be kept in such a bronchitis tent night and day 
through the entire attack. 

In the way of drugs there is no remedy so efficacious in diminishing the severity 
of the attack as small doses of antipyrin; that is to say, \ to 1 grain of antipyrin 
every three or four hours to a child of one or two years, or 2 grains every three or 
four hours to a child of five or six years, care being taken that the drug does not 
too greatly relax the skin or depress the circulation. There is a widespread belief 
among the laity that quinine in small doses is not only a prophylactic against 
whooping-cough for other children in the family who have not as yet contracted the 
disease, but that it is also of curative value. Some physicians have used a spray 
of a weak solution of quinine in the throat with asserted advantageous results, 
but its value is doubtful, and its bitter taste makes its use impossible in a large 
proportion of cases. Vaccine treatment using 50,000,000 of the Bacillus pertussis 
has given excellent results, the dose being repeated about every five days. 

The development of complications, such as bronchopneumonia, necessitates the 
institution of those lines of treatment which will be found suggested for that disease. 
For the relief of the individual paroxysms of cough several remedies may be employed, 
of which the best is probably chloroform. It is needless to say that this drug 
should be used with great caution, and the patient's parents and the nurse should 
be instructed never to use it on a cloth, but, when the paroxysm is threatened, 
to pour the remedy over the back of the hand and place the hand under the child's 
nose. Under these circumstances a sufficient quantity of the chloroform is often 
inhaled to relax the spasm, without producing any of the marked physiological 
effects which would certainly be obtained to an undesirable degree if the drug were 
poured on to a napkin. This method also prevents an overdose of chloroform 
being given, since the excess of the drug rapidly runs off the hand or evaporates. 
As the hurry of an approaching paroxysm often makes the attendant careless as 
to the quantity which is poured out of the bottle, the physician should insist that 



106 DISEASES DUE TO A SPECIFIC INFECTION 

the chloroform be used in no other way than that which has just been described. 
If the parosysms are too severe to be controlled in this way, nitrite of amyl may 
be occasionally employed. 

An innumerable array of drugs have been recommended for the palliation and 
cure of whooping-cough. Suffice it to say that most of them are entirely useless. 
Even such powerful nervous sedatives as the bromides cannot act advantageously 
in many of these cases, and the use of more powerful ones such as chloral and opium 
are contra-indicated for evident reasons. The physician should always remember 
that whooping-cough is a disease which is bound to run its course, uninfluenced 
in its duration by any treatment which he can employ. The most that the physician 
can do is to prevent complications, treat them if they arise, and endeavor to modify 
the frequency and severity of the individual parosysms, being careful in so doing 
that the remedy is not worse than the disease, in the sense that it produces digestive 
or circulatory disorders which are distinctly disadvantageous. 



INFLUENZA. 

Definition. — Influenza is sometimes called la Grippe. It is a pandemic disease; 
that is, one which appears in widely separated parts of the world simultaneously. 
It is also highly infectious, and the infection is produced by the bacillus of Pfeiffer. 
Influenza of this type is to be separated, theoretically at least, from that condition 
sometimes called "common cold" or "coryza," which often causes somewhat 
similar symptoms in a milder form, although during the presence of an epidemic 
of la Grippe the differential diagnosis may be impossible. At the present time 
the term "influenza" is often employed when the physician is unable to reach a 
diagnosis, and as a consequence is greatly abused, particularly in the early stages 
of typhoid fever and tuberculosis. 

Leichtenstern has divided the disease into two varieties, namely, true epidemic 
influenza (influenza vera) due to the bacillus of Pfeiffer, and endemic influenza 
due to the same cause and occurring for some years after an epidemic has been 
present. Both of these forms are to be separated from ordinary pseudo-epidemic 
influenza or an attack of ordinary cold in the head. A peculiarity of true influenza 
in its epidemic form is the large percentage of persons which it attacks within a 
short space of time, more than any other epidemic disease except dengue. 

History. — At various times in the past great epidemics have broken out and 
raged over the entire world, and have been followed by long periods of immunity. 
Thus, when the great epidemic of 1889 occurred, only a few physicians, and they 
of advanced years, had ever seen a case, for the previous epidemic had occurred 
in 1847 and 1848. 

Pandemics have occurred during the last century in 1830-33, 1836-37, 1847-48, 
and 1889-90. In 1889 the disease began in remote parts of Russia in October, 
reached Moscow in November, ten weeks later it got to Berlin, a month later to 
London, and soon after to New York and Philadelphia, and thence it spread all 
over the continent of North America. Within the next few months nearly the 
whole civilized world was affected by it. Since the last outbreak the disease has 
been endemic, but it is an attenuated form of the infection. An individual locality 
is rarely subject to an epidemic for more than two months, but sporadic outbreaks 
occur for a long period afterward. 

Etiology. — It is interesting to note that the word influenza is derived from the 
Latin sentence ab coeli occultes quadam influentia — from some hidden influence 
in the sky. Influenza, if entirely dependent upon a microorganism for its infectious 
character, must also be dependent upon certain telluric influences, at present 
unknown, which render the human race more susceptible to the effects of the germ 



INFLUENZA 107 

at certain times or which render the germ more capable of producing infection 
at certain periods. 

There are two chief factors involved in the production of an attack of influenza, 
namely, the presence of the bacillus, usually received directly from another patient 
by contact, or through the air; and, second, atmospheric states which are favorable 
to the growth of the germ or to the production of individual susceptibility. A 
third factor, always of importance in connection with infectious diseases, is the 
presence of preexisting disease which decreases the general vital resistance of 
the patient. 

The bacillus of Pfeiffer was first isolated by that investigator in 1892. The 
organism is small and non-motile, and can be well stained by Loeffler's methylene 
blue or by well-diluted watery solutions of carbol-fuchsin. It develops in myriads 
on the nasal and bronchial mucous membranes and in the secretions of those parts. 
A number of observers, and more particularly Ricciardi, have shown that the 
bacillus is readily distributed and spreads most actively by droplets of mucus. 
Even after the patient has recovered from an attack his nasal secretions may 
reinfect himself or other persons for a period of weeks, and therefore all handker- 
chiefs, towels, and pillowcases used by him should be boiled before being used by 
others. The room occupied by the patient should be fumigated with formaldehyde 
after his recovery occurs and before anyone else occupies it. 

It is a noteworthy fact that during an epidemic of influenza other infectious 
diseases seem to be less common. This is particularly true of malarial fevers, 
if the statistics collected by Anders, of Philadelphia, are correctly interpreted. 
On the other hand it is very common, and indeed it is almost constantly the case, 
to find that the illness is due quite as much to associated infection with the pneu- 
mococcus and pyogenic cocci as to the influenza bacillus. That is to say the 
infection is usually compound or complex and not single. Thursfield reports 
two cases of influenzal septicemia, with recovery of both. He believes that the 
organisms described as the B. influenza are not identical but form a group, like 
the typhoid-colon family, with different pathogenic powers. Lesions produced 
by the various members of the group include influenza, endocarditis, a septicemic 
form of cerebrospinal meningitis, septicemia, pertussis, and suppuration in the 
middle ear and nasal sinuses. 

Incubation. — The period of incubation is probably from twenty-four to seventy- 
two hours, but in some cases it seems to be longer than this. 

Symptoms. — The onset of symptoms of epidemic influenza is nearly always 
sudden. A person feeling perfectly well may suddenly be seized by a sense of 
chilliness or a severe rigor, followed by severe aching pains in the back and in the 
legs. There is usually congestion of the nasal mucous membrane, so that the patient 
seems to have a severe cold in the head. The chill is quickly followed by fever 
which may rapidly rise to a point as high as 105°, although as a rule 103° is the 
more common acme. Associated with these early symptoms there is usually a 
sense of severe illness and a feeling of great wretchedness, so that the patient not 
only expresses himself as feeling very ill, but seems so to the physician. 

About this time the symptoms are wont to be associated with additional ones 
indicating involvement of certain viscera. Most frequently the respiratory system 
is affected, and, in addition to more or less intense congestion of the nasal mucous 
membrane, an acute bronchitis develops; the physical signs in the chest being 
typically those of acute bronchitis with excessive, unproductive cough and a 
sense of thoracic soreness. When the nasal mucus is examined it is seen to be 
unusually thin, excoriating to the nose and upper lip, and if any bronchial mucus 
is expelled it is also of this character. As the disease progresses the sputum becomes 
greenish-yellow and thick. 

The general state of the patient at this time is often one of profound depression, 



108 DISEASES DUE TO A SPECIFIC INFECTION 

far in excess of that which usually accompanies such signs of bronchitis. The 
action of the heart may be feeble and the skin is relaxed and clammy, or it may be 
very hot and dry. 

If convalescence is not soon established the disease often develops into a peculiar 
form of pulmonary congestion or pneumonia, in which the sputum may be blood- 
tinged and frothy or in which no sputum may appear. A peculiarity of this pul- 
monary involvement, in one of its forms, is the fact that it moves from place to 
place with remarkable rapidity. An area of impaired resonance which existed 
yesterday is clear today, and still another area of congestion develops elsewhere— 
a form of wandering congestion. When true pneumonia develops it may be 
croupous in type and be due to mixed infection by the bacillus of Pfeiffer and by 
that of true pneumonia, or it may be in the form of bronchopneumonia. The 
latter type is the more common, but both forms are apt to be serious and particularly 
so in the feeble, the aged, the very young, and in alcoholic or renal cases. Pneu- 
monia and heart-failure due to an action of the toxin of the disease on the heart 
muscle are the chief causes of death in all epidemics. 

Pleurisy followed by empyema is not very rare. 

In studying a case of influenza accompanied by pulmonary signs the physician 
must always bear in mind the possibility of the presence of associated tuberculous 
infection, because an attack of influenza not only often predisposes to this disease, 
but in addition permits unrecognized foci of early tuberculous infection to become 
active. 

In some cases of influenza the heart seems to bear the chief brunt of the attack 
so that repeated attacks of syncope ensue. These instances are met with chiefly 
among patients who have persisted in remaining at work during the early stages 
of the disease, or who have had, previous to the attack, an impaired heart muscle. 
Thus, a heart dilated as the result of excessive exercise may succumb readily, or 
one in which early but hitherto unrecognized degenerative changes were developing 
may suddenly fail. Often the symptoms of influenza are chiefly gastro-intestinal 
or nervous. 

The gastro-intestinal form of the disease may have its onset in severe diarrhea 
and vomiting, with collapse and violent abdominal pain. In some cases the 
pain is entirely absent, and profuse watery stools are present. Jaundice may be 
present, due to an extension of the gastro-intestinal eatarrh to the common biliary 
duct. 

In the nervous form the symptoms consist of profound nervous and mental 
depression, or in severe neuralgic pain which may or may not be due to neuritis. 
Mental disturbances in the course of an attack of influenza are by no means rare. 
Indeed, it may be said that no other acute infectious disease is so commonly com- 
plicated, or followed, by such a condition. Leichtenstern states that he met with 
fewer psychoses among 2000 cases of typhoid fever and 3000 cases of pneumonia 
than he found among 439 cases of influenza. These psychoses may be of the 
exhaustion type, but usually are due to a toxic state induced by the malady. The 
mental disturbance may develop during the stage of onset, the febrile stage, or 
the stage of decline or convalescence. The latter cases are usually of the exhaustion 
type. The prognosis in these cases as to the state of the mind is usually good 
unless there is a bad history as to heredity. 

Very rarely meningitis develops, and still more rarely true encephalitis. The 
meningitis is primarily due to the influenza bacillus but other secondary organisms 
are nearly always found at autopsy. It usually occurs in children under one 
year of age and the mortality is ninety per cent. Lumbar puncture reveals a 
turbid fluid under high pressure with many leukocytes and an excess of polynuclear 
cells. In some instances, however, although the meningeal symptoms are most 
marked during life no definite lesions can be found at autopsy. Particularly is this 



INFLUENZA 109 

true in young children. In other cases extensive hemorrhages into the pia mater 
may be produced or a sharp perivascularitis in the vessels of the brain may develop. 
In still others there may develop a chronic perivascularitis which induces permanent 
palsies. It is usually met with in infants. Cases of cerebral abscess have also been 
ascribed to this disease. In rare cases toxic neuritis develops, and this may be 
single or multiple. Even paraplegia due to this cause may arise. Not only may 
this type of influenza affect the nerves of sensation and motion, but specialized 
nerves such as the vagus, thereby causing disturbances of the circulation such as 
paroxysms of tachycardia and bradycardia. In an analysis of 29,000 cases Lee 
found that 7000 were of the nervous type. In some instances the disturbance of 
circulation is due more to an influence exercised upon the vasomotor nervous system 
than to any direct affect upon the nerve supply of the heart, so that attacks of 
syncope come on from acute vascular relaxation. 

Complications and Sequelae. — It is difficult to separate the complications of in- 
fluenza from the ordinary symptoms of the disease because its natural course 
presents such diverse manifestations in different organs. Without doubt 
pulmonary, cardiac, and renal disorders are the most common complications. 
In many cases death is due to an attack of pneumonia, which rapidly carries off 
the patient whose vitality is already sapped by the onset of la Grippe. In other 
instances the kidneys, which have been impaired before the attack, suffer from an 
acute congestion or true nephritis superimposed upon a subacute or chronic 
state, and so uremia speedily comes on, with its helpmate, pulmonary edema. 

Patients with influenza develop cardiac complications in three chief classes: 
either they already have mild cardiovascular degeneration which enables the 
influenzal toxin to work havoc with the cardiac muscle, or they have dilated feeble 
hearts, or, again, as already stated, they persist in remaining at work after the 
attack begins and refuse to go to bed. These patients not only have serious 
cardiac difficulty during the attack, but very frequently suffer from cardiac weak- 
ness and distress for many weeks after convalescence should be well established. 
The man who persists in remaining out of bed when attacked by this disease, 
even if mildly ill, literally " takes his life in his hand." 

In children, as well as adults, severe middle ear inflammation is a very common 
complication even in mild cases. 

The German collective investigation of the epidemic of 1889-90, based on an 
analysis of 3185 cases, gave the following results as to the relative frequency of 
complications, which results, however, differ materially from clinical experience 
in America so far as the cardiac complications are concerned: 

1. Diseases of the respiratory organs, exclusive of pneumonia, 48.76 per 
cent. 

Of these complications pleurisy was the most frequent, being present in 27 per 
cent, of the entire number of cases. Pneumonia was present in from 6 to 8 per 
cent, of all cases. 

2. Diseases of the nervous system, 45.77 per cent. 

3. Diseases of the ear, 37.95 per cent. 

4. Hemorrhages, 25.33 per cent. 

5. Diseases of the heart and vascular system, 14.09 per cent. 

6. Diseases of the digestive organs, 10.36 per cent. 

7. Polyarthritis, 7.28 per cent. 

8. Diseases of the eye, 7.03 per cent. 

9. Albuminuria and nephritis, 4.52 per cent. 

Diagnosis. — It is so easy to make a diagnosis of influenza during the presence 
of an epidemic that physicians are wont to be careless in examining the patient 
thoroughly, and so may overlook complications of importance or decide that the 
case is one of influenza when in reality the chills, the fever, the aching, and the 



110 DISEASES DUE TO A SPECIFIC INFECTION 

prostration are due to an oncoming typhoid fever or an acute tuberculosis or malaria. 
All of these diseases, and also ulcerative endocarditis and sepsis, should be carefully 
excluded before a diagnosis of influenza is made. 

Treatment. — Above all other things in the treatment of influenza is rest in bed. 
This is as true of mild as of severe cases and of the patient who is stalwart as of 
the patient who is feeble. A robust man who fails to rest almost always suffers 
from a severe attack or from sequelae, such as cardiac disorder and giddiness, which 
may invalid him for weeks. Aside from rest in bed little medicine is needed except 
for the purpose of relieving symptoms which are troublesome. For the relief of the 
excessive pain in the back and limbs the coal-tar antipyretics have been employed 
by the ton. Although they give ease they are harmful if the doses are large, and 
often fail if they are used in moderate amounts. They tend to increase nervous 
and circulatory depression, and to decrease the ability of the patient to resist the 
infection from which he is suffering and the possible secondary infections which 
may occur. If the patient will rest they may be used moderately; if he will not 
rest they should not be used, for they not only do harm directly, but by diminishing 
discomfort they also enable and encourage him to remain out of bed. 

A very useful drug for the relief of the aching and pains in the back and limbs 
is salicin in 5 grain doses every five hours in capsules. Many practitioners believe 
that this drug alone, or when combined with 3 grains of cinchonidine, acts as a 
specific in the cure of the affection. Should the pain in the back be intense it may be 
relieved by the application of hot stupes or compresses, or by rubbing with soothing 
liniments. A more ancient but nevertheless very useful remedy for this condition, 
particularly in the early stage of the malady, is Dover's powder in the dose of 
from 2 to 10 grains once or twice a day. At one time used as a matter of routine 
in all infections, it has fallen into an undeserved disuse. 

Headache, if it be due to congestion, may be modified by the use of an ice-bag, 
or by the administration of 1 to 2 grains of caffeine with 10 grains of bromide of 
sodium or potassium every few hours. This formula can be given in the form of 
an effervescent granular salt without the use of the coal-tar products often added 
by manufacturers of headache cures. Hot foot-baths also decrease headache. 
Menthol pencils may be used locally for neuralgia or a spray of chloride of ethyl 
may be used for the same purpose. 

As in all infectious maladies, it is of the greatest importance that the organs of 
elimination be kept active. The bowels may be first moved by a grain or two of 
calomel, followed in twelve hours by a Seidlitz powder, or, if constipation has been 
marked, they may be opened at once by citrate of magnesium. For the purpose 
of keeping the kidneys active 5 grains of citrate of potassium or of bicarbonate of 
potassium may be given every four hours in copious draughts of water if the urine 
is acid, or the same amount of benzoate of ammonium if the urine is alkaline. 
The latter drug is best given in kon seals, and possesses the additional advantage 
of acting favorably upon the respiratory mucous membrane and upon the muscular 
pains. A hot compress or poultice applied over the loins will often establish renal 
secretion when it seems scanty. 

Dryness and soreness of the mucous membrane of the respiratory tract, in the 
stage of onset, may be much relieved by telling the patient to inhale steam which 
may be medicated by the addition to the water from which it arises of a few grains 
of menthol or of equal parts of menthol, oil of eucalyptus, and oil of pine. In 
other instances the patient may add to the boiling water a tablespoonful of com- 
pound tincture of benzoin. The medicated steam may be taken directly from an 
inhaler or the vapor may be set free in the air of the room by the use of a bronchitis 
kettle. When the nasal mucous membrane is so congested and occluded that 
breathing is difficult and oppression is marked, adrenalin chloride, 1 : 5000, with 
chloretone may be sprayed into the nostrils or applied on pledgets of cotton. It 



ACUTE POLIOMYELOENCEPHALITIS 111 

loses its effect if applied too often, but it does not do so as rapidly as does cocaine, 
nor is it dangerous in its systemic effects. 

For the relief of the congestion of the respiratory mucous membrane, when the 
illness has lasted for several days and the secretion is thick and tenacious, chloride 
of ammonium in 5 grain doses four times a day may be administered combined with 
codeine or heroin to relieve cough, or terpin hydrate may be used with the same 
sedatives in the form of the well-known elixir of terpin hydrate with heroin. For 
the persistent cough of convalescence, oil of sandal-wood in 5 minim doses four 
times a day is very useful. 

Circulatory and nervous stimulants are not to be used unless there is distinct 
evidence of their need. Alcoholic drinks are as a rule to be excluded, unless the 
patient uses them habitually when well, when they have to be given, preferably 
in the form of an old brandy or good whiskey. Great care must be taken that the 
patient does not overuse them in his endeavor to make himself feel stronger. For 
acute circulatory failure aromatic spirit of ammonia or Hoffmann's anodyne are 
the remedies of choice. When the failure of the cirulation is associated with 
nervous depression the use of strychnine is indicated, but it is greatly abused and 
should not be given day after day except as a tonic in convalescence, as it loses 
its power, is not a true stimulant but a nervous irritant, and often causes great 
irritability if not employed skilfully. 

As influenza is a disease which produces great prostration, a diet which is easily 
digested and nutritious is essential for the maintenance of strength, particularly 
in the very young, very feeble, and very old. Animal broths, oysters, and predi- 
gested foods are useful, and they may be fortified with advantage by barley-gruel, 
the digestion of which may be aided by the use of taka-diastase. Indeed, the 
various vegetable gruels with taka-diastase are in many cases better than the 
animal broths. Arrowroot and milk-toast and eggs are also useful. 

Prophylaxis. — There can be no doubt that much can be done to prevent the 
spread of la grippe from one person to another by isolating the ill and by forbidding 
healthy persons to occupy the sick-room after it is vacated, until it is thoroughly 
disinfected. This is particularly advisable when the old and feeble are about the 
house and when persons who are still weak from one attack are exposed. Every 
effort should be made to keep the malady out of the non-medical wards of hospitals, 
insane asylums, and almshouses. Patients in these institutions when taken ill 
should be isolated, and the bedding, napkins and handkerchiefs be promptly disin- 
fected. The sputum should be expelled upon pieces of rag and then burned. 

All rooms, clothes, and books used by patients suffering from influenza should 
be disinfected as carefully as if the patient had suffered from some more fatal 
malady. 

ACUTE POLIOMYELOENCEPHALITIS. 

Definition. — This infectious disease is sometimes called infantile spinal paralysis, 
because it most commonly presents spinal symptoms. It is also called acute infantile 
palsy, and acute atrophic paralysis. In its spinal form it is characterized by fever 
and sudden loss of power in one or more of the limbs, most commonly the lower 
extremities. As a rule, the loss of power is complete, but occasionally it is local- 
ized in certain groups of muscles. Immediately after the development of the 
paralysis, wasting of the muscles begins to take place and may be extreme. There 
is no disturbance of sensation. 

Etiology. — Within recent years it has become more and more evident that acute 
anterior poliomyelitis is due to an infection. That the disease at times occurs in 
epidemic form was noted by Colmar more than sixty years ago. Since 1907 out- 
breaks have occurred in many widely separated States of the Union, in Canada, 



112 



DISEASES DUE TO A SPECIFIC INFECTION 

Fig. 28 



"t r-'- 



•1881-1893- 



-x — 1894-1901-*-' 02 '04 '00 '08 '10 



9000 
8000 
7000 



6000 ft 



5000 , 



4000 w 
3000 i 



2000 

1000 




Relative prevalence of infantile paralysis in the United States and Europe and Australia, 1881 -.1910. 
The solid black line refers to the United States; the dotted line to the following countries: Italy, 
Sweden, Norway, Germany, Austria, France, England, and Australia. Part of this increase is due to 
better recognition. (Lovett.) 

Fig. 29 







' ■■ 




































•jUU ■■■ 








































<iu\J ■■■ 
















































































HI B" 
















































































« HM_^_ 




H ; H 
































— r0 'f ■■■■ llllll BE Ell 












d 








- -3 -]<B z ■:---- !- 1 


^tf- 1 ^- -:■--: = c-- 4 5--S^ 


p- p : : j[i 


1 ,o o m O G j < 


- - >H O '° O Q O Q C 

§ h t] it 1 vl "il h 

jiiLjiiijijijij: 


1 ,1 M & £ ^--S:f3: §7 


lii-itfiSiiSSSi 


tSi£:±±:Kfi:±E3± 



Chart showing graphically, age incidence of 1076 cases of poliomyelitis recorded in 1910. 
(Department of Health of Pennsylvania.) 



ACUTE POLIOMYELOENCEPHALITIS 



113 



Cuba, Austria, Germany, and Melanesia. In the last decade its occurrence has 
greatly increased in all parts of the world. 

Flexner and Noguchi have grown the virus outside the body anaerobically. 
It developed in minute colonies of globoid bodies (0.15 to 0.3 microns in size). 
These cultures are capable of causing the typical disease in monkeys. It is killed 
by 1 to 500 of potassium permanganate or 1 per cent, of menthol in oil. 

The biting stable-fly (Stomoxys calcitrans) has been accused of transmitting 
the disease but this has been denied. House flies undoubtedly carry the infectious 
agent on their bodies. 

The disease is distinctly one of early child life, the greatest number of cases 
developing in the first three years of life, it being comparatively rare after the 
tenth year (Fig. 29). It is far more apt to develop in the summer than in winter, 
and has its greatest incidence in July and August. After this season it is most 
frequent in September and in June. The period of incubation may vary from two 
days to three weeks. 

One attack protects to some extent from another. The infection probably is 
spread by the nasal secretions of those who are convalescent or who act as "carriers." 



Fig. 30 



ant 




a. spin, post: 



a. spin. post. 



Dots show chief areas of disease in acute poliomyelitis. 



Prevention. — Patients in the acute stages should be isolated and their nasal 
discharges destroyed. They should be protected from flies which may carry the 
disease for at least two weeks. Kling found the virus in the nasal discharges, how- 
ever, six months after the illness. Dust should be avoided and the throat gargled 
with a 1 or 2 per cent, solution of hydrogen peroxide or treated by a spray of 
menthol in oil, 5 grains to the ounce. This may also be used in the nose. Urotropin 
may be given in 5-grain doses, i. e., as a prophylactic. Patients suffering from the 
disease should be quarantined for three weeks after the acute symptoms cease. 

Pathology and Morbid Anatomy. — As Flexner and his colaborers have well put 
it, epidemic poliomyelitis is a general disease of the nervous system, although 
the most prominent and important symptoms are those following injury to the 
motor neurones of the spinal cord and brain. The essential lesion of this disease 
is an acute inflammatory process in the anterior cornua of the spinal cord, with 
8 



114 DISEASES DUE TO A SPECIFIC INFECTION 

associated hyperemia of the membranes covering the anterior surface of the cord. 
The branches of the anterior spinal artery (Fig. 30) bear the brunt of the attack 
and are intensely engorged. Their finer branches are ruptured so that extrava- 
sations of blood take place into the gray matter. As a result of these changes 
the typical picture of tissues suffering from an acute inflammatory process is 
presented, for serum, leukocytes, and red cells crowd the nervous protoplasm. 
The ganglion cells of the gray matter in the anterior horns undergo marked degen- 
erative changes. They undergo cloudy swelling and the nuclei become granular, 
or if the change is still more severe the nuclei disappear and the neurones lose their 
dendrites and become vacuolated. As a final stage the cell undergoes shrinkage, 
becomes a small, granular mass, and finally disappears. The damaged areas, in 
old cases, are occupied by connective tissue and are much shrunken, so that the 
affected gray horn is much smaller than its fellow. The anterior nerve fibres, which 
have their origin in this part of the cord, also atrophy. Associated with these 
changes in the anterior cornua of the cord there is often some involvement of 
fibres in the anterolateral tracts, because, it will be recalled, some of the fibres, 
or axones, which leave the anterior horns pass upward and downward in these 
columns to enter the anterior horns above and below to associate their function, 
and it is also due to the inflammatory process extending into the white columns. 

The degree of the inflammatory process in the gray matter varies very greatly 
in different cases and may involve the cells supplying but a few muscles. It may 
affect chiefly that part of the gray matter which is most anterior or that nearer the 
commissure. In rare cases it would seem probable that no true inflammatory 
process develops in the cord, but that simple degenerative changes occur in the 
neurones in the anterior horns. 

Symptoms. — The symptoms of acute poliomyelitis of the mild form usually 
take the following course : A child in good health has a restless and feverish night, 
and seems on the next day to be somewhat out-of -sorts. In the course of twenty- 
four or forty-eight hours it not infrequently happens that the parents consider 
the child recovered from its acute illness, and it may be some days or weeks before 
the mother notices that one or both of the lower limbs are lacking in power. Not 
rarely it is found, as the child sits in its mother's lap, that one leg moves while 
the other hangs like a flail, or the mother notices that the child is unable to push 
its leg into its clothing as efficiently as it could do before it was taken ill. These 
may be considered as the symptoms of a comparatively moderate case. There 
is usually marked leukocytosis chiefly of the lymphocytes. Spinal puncture gives 
a fluid containing an excess of cells nearly all of which are lymphocytes. In the 
earlier stages the mononuclear cells may be in excess. 

In instances in which the onset and course of the malady is more severe, we find 
that fever is quite marked, often rising as high as 102.5°, and continuing at this 
point for several days. Occasionally, at onset, it may reach as high as 105°, and 
with this febrile movement there may be headache, loss of appetite, and vomiting. 
Sometimes diarrhea occurs. In these instances the manifestation of loss of power 
is usually so marked that its presence is recognized within a few hours of its onset. 
Even in these cases, however, it not infrequently happens that the child is supposed 
to have suffered from an attack of acute gastric catarrh or indigestion until its 
inability to make certain movements calls attention to the palsy. Occasionally 
pain is a symptom of some importance, if, as already pointed out, the lesions in 
the anterior horns extend sufficiently backward to involve some of the sensory 
fibres beyond the commissures. These pains are usually felt about the joints. 
In some cases they come on not as a symptom of onset, but as a sequel, and seem 
to be due to an associated neuritis. At times a fine fibrillating thrill is seen in 
the muscles about to be chiefly affected. 

The degree of the paralysis varies greatly in different cases. In some instances 



ACUTE POLIOMYELOENCEPHALITIS 115 

only one or two muscles seem to be affected. In others, the whole limb may be 
paralyzed, or both lower limbs and one upper limb may manifest loss of power. 
Even when the paralysis is quite widespread, it is rare for the cranial nerves to 
be affected, and equally rare for the sphincter muscles to lose power. 

There is still a third type of case in which convulsions appear at the time of 
onset. This type is described as polioencephalitis. These convulsions may be 
cerebral or epileptiform in character, and may be followed by deep coma lasting for 
many hours. A fourth type presents a very typical picture of cerebrospinal men- 
ingitis arising from the diplococcus of Weichselman. Paralysis may not be present, 
but there is marked headache, vomiting, pains in the back, rigidity, and Kernig's 
sign. Later, if life persists the paralysis becomes noticeable. 

In other instances a child in previously good health develops fever more or less 
severe. There may be headache and vomiting without the onset of convulsions. 
In some cases it passes into stupor. In other instances it is delirious and exceed- 
ingly irritable with excessive hyperesthesia. Kernig's sign is marked. Ocular 
palsies may be present, even with or without facial palsy, unilateral or bilateral. 
If the patient recovers consciousness returns, the signs become normal, but on 
attempting to let the child stand up he suffers from vertigo and ataxia. In some 
instances marked symptoms of hydrocephalus develop. Not infrequently in 
these cases, after recovery from the acute illness is established, there remains 
strabismus and sometimes there is dimness of vision which may progress to com- 
plete blindness. Very remarkable recovery from this blindness, however, some- 
times ensues. In those cases of the cerebral type which closely resemble tuber- 
culous meningitis, facial and ocular palsy, without Kernig's sign, accompanied 
by complete muscular relaxation and Cheyne-Stokes respiration, occur. While 
death frequently takes place in these cases a surprising number survive. 

In some instances the disease seems to be progressive in its type, the full degree 
of paralysis not developing at once, but beginning in one part and then spreading 
to adjacent parts. Rarely one attack speedily follows another, involving a diff- 
erent set of muscles. 

In very rare instances the paralysis may develop without any history of the 
symptoms of onset already described. Cases are on record in which the paralysis 
has been almost universal, but it is a noteworthy fact, in regard to the paralysis 
of acute poliomyelitis, that it is far more widespread in its early stages than later 
on, this being due to the fact that as the inflammation subsides certain cells which 
have not been irreparably damaged regain part or all of their functions, and so 
adequately supply the muscles under their control, or collateral muscles supply 
the power needed. 

Occasionally the onset of the symptoms may resemble Landry's paralysis, since 
the paralysis starting in the lower extremities speedily travels upward and may 
produce grave respiratory difficulty through interference with the diaphragm. 

The bulbar type may cause rapid death and paralysis of the cranial nerves. 
Rarely the symptoms are those of a polyneuritis. 

Wickham has classified the type as follows: 

1. Ordinary spinal paralysis, anterior poliomyelitis. 

2. Progressive paralysis, usually ascending, less often descending; Landry's 
paralysis. 

3. Bulbar paralysis; polioencephalitis of pons. 

4. Acute encephalitis, causing spastic mono- or hemiplegia. 

5. Ataxic form. 

6. Polyneuritic form. 

7. Meningitis form. 

8. Abortive form. 

The period of recovery usually extends from one to three months. The muscles 



116 DISEASES DUE TO A SPECIFIC INFECTION 

which fail to recover soon lose their contractility to faradism and then to galvanic 
electricity. The loss of faradic responses may be present as early as the eighth 
or ninth day, but in other instances some response is maintained, for a number 
of weeks. At the end of a few weeks the reactions of degeneration are observed. 
As would be expected from the lesions already mentioned and described when 
discussing the pathology of the affection, sensation is usually unimpaired. Reflex 
activity is, of course, diminished or lost because of the spinal lesions and the atrophy 
of the muscles. As secondary lesions to the paralysis we find shortening of the 
muscles with consequent contractures and deformities. 

The legs are affected more frequently than the arms in the proportion of 3 to 1. 
The muscles below the knee suffer more frequently than those above the knee, 
and the tibial and peroneal muscles suffer more frequently than those of the calf. 
Lovett and Richardson found the proportion to be one leg, 27.97 per cent.; both 
legs, 23.48 per cent.; back, 23.29 per cent.; both arms and both legs, 11.13 per 
cent.; one arm only, 7.25 per cent. In the forearms the supinators usually escape, 
but the deltoids suffer more frequently than any other muscles in the upper 
extremity. 

Diagnosis. — The acute poliomyelitis of childhood is usually readily diagnosed. 
Care must be taken that the muscular pains when they occur are not thought to 
be due to rheumatism. None of the other spinal lesions of childhood have such a 
characteristic onset, but postdiphtheritic paralysis and multiple neuritis due to 
lead or arsenic may produce similar symptoms although their onset is not so sudden 
and there is no fever. The meningeal type must be separated from cerebrospinal 
meningitis by an examination of the cerebrospinal fluid which in the latter disease 
is turbid and contains the diplococcus and an excess of polynuclear cells. From 
tuberculous meningitis it is differentiated by the aid of the von Pirquet and Moro 
tests, by the finding, very rarely, of the tubercle bacillus in the fluid and by the 
possible discovery that the child has been exposed to tuberculous persons. Pneu- 
mococcic meningitis must also be considered. 

Prognosis. — This is usually good so far as life is concerned, although if the at- 
tack has been severe, vital resistance may be so diminished that other affections 
may readily cause the death of the child. The degree of ultimate paralysis can 
be determined only after two or three weeks of careful observation, when some 
idea as to the number of muscles which may recover can be obtained, particularly 
if electricity is used to determine the electrical contractility of the affected muscles. 
The percentage of complete recovery after the attack is usually reckoned at about 
25 per cent. 

Treatment. — In the treatment of acute poliomyelitis little can be done in the 
way of directly combating the disease. The child should be put at absolute rest 
in a quiet and darkened room. Sweet spirit of nitre and citrate of potassium should 
be given in small and frequent doses to diminish fever and to cause mild perspiration. 
The use of as large doses of hexamethylenamine as the stomach and kidneys will 
stand (10 to 30 grains a day) inhibits the growth of the infection in the nose and 
tends to protect others, but can do little good to the patient already stricken. Hot 
applications have been recommended to be applied to the back. It is difficult 
to understand how they can be of much value. Some mild counter-irritant over 
the spine, such as a spice plaster, or a pepper plaster, may be advantageous. The 
whole object of the physician must be to produce nervous quiet and aid in 
diminishing the inflammatory process in the cord by avoiding excitement of the 
nervous system. 

After the acute stage of onset is past, and the paralysis is present, that is to 
say, after sufficient time has elapsed for the acute stage of the inflammation to have 
passed by, or, in other words, in three or four weeks after onset, moderately large 
doses of strychnine may be given, but care must be taken that the doses are not so 



DENGUE 117 

large as to produce twitching or great nervous irritability. At this time, too, the 
slowly interrupted faradic current may be applied to the paralyzed muscles, and 
particularly to those which are semiparalyzed, in the hope that in this way their 
nutrition may be maintained. It must not be forgotten, however, that the greatest 
care must be exercised that the muscles are not overfatigued, since if they are 
exhausted they will more rapidly atrophy than if no electricity was employed. 
If electricity is used before the spinal cord has recovered from the acute stage of 
the inflammation, it will make the condition worse. In many instances it is advis- 
able to use electricity on one day and careful, gentle massage on the next. The 
electrical current should never be employed in such strength as to give the child 
pain or distress. 

As general tonics for the nervous system the hypophosphites, glycerophosphates, 
cod-liver oil, and iron may be used. 

Should any tendency to deformity take place, this must be treated by the methods 
commonly resorted to by orthopedic surgeons. Rapid recovery should not be 
expected in these cases. Careful treatment for months is necessary to get the best 
results. 

DENGUE. 

Definition. — Dengue is an acute infectious, but non-contagious, usually epidemic 
fever, which is probably dependent for its development upon the presence of some 
specific organism the exact nature of which is still obscure, although McLaughlin 
and Graham believe that they have succeeded in isolating it. The disease is 
characterized by two febrile attacks with severe pains in the muscles and joints. 
Because of these latter symptoms it is often called "breakbone fever," and from 
the peculiar gait caused by this condition "dandy fever." A large number of 
other popular names have been given it, such as " three-day fever," "bouquet 
fever," or sometimes, as a corruption of the last name, "bucket fever." 

History and Distribution. — The earliest accurate description of dengue that we 
possess is that of Brylon, who described the outbreak of 1779; later the celebrated 
epidemic in Philadelphia, in 1780, was described by Rush. Since then it has 
occurred in a considerable number of epidemics in various subtropical parts of the 
world such as Batavia, Spain, India, Bermuda, Brazil, the West Indies, and in 
various parts of the Southern United States. Within twenty years it has also 
visited Turkey, Greece, Fiji, and Tripoli. It is distinctly a disease of warm 
climates, and, so far as I know, has never been met with north of Philadelphia. 
The disease spreads from point to point along lines of travel, being carried by 
infected individuals and perhaps by clothing. 

A peculiarity of dengue is the rapidity of its spread and the few people in a com- 
munity who escape its attack. In this respect it surpasses epidemic influenza. 
No age, sex, or race escapes, and in an incredibly short time after the first case 
is seen a multitude may be down with it. As Manson well says, it "bursts" upon 
a place. The spread of an epidemic is always arrested by the appearance of cold 
weather. High altitudes are also unfavorable to its spread. 

Etiology. — As the result of valuable researches carried out by Ashburn and Craig 
and by Vedder of the United States Army in the Philippines, in which they 
observed over six hundred cases, they conclude that the disease is not contagious. 
They also assert that no organism, either bacterium or protozoon, can be demon- 
strated in either fresh or stained specimens of blood with the microscope. 

The red blood count in dengue is normal. 

There occur no characteristic morphological changes in the red or white cor- 
puscles in this disease. 

Dengue is characterized by a well-marked leukopenia, the polymorphonuclear 



118 DISEASES DUE TO A SPECIFIC INFECTION 

leukocytes being decreased, as a rule, while there is a marked increase in the small 
lymphocytes. 

The intravenous inoculation of unfiltered dengue blood into healthy men is 
followed by a typical attack of dengue. 

Graham, of Beyrouth, believes that the infection is conveyed by the mosquito, 
the Culex fastigans. In several instances Graham placed persons suffering from 
dengue in apartments in which all mosquitoes had been destroyed by chlorine gas, 
and allowed healthy individuals to associate with the sick. In no case of this kind 
was the disease contracted. In addition to this negative evidence Graham offers 
positive evidence, which he obtained by allowing mosquitoes which had bitten 
affected persons to bite two healthy individuals who resided in a district where 
no cases of dengue were present. Both of these men developed the disease, one 
on the fourth and the other on the fifth day after they were bitten. They were 
kept under mosquito nettings until they had completely recovered and the infected 
mosquitoes were all killed. No other cases of dengue occurred in the village where 
these experiments were made. 

That mosquitoes convey the disease is believed by Ashburn and Craig from 
their reseraches in the Philippines. 

Symptoms. — Dengue is characterized by a train of symptoms which is quite 
remarkable. In the first place, the suddenness of its onset is noteworthy. A 
patient may be in perfect health at one hour and sick in bed with well-developed 
symptoms the next. In any event the onset is sudden, and sometimes it is ushered 
in by a chill or by pains in the limbs. Fever rapidly develops and may reach as 
high as 106° or 107°, but usually the acme is 103° to 105°. There is intense headache 
and the pains in the limbs are so excruciating that the term "breakbone fever" 
is well applied. The discomfort of the patient is increased by the pain caused by 
moving the body. The tongue is usually heavily coated, and nausea and vomiting 
may be distressing symptoms. 

With the onset of the fever there develops a rash which is of the nature of erythema. 
In from one to three days, usually two days, the fever suddenly ends by crisis and 
simultaneously the patient not only sweats freely, but also has free diuresis, diarrhea, 
and nosebleed. This nosebleed, by relieving the cerebral congestion, greatly 
decreases the headache, and the rash rapidly fades. 

In other instances the fever gradually falls by lysis, but this is less common 
than crisis. The fever having fallen to normal the patient, still feeling weak, is 
able to be about, although he suffers from twinges of pain in the joints and muscles, 
which impress upon his mind the fact that he is as yet ill. After a remission of 
several days, usually from two to four, the fever returns with some violence, but it 
is rarely as severe as in the primary paroxysm, and it usually lasts only a few hours. 
With the appearance of this secondary fever a roseolous rash develops, and with 
its development the patient may have a return of his bone and joint pains to a 
very severe degree. Although the fever soon disappears the rash lasts for several 
days and may end in a slight desquamation. Taking it all in all, the secondary 
attack is usually much milder than the first. 

The rash of the second attack is roseolous, and is peculiar in that it is usually 
first seen on the hands, both in palmar and extensor surfaces, and thence rapidly 
spreads to the entire body. The spots are as large as a pea, circular in appearance, 
dusky red, and perhaps elevated. As the disease progresses they may coalesce, 
leaving patches of healthy skin between. This rash is more apt to be profuse and 
to coalesce around the joints than elsewhere. The roseola fades as it begins, first 
on the hands, then on the arms and body, and lastly on the legs. The desquamation 
may last for weeks, but it is so fine that it may be overlooked. The skin never 
peels as after scarlet fever. In some instances the patient passes on to rapid 
convalescence after the terminal or roseolous rash fades, but in others he remains 



DENGUE 119 

miserable for a long time from wandering pains in his joints or in the soles of his 
feet. The muscles are sore on pressure and stiff on moving after a long rest, and 
debility may be persistent. In some instances insomnia or furunculosis delays 
complete recovery. 

In certain epidemics there is sufficient degree of swelling and redness about the 
joints to suggest the presence of acute rheumatism. 

Relapses of dengue occur not infrequently. 

Diagnosis. — Dengue may be separated from rotheln, which it resembles during 
the period of its secondary rash by the lymphatic swellings of the latter disease. 
The differentiation is also accomplished by the sudden severe onset and the pain 
in the joints. It is distinguished from scarlet fever by the lack of sore throat 
and by the peculiar scarlet hue of that disease, and from syphilitic roseola by the 
absence of a history of venereal infection, and the fact that associated symptoms 
of the early secondary stage of syphilis are absent. On the other hand, it is to be 
recalled that many syphilitics, with the onset of the roseola of that disease, suffer 
from a chill and general wretchedness, with pains in the bones. Influenza is sepa- 
rated by the absence of catarrhal symptoms and by the presence of the rash in 
dengue. Acute articular rheumatism and malarial infection are two other diseases 
which must be borne in mind when the diagnosis of an individual case is in question. 

Prognosis. — The prognosis in a case of dengue is always favorable if the patient, 
prior to the attack, is in good health, and not debilitated by some other malady 
or old age. Death may be said not to be known as a result of this malady in 
ordinarily healthy persons. Convalescence, after a severe attack, is, however, 
very often quite slow, and if the patient is living in a hot climate recovery may not 
be complete until a change of residence is made. 

When dengue attacks the aged and feeble, or very young children, it sometimes 
indirectly causes severe illness and death by predisposing the patient to other 
infections so that there develops a severe bronchitis or bronchopneumonia, or some 
other evidence of another acute infection. In such cases the prognosis depends 
chiefly upon the character of the secondary ailment. 

Treatment. — In discussing the treatment of this disease it is to be recalled that 
it presents very different degrees of severity in different cases. In many persons 
the symptoms are so mild that the patient seems scarcely at all ill, and in others 
the manifestations are so severe that convulsions and unconsciousness may be 
present. In the mild cases no drugs are needed, but in the severe cases active 
treatment may be essential. In general terms it may be stated that the treatment 
of the patient suffering from dengue consists in absolute rest in bed from the earliest 
stage of onset till the conclusion of the second stage of fever. Indeed, the longer 
he will consent to rest in bed after the fever develops, the more rapidly will complete 
convalescence be established. 

So far as drugs are concerned, there are no specifics for this disease, which, 
if permitted, will usually run its own self-limited course to recovery. When the 
pains are intolerable they may be controlled by moderate doses of morphine given 
hypodermically or by the use of acetanilid or phenacetin. A gentle antipyretic 
and sedative mixture, containing 5 grains of potassium citrate and 30 minims of 
sweet spirit of nitre in a dessertspoonful of water, is useful to keep the kidneys 
active. An ice-bag may be applied to the head to relieve the cephalalgia, and if the 
face is very much flushed, and the head throbs a hot foot-bath is advisable. Some- 
times a hot bath is useful to develop the rash and relieve the pains in the body 
and limbs. In these cases the salicylates may also be used for the same purposes, 
10 grains of sodium or strontium salicylate, or of aspirin, being given every three 
or four hours. 

W 7 hen the circulation is strong and full McLaughlin asserts that large doses 
of tincture of gelsemium serve to quiet the excited pulse and to relieve the neuro- 



120 DISEASES DUE TO A SPECIFIC INFECTION 

muscular pains. The dose he recommends, namely, 20 to 30 minims every three 
or four hours, seems to the writer much too large and capable of causing serious 
depression; but as McLaughlin has had large experience with the disease, his 
views demand respectful attention. The fever is rarely sufficiently high or pro- 
longed to require treatment. Should it require attention tepid spongings are 
usually sufficient to control it within safe limits; but should it reach as high as 
105° or more, then it must be reduced by cold spongings, or even by the use of the 
cold bath, with active frictions. Should nervous symptoms be very manifest 
and convulsions be threatened, chloral should be given in the dose of 5 grains by 
the mouth, or 10 grains by the rectum, if the patient is a child, and bromide of 
sodium added to aid it in its sedative action. 

The patient should be urged to drink water freely, if his stomach will retain 
liquids, in order to keep his kidneys active in eliminating the poisons of the disease. 
When the stomach is not retentive a pint of cold water may be given by the rectum 
every eight hours. Should diarrhea be troublesome it can be best controlled by 
giving castor oil to cleanse the bowels, following it by opium. 

MENINGOCOCCI MENINGITIS. 

Definition. — Meningococci meningitis, cerebrospinal fever, sometimes called 
"cerebrospinal meningitis," "spotted fever," or "petechial fever," is an acute, 
often malignant, infectious, but rarely contagious disease, due to the diplococcus 
of Weichselbaum, which is sometimes called the meningococcus or the Diplococcus 
intracellularis meningitidis. It is characterized by a rapid course, rigidity of 
the neck, retraction of the head and the formation of inflammatory exudates 
under the membranes which cover the brain and spinal cord. It is to be clearly 
understood that a number of pathogenic microorganisms are capable of producing 
inflammation of the pia arachnoid, and consequently all the symptoms of true 
epidemic cerebrospinal meningitis. Such cases are not instances of this disease, 
but rather are to be considered as sporadic cases of meningeal infection. Indeed, 
it is a noteworthy fact that the sporadic cases of cerebrospinal meningitis which 
are due to the pneumococcus, may be more virulent than those due to the specific 
organism just named. While, therefore, the epidemic form has been proved to be 
always due to the Diplococcus intracellularis meningitidis, it is not correct to call 
all cases of cerebrospinal meningitis instances of cerebrospinal fever. 

History. — No definite description of this disease is to be found in medical literature 
prior to the nineteenth century. In 1805 the first case was described by Vieusseux, 
in Geneva, Switzerland, where several deaths took place from the disease. In 
America it first appeared in Medfield, Massachusetts, in 1806. During the next 
ten years the malady broke out in different parts of Europe and America, but 
disappeared after 1816 till 1822, when it reappeared in France. In 1828 it broke 
out in Ohio. It was not, however, till 1839 that it became sufficiently prevalent 
in any one place to cause a very large number of deaths. In that year, at Versailles, 
it ravaged the town and garrison and produced a mortality of nearly 75 per cent. 
Scattered epidemics have since occurred in the United States at intervals of every 
few years, and it is constantly present in scattered cases in the central part of the 
State of New York. (Eisner.) A noteworthy point in connection with the disease 
is the fact that it suddenly appears simultaneously in widely separated areas, and 
without any dependence upon lines of travel. Thus during a recent period of 
twelve months many cases occurred in New York, but none in Philadelphia, which 
is only ninety miles away. Certain atmospheric influences may make this possible, 
but the cause is not definitely understood. 

Etiology. — There can be no doubt that cerebrospinal fever is due to the diplococcus 
already named, but the same anatomical conditions and a similar clinical picture 



MENINGOCOCCI MENINGITIS 121 

may be produced by other bacteria, for example, the pneumococcus and other 
pyogenic cocci. In cases of cerebrospinal meningitis which have appeared 
sporadically and presented all the signs of the epidemic disease the streptococcus, 
the Staphylococcus pyogenes, the pneumococcus, the gonococcus, and even the 
bacilli of influenza and typhoid fever have been found as apparently the only 
cause of the affection. Dopter has isolated another organism capable of causing 
meningitis resembling the specific disease under discussion, a parameningococcus. 
A similar acute serofibrinous meningitis may accompany pyemia or septicemia, 
or may be due to injury, with infection or extension of infective processes from the 
frontal, ethmoidal, sphenoidal, or mastoid sinuses, middle or internal ear. Such 
forms of meningitis are often called consecutive, incidental, or secondary, and are 
to be distinguished from the epidemic malady. 

Infection probably takes place through the respiratory passages, particularly 
in the nose, and Albrecht and Ghon have described epidemics of rhinopharyngitis 
due to the meningococcus when an epidemic of cerebrospinal meningitis has 
been affecting other persons. Flexner thinks the infection follows the lymphatics. 

Many healthy persons act as meningitis carriers during epidemics. Thus 
Bruns and Hahn examined 600 persons in health belonging to families suffering 
from the disease and found 224 of them were nasal carriers. 

As a rule the organism does not persist in the nasal passages of convalescents 
but it has been found as late as the forty-third day after the onset of the disease. 

Climatic conditions undoubtedly exercise some influence, for the disease confines 
itself almost entirely to the colder parts of the temperate zone, but this is not to 
be taken as indicating that it is a disease of the winter months. On the contrary, 
it appears about equally frequently in winter and summer. While it is true that 
unhealthy surroundings favor all diseases, it is also true that they do not seem to 
greatly influence this malady, for it occurs on high and on low land, when it is 
dry and when it is wet, on hill and in marsh, with equal frequency. As Stille 
says, " It has passed by large cities reeking with all the corruptions of a soil saturated 
with ordure and populations begrimed with filth, to devastate clean and salubrious 
villages and the families of substantial farmers inhabiting isolated spots." 

The disease affects children and young adults far more frequently than persons 
in advanced life. It is slightly contagious, but cases of undoubted transference 
from one patient to another occur as in one notable case reported by me. The 
specific germ if expelled in the nasal mucus by the infected patient may find entrance 
into the nasal spaces of the healthy in fine spray or in the form of dust. The occur- 
rence of the malady in a number of persons living in the same district is usually 
due to the fact that they have all been exposed to the same cause. 

Prevention. — We know of no method of preventing epidemic cerebrospinal 
meningitis, but physicians and others who are attending cases, should wash the 
nasal mucous membrane with normal salt solution to aid in preventing infection 
and full doses of hexamethylenamine should be taken to exert an antiseptic influence 
in the nasopharynx. Iodine tincture 1 part, glycerin 2 parts, and water 4 parts 
may be applied to the pharynx. All cases should be isolated. 

Meningococcus vaccine containing from 500,000,000 to 1,000,000,000 cocci in each 
cubic centimeter has been used for the prevention of the spread of cerebrospinal 
meningitis, particularly on the part of "carriers," in whose nasal pharynx the 
specific microorganisms may be found. Usually three injections are used at 
intervals of seven days. The first of 500,000,000 and the second and third of 
1,000,000,000. 

Frequency. — From what has already been said, it is evident that this disease 
is met in epidemic form, but is comparatively rare. Many practitioners never 
meet with a single or sporadic case in a long career; whereas, others may be so 
unfortunate as to meet several outbreaks. 



122 DISEASES DUE TO A SPECIFIC INFECTION 

Pathology and Morbid Anatomy. — In fulminating cases death may occur before 
the meningeal exudate forms; in these the meninges may exhibit no exudate, 
showing only intense hyperemia and edema, but the membranes and cerebrospinal 
fluid are usually rich in the specific organism. Death in such cases seems to 
depend on the toxic action of the bacteria-laden serous exudate. 

The characteristic lesion of this disease is an acute inflammatory exudate of the 
pia-arachnoid enveloping the brain and spinal cord. This membrane becomes 
infiltrated, and the surface appears to be covered by a white or creamy-white 
exudate, which is most conspicuous in the sulci. The ventricles may contain a 
cloudy, opaque, or even distinctly purulent fluid. The inflammatory exudate 
is most copious at the base of the brain and on the dorsal surface of the spinal cord, 
particularly in the lower thoracic and lumbar regions. When the disease affects 
children the lateral ventricles are often found at autopsy to be distended with 
purulent fluid, but in adults this condition is rarely marked. In the early 
stages of the disease the diplococcus is found in large numbers in the leukocytes 
contained in the exudates, but when death occurs late in the course of the malady 
the germ may be demonstrated with difficulty, if at all. 

In addition to the lesions in the meninges the nerves and ganglia exposed to 
the toxic action of the exudate undergo inflammatory and degenerative changes. 
The involvement of these nerves may leave irreparable damage, manifested by 
blindness, deafness or other phenomena, dependent upon the structures involved. 
Secondary alterations in other parts of the body may be present. These are due 
to the toxins of the disease or to the presence of the microorganisms in the affected 
areas. Thus, we find petechia? in the skin and mucous membranes and some- 
what similar punctate extravasations of blood in the endocardium. Not rarely 
multiple abscesses are found scattered through the body and multiple suppurative 
arthritis may be present. Hyaline and granular degeneration of the voluntary 
muscles is also demonstrable, and the heart muscle, kidneys, and liver may manifest 
necrotic, degenerative, or inflammatory changes. Occasionally there is found, 
associated with the meningitis, croupous pneumonia, ulcerative endocarditis, and 
otitis media. These pathological conditions are characteristic of the severe forms 
of the disease. 

In some cases the lesions are much more moderate, in that hyperemia or intense 
congestion of the pia mater only is seen, although the sulci between the convolutions 
of the brain may contain fibrin or pus. 

Incubation. — The period of incubation is from one to four days. 

Symptoms. — The symptoms of epidemic cerebrospinal meningitis may be grouped 
into five classes — viz., the moderate, the malignant, the intermittent, the typhoid, 
and the chronic form. 

In the moderate form, after an unknown period of incubation, the patient suffers 
from a sudden chill, which may be preceded by, headache and dizziness. The 
headache rapidly becomes very severe and is accompanied by severe pain in the 
back and down the backs of the thighs, the muscles of which are often tense or 
fixed. The fever which follows the chill is usually moderate, rarely exceeding 
102°, and it presents no characteristic curves. On the contrary, it is exceedingly 
irregular and does not show any constant morning and evening variations. Very 
rarely hyperpyrexia may develop. 

As the disease develops the tenseness of the muscles of the legs extends to those 
of the back, neck, and arms, and, finally, they may become almost rigid, and 
contracted to such a degree that the patient develops opisthotonos. The abdomen 
is rigid and scaphoid. Not rarely spasmodic movements of the muscles of the 
face develop as the result of irritation of the roots of the cranial nerves, and by 
reason of this same cause strabismus, ptosis, amaurosis, and diplopia may be present. 
The conjunctiva are usually reddened. 



MENINGOCOCCIC MENINGITIS 



123 



Delirium is a very frequent symptom, and is sometimes so severe as to be mani- 
acal. From this state the patient may pass into coma. 

The pulse and respiration are not greatly affected, except that as the disease 
progresses they may become feeble. Toward the end of the attack, if it be fatal 
in its nature, Cheyne-Stokes breathing may develop and the pulse become rapid 
and small. 

An eruption develops on the skin in about one-half of the cases. When it appears 
about the mouth it is herpetic, but on other parts of the body it is usually petechial, 
although herpes of the skin of the trunk and about the genitals may appear. At 
times a general erythema may be present or in its place an urticaria is developed. 

The presence of arthritis has already been referred to. It appears in about 
20 per cent, of the cases, and, as it is septic in nature, it may cause serious changes 
in the joints and result in permanent deformity if the patient survives. 

The blood shows no marked changes, save that the inflammation of the meninges 
results in a leukocytosis of the polymorphonuclear cells. 

As an almost constant symptom, mention should be made of "Kernig's sign," 
which consists in the fact that in inflammatory processes in the membranes of the 
cord it is not possible to extend the leg on the thigh when the thigh is at right 
angles to the plane of the body. Rarely this sign is unilateral (Fig. 31). 



Fig. 31 




Kernig's sign, showing the strong contraction of the flexors on attempting to extend the leg. 

(After Osier's case.) 

When the leg on one side is passively flexed, the patient being in the dorsal 
decubitus, the other leg is actively flexed. This is called Brudzinski's contra- 
lateral reflex. If the head is lifted from the pillow the thighs are flexed on the 
abdomen and the legs on the thighs. 

In the malignant type of the disease the onset is remarkably sudden. The patient 
is seized by a chill, followed by headache, unconsciousness, and death. Convulsions 
occur more commonly in children than in adults. The fever may be absent, the 
pulse slow, the breathing labored, the urine greatly decreased in amount and loaded 
with albumin, and the stupor profound. The patient in such an instance is probably 
overwhelmed by toxemia, so that death may ensue in a few hours. 

In the intermittent form, which is probably due to the Streptococcus pyogenes, 
or Staphylococcus pyogenes alone, or to association of those organisms with the 
specific coccus of Weichselbaum, the fever intermits, as in malarial fever, but 



124 DISEASES DUE TO A SPECIFIC INFECTION 

the intermittence is irregular, as in sepsis, and is not distinctly periodic, as in 
malaria. The typhoid form is characterized by symptoms of apathy, feebleness, 
and abdominal disorders. 

The chronic form consists in the prolongation of the ordinary type, with special 
symptoms, such as headache, pains in the nerves, vomiting, and progressive emacia- 
tion, with secondary arthritic changes and increasing inability to move the limbs. 
Here, again, it is probable that the maintenance of the illness is due to septic 
organisms rather than to Weichselbaum's coccus. 

While for the sake of description these several types of the disease have been 
named, it is, of course, true that it may manifest various degrees of severity in 
the same case at different periods. Some cases which seem quite severe at the 
onset gradually ameliorate and pass into the chronic or subacute form. The 
fact that the malady presents widely different types is well illustrated by the 
seemingly exaggerated, but nevertheless correct, statement of Hirsch that the 
duration of epidemic cerebrospinal meningitis may be between several hours and 
several months. N. S. Davis stated that its duration in his experience varied 
from twenty-four hours to twenty-eight days. I have seen death occur in eighteen 
hours. 

Complications and Sequelae. — The complications and sequelae of epidemic cerebro- 
spinal meningitis are very numerous. During the attack croupous pneumonia 
not only often develops and aids materially in producing a fatal issue, but acute 
pleurisy also is not uncommon. So, too, inflammation of other serous membranes, 
such as the pericardium and the endocardium and the synovial membranes, is 
often met with, because the coccus has an affinity for these membranes in all parts 
of the body. In the nervous system the most common sequelae are blindness or 
impaired vision due to optic nerve atrophy, ptosis due to oculomotor paralysis 
following neuritis or to changes arising from the inflammatory exudate at the point 
where the nerves leave the membranes, and deafness arising from the effects of the 
acute inflammation or infection upon the auditory nerves. Sometimes the deafness 
arises from an otitis media due to the specific coccus. Aside from chronic naso- 
pharyngeal disease and scarlet fever, this disease is responsible for deafness in a 
larger proportion of cases than any other malady. 

Diagnosis. — While it is true that in a majority of cases the diagnosis of this 
disease is readily made, it is also a fact that many other diseases may produce 
symptoms which so nearly resemble those of epidemic cerebrospinal meningitis 
that it may be absolutely impossible to make a symptomatic differentiation. In 
the first place, it must not be forgotten that cerebrospinal meningitis is, as its 
name implies, an inflammation of the cerebrospinal membranes, and this change 
may be produced by a host of causes, none of which have any true relationship 
with the true epidemic form of the disease. As already pointed out in this article, 
and in that on typhoid fever, the bacillus of Eberth may cause a train of symptoms 
and morbid changes which is identical with that due to the diplococcus of Weichsel- 
baum, yet such a case would not be one of epidemic cerebrospinal meningitis. 
It is evident, therefore, that cases of retraction of the head, rigidity of the limbs, 
and twitchings of the face should not be called true cerebrospinal fever unless 
the specific diplococcus can be demonstrated, or unless the disease can be found 
to be present in other patients in the vicinity. In the midst of an epidemic of 
typhoid fever the development of cerebrospinal symptoms should be credited to 
this infection rather than to the specific fever now under discussion. If any 
doubt exists as to the true nature of the affection, it should not be forgotten that 
herpes is very rare in typhoid fever and in typhus fever, but is common in true 
cerebrospinal fever. Both these fevers run a course which is marked by a natural 
limit; whereas, epidemic cerebrospinal meningitis does not begin to decline after 
the lapse of a definite course, but is exceedingly irregular in its duration. 



MENINGOCOCCIC MENINGITIS 



125 



Croupous pneumonia is the infection, above all others, which is capable of 
misleading the physician in his diagnosis of cerebrospinal fever. It has already 
been stated that pneumococcus is often found to be the cause of inflammation of 
the meninges, and in children in particular the cerebrospinal symptoms may be 
so well developed that unless the physician examines the lungs very carefully, 
he may diagnosticate cerebrospinal meningitis when in reality the true cause lies 
in the lung. It would seem that two types of cerebrospinal symptoms develop in 
pneumonia, namely, those due to the secondary meningeal infection with the 
pneumococcus and those in which there is no true infection, but simply irritation 
produced by the toxemia of the pneumonia. 

Some cases of acute poliomyelitis, both in adults and children, may so closely 
resemble meningococcic meningitis that a differentiation can be made only by 
the discovery of the specific diplococcus. (See Acute Polioencephalitis.) 



Fig. 32 




A, space between the third and fourth lumbar vertebrae which can be used for puncture; or B, the 
space between the fovrth and fifth lumbar vertebrae. 



Tuberculous meningitis is very rarely so sudden in onset as is the true epidemic 
form, and careful physical examination of the patient will usually reveal a primary 
tuberculous focus if meningeal tubercles are present. The von Pirquet or Moro 
tests may aid in the diagnosis. When the inflammation is tuberculous the leukocyte 
count is not materially increased, whereas, in the specific type it may vary from 
9000 to 26,000. 

When cerebrospinal symptoms develop in the presence of an epidemic of influenza, 
the differentiation between true cerebrospinal meningitis and that due to influenza 
may be impossible, although the fact that the case is single points to the influenza 
bacillus as the true cause rather than that the attack is a sporadic case of the 
disease now under discussion. The cerebrospinal symptoms of influenza are 
rarely so severe or so persistent as those due to epidemic cerebrospinal fever. 

The greatest aid that we have in differential diagnosis is by means of lumbar punc- 
ture. This operation consists in inserting a large hollow needle between the third and 
fourth or fourth and fifth lumbar vertebra?, a little to the side of the median line 
and just below the spinous process. The needle as it enters should be directed 
upward and inward. In children the fluid is reached when the needle is inserted 
about 2 cm., and in adults when it has reached the depth of from 4 to 6 cm. As 
soon as the membrane containing the fluid is punctured it flows from the needle 
in drops, which should be caught in a sterile test-tube in such a way that the fluid 
does not run down its side. If the infection is due to the specific organism, the 



126 



DISEASES DUE TO A SPECIFIC INFECTION 



pressure is greatly increased, so that the fluid may escape with a spurt. This 
fluid is clear if tuberculous meningitis is present, but cloudy if the diplococcus of 
Weichselbaum is the cause of the illness. If the fluid also has a yellowish or greenish 
color it is significant of a virulent infection. Under these circumstances, too, 
the faint trace of albumin found in the normal fluid is very distinctly increased 
in proportion to the severity of the attack, and the absence of dextrose as shown 
by the ordinary copper tests is pathognomonic of meningitis. The poly nuclear 
cells are also greatly increased and their excess is a gauge of the severity of the 
infection. The careful staining of a single specimen or a more exhaustive bacterio- 
logical examination may reveal the presence of the diplococci, most of which are 
intracellular. 

Fig. 33 




Introduction of needle between the last two lumbar vertebrae. The syringe is used as a convenient 
handle for the needle, and is unscrewed after the puncture is made. 



Demonstration of the meningococcus in the nasal mucus is an important addition 
to other signs. Netter and Debre in 100 tests in 49 patients found it in 78.33 per 
cent, in the first week, in 60 per cent, in the second week, and in 50 per cent, in the 
third week. Even after the fifth week it was found in more than 15 per cent., but the 
disease may occur without the specific coccus being present in the nose, and a men- 
ingococcus rhinitis neither preceded nor followed by meningitis is not of excep- 
tional occurrence. 



MENINGOCOCCIC MENINGITIS 127 

Prognosis. — The prognosis of true epidemic cerebrospinal meningitis is 
grave, but its rate of mortality varies in wide limits, namely, from 20 to 75 per 
cent. In children under two it is almost always fatal, and before puberty its 
mortality is very high. The most violent cases usually meet death by the fifth 
day, but it is not to be forgotten that many others reach the fourteenth day before 
death occurs. Then, again, it sometimes happens that after several days of 
severe symptoms the general aspect of the case improves, but the favorable signs 
only persist for a few hours and then the symptoms return with renewed vigor. 
Further than this, patients who seem about to recover not rarely suffer from a 
relapse which may prove fatal. Koplik asserts that the character of the spinal 
fluid is of great prognostic value. If it is thick and purulent the outlook is bad; 
but if it is of a straw color and clear it is better. 

Treatment. — The treatment of true cerebrospinal meningitis whether it appear 
in sporadic or in epidemic form consists in the use of antimeningococcus serum 
as first prepared by Flexner. It is not an antitoxic serum but acts on the coccus. 
This serum is that of the horse which has been inoculated by the Diplococcus 
intracellularis and its products. It has been proved that the subdural injection 
of this serum, if given early enough and repeated at proper times and in proper 
doses reduces the mortality from about 80 per cent, to about 20 per cent, and also 
shortens the duration of the disease. It also prevents to a large extent the patho- 
logical changes in the meninges and elsewhere which produce the secondary lesions, 
which so often develop in those who recover without the use of the serum, such as 
deafness, blindness, and deformities. The subdural injection of the serum results 
in a remarkable diminution in the growth and number of the specific coccus of 
the disease, as they are seen in the cerebrospinal fluid. Further than this the 
abnormal turbidity of this fluid is overcome so that it becomes limpid and approxi- 
mately normal in appearance. 

The use of the serum is often followed by a sharp fall in temperature almost 
like the crisis of pneumonia. Consciousness returns, the mind becomes clear 
and headache and vomiting cease usually within twenty-four hours. Kernig's 
sign and stiffness of the neck, however, often persist for a day or two more. 

Thirty c.c. of serum is injected into the subarachnoid space after 30 c.c. of cere- 
brospinal fluid is withdrawn by means of lumbar puncture and the dose is repeated 
daily until marked improvement ensues. If a tendency to relapse occurs it is 
again resorted to. In no case should the clinical diagnosis wait for confirmation 
by the laboratory but the antiserum should be given at once. The earlier it is 
used the better it acts. Used late it may do little good save to prevent relapse. 

In making the lumbar puncture, for the purpose not only of drawing off fluid 
for diagnostic purposes but with the object of injecting the specific serum, it is well 
to use a special apparatus and not to employ for injection purposes an ordinary 
syringe. This apparatus consists of a strong, hollow needle or cannula fitted 
with a by-pass which is governed by a small valve and which is attached to one 
side of the cannula rather than at its external orifice, as it may be necessary to 
dislodge some obstruction in the cannula by inserting a trocar. To a piece of 
tubing attached to the by-pass is attached a straight glass tube, which is either 
gauged by marks made upon it, or is fitted with a gauge resembling that of 
a thermometer. By this means an estimation of the pressure of the cerebrospinal 
fluid is obtained. This is important, because it is unwise as the fluid is with- 
drawn to permit the pressure to fall too low, and when the specific serum is 
injected it is important that the pressure should not be too high. By the use of 
a burette attached to the end of the cannula and into which the serum is poured, 
the injection can be given; the pressure of the injection being modified by the 
height at which it is held. 

The treatment of true cerebrospinal fever, except by antimeningococcic serum 



128 DISEASES DUE TO A SPECIFIC INFECTION 

is not satisfactory. We know of no remedies which exercise any true curative 
influence, and all the physician can do is to keep the patient during the acute 
stages in a quiet, darkened room, and to give sedatives in sufficiently large doses to 
prevent convulsions of sufficient violence to exhaust the patient. Chloral is a 
powerful and useful drug for this purpose, being given in the dose for an adult of 
20 grains by the mouth, or 60 grains by the rectum, in starch-water. Pain is to 
be relieved, if excessive, by the use of morphine in adequate doses, as much as 
J a grain being used if needed, particularly at night, to give rest and sleep. 

Mention has already been made of lumbar puncture for diagnostic purposes. 
When headache, high temperature, rigors, or stupor are marked, the relief of the 
pressure upon the brain and spinal cord by this means may be temporally effected, 
but that it aids the patient permanently is very doubtful. The amount of fluid 
withdrawn should equal 40 to 50 c.c. 

Relief from the severe pains in the limbs and back may be obtained in some 
cases by immersing the patient for long periods of time in a hot bath of plain or 
salt water at 99° or 100°. 

The fever is rarely high enough to need treatment. If it is above 105°, the 
ice-bag and the use of cool spongings with frictions may be resorted to. 

In all cases the diet should be one which is easily swallowed and easily digested, 
and everything should be done to support the system. This is particularly neces- 
sary in the prolonged types, in which marked emaciation is often present. 

CROUPOUS PNEUMONIA. 

Definition. — There is no condition of the lungs which is so apt to be confused 
in the mind of the student as that designated pneumonia. This is because the 
word "pneumonia" is used by some medical men to designate a single disease 
affecting the lung and by others as signifying any state in which, as the result of 
an inflammatory process, a part of the lung becomes congested or consolidated. 
The latter is the better use of the word, and when the physician desires to state 
that a definite lesion is present he should specify the type of pneumonia by em- 
ploying an adjective to qualify the noun — i. e., he should speak of the various forms 
of pneumonia as croupous or lobar pneumonia, catarrhal or lobular pneumonia, 
and of tuberculous pneumonia. The term "pneumonia," while commonly used 
to signify croupous pneumonia, means nothing more definite than consolidation of 
the lung. 

Croupous Pneumonia is sometimes called Lobar Pneumonia, Pneumonitis, 
Lung Fever, or Fibrinous Pneumonia. 

Croupous pneumonia is an acute infectious systemic disease depending for its 
existence, when in its typical form, upon the activity in the body of the specific 
organism known as the Micrococcus lanceolatus, sometimes called the pneumococcus 
of Fraenkel. As the result of this infection, there takes place in the lung an acute 
inflammation accompanied by the exudation into the air vesicles of an adhesive, 
croupous, or fibrinous exudate, which produces consolidation of the lobe or lobes 
affected. In addition to these changes the patient suffers from a greater or less 
degree of toxemia, due to the poisons made by the infecting microorganisms and 
from the changes produced in the tissues of other organs than the lungs by the 
growth of the micrococcus or by its toxins. This disease is also characterized by 
the fact that it usually lasts about nine days and ends by crisis, although this 
crisis may occur as early as the third day or even earlier in very rare instances. 

While it is true, as already stated, that croupous pneumonia is, in its typical 
form, due to the Micrococcus lanceolatus, it is also a fact that lobar pneumonia 
or consolidation of the vesicular portions of a lobe or lobes may arise from infection 
by other microorganisms. Such an occurrence is, however, rare, the non-specific 



CROUPOUS PNEUMONIA 129 

infection resulting usually in abortive changes in the pulmonary parenchyma, or 
running a course at variance with that commonly pursued by the true infection. 

Etiology. — The development of croupous pneumonia is dependent upon many 
causes, some of which we do not know. These causes are those external to the body 
which produce conditions in the individual favorable to the growth of the specific 
germ, and internal causes which exert similar influences. The importance of 
these conditions is shown by the fact that the pneumococci are periodically or 
continuously present in the oral secretions of a large percentage of healthy human 
beings and further they are present in greater number and greater virulence in 
December and January, and in less number and virulence between April and Novem- 
ber. Although the organism is capable of rapidly increasing in virulence, this 
cannot be held to account for all cases of infection, as even the most virulent strains 
are sometimes found in normal persons. 

So far as season is concerned, there can be no doubt that the summer and autumn 
months are the ones in which the fewest cases occur. Thus, the combined statistics 
of Seitz, in Munich, and Jurgensen for six large German towns, and of Sturgis 
for Westminster Hospital, London, show that in winter the incidence is 31.7 per 
cent.; in the spring, 34.6 per cent.; in the summer, 15.1 per cent., and in the autumn, 
18.5 per cent. The following chart is based upon 35,828 cases occurring in hospitals 
in the United States, Germany, and Austria, and 19,000 cases occurring in the 
Confederate army during the year 1862, collected by Joseph Jones. 

Exposure to cold was thought for many years to be a cause of croupous pneu- 
monia, but we know that this acts only as a predisposing cause which decreases 
the general systemic, or local, power or resistance to infection; in other words, 
it is prone to affect all persons whose vital resistance is diminished. Living in 
poorly ventilated rooms is a predisposing cause, as is prolonged physical or mental 
strain, or any condition which saps vitality. A very interesting illustration of the 
effect of fatigue, bad air, and exposure in the production of croupous pneumonia 
has been recorded by Connell, of Leadville, Colorado, who reports the common 
occurrence of the disease in miners and others who go on long railway journeys 
for a day's outing and live during that time in badly ventilated railway cars. 

Croupous pneumonia is also a disease peculiarly apt to attack those of advanced 
years, and a very large proportion of deaths among the aged is due to this cause, 
such patients seeming to possess little resistance to its attack. This inability to 
resist the infection depends upon at least two causes — viz., a feeble heart muscle 
which cannot meet the circulatory demands of the disease nor resist the depressant 
effects of its toxins; diseased kidneys, or kidneys impaired in function, whereby 
toxic materials cannot be speedily eliminated and, as the general result of which the 
vital resistance of all the tissues is diminished, so that not only the specific organism 
is permitted full sway, but the patient is also placed in a favorable condition for 
the growth of other infecting microorganisms which aid in producing a fatal 
issue. It is because of these facts that pneumonia so frequently attacks those 
who are already in ill health, or who are suffering primarily from some other malady, 
and it is for these reasons that it so often ends in death. Acute and chronic alcohol- 
ism greatly predispose to croupous pneumonia, and it is a singularly fatal disease 
in persons addicted to alcohol. In many cases it is a terminal infection. 

Sometimes an injury to the chest wall will be followed by acute croupous pneu- 
monia, probably because the trauma to the lung renders it susceptible to infection. 
Numerous experimental observations have confirmed this clinical fact, which may 
be of great importance from a medicolegal stand-point, as well as from the purely 
clinical aspect. Without doubt local injury renders a part peculiarly susceptible 
to infection by any pathogenic microorganisms which may enter it, and as the 
pneumococcus is a constant inhabitant of the mouth in healthy persons, a source 
of infection is ever present. 
9 



130 



DISEASES DUE TO A SPECIFIC INFECTION 



There can be no doubt that the disease is capable of being spread from one patient 
to another. On several occasions I have seen pneumonia contracted by the wife, 
or daughter, of a patient who was engaged in nursing him, and repeatedly it has 
occurred that the introduction of a case of pneumonia into a ward of a hospital 
has resulted in the development of the disease in other patients. Thus, out of 
eleven women suffering from typhoid fever on admission to my wards in the Jefferson 

Medical College Hospital, no less than 
Fig. 34 eight suffered from croupous pneumonia 

after the introduction of a single case of 
this disease. 

Unlike many of the acute infectious 
diseases, one attack does not protect 
against another, but rather predisposes 
the patient to subsequent attacks. 

Distribution. — Croupous pneumonia is 
met with in all parts of the world, but 
it is more common in the temperate 
than in the tropical zones. In the United 
States its greatest mortality occurs in the 
great Northwestern States east of the 
Rocky Mountains, in which district it 
causes 120, or more, deaths per 1000 
deaths from known causes. Only a few 
areas in the States east of this area have 
so heavy a mortality, even if large cities 
like New York, Philadelphia, and Chicago 
are included. 

Frequency. — Statistics as to its fre- 
quency are to a large extent vitiated by 
the fact that in many health reports the 
difference between the various forms of 
pneumonia is not specified. There can be 
no doubt, however, that it is one of the 
most common and most fatal of all acute 
infectious diseases, and that its frequency 
and mortality are increasing. The United 
States census shows the total mortality 
per annum from pneumonia to be 
105,971, of whom 58,340 were males 
and 47,631 were females. The propor- 
tion of deaths was 106.1 for each 1000 
deaths from all known causes. Its average mortality is about 1.5 to 2.3 per 1000 
persons living. 

At times croupous pneumonia may occur in epidemic form and cause an extra- 
ordinary increase in the death rate of a given district. Thus, the mortality from 
this disease in Chicago, as shown by Reynolds in his official report covering the 
period from January 1 to June 1, 1903, became remarkably high. There were 
2891 deaths from pneumonia, as compared with 1321 from consumption and 1238 
from all other communicable, contagious or infectious diseases, including diphtheria, 
erysipelas, influenza, measles, puerperal fever, scarlet fever, smallpox, typhoid 
fever, and whooping-cough. This is an excess of 382 pneumonia deaths over the 
deaths from all the other preventable diseases— 1570, or 118.8 per cent., more than 
the deaths from consumption, and 1653 or 133.5 per cent., more than those from 
the other specified diseases. 





3 

»-a 




3 


a. 


3 


2 


"■a 


ii) 
s 
< 


Sk 
3£ 




> 
O 
S5 


q 


5400 


























5200 


\ 
























5000 


























4800 


























4600 


























4400 


























4200 


























4000 


























3800 


























3600 


























3400 


























3200 


























3000 


























2800 


























2600 


























2400 


























2200 
























2000 


























1800 


























1600 


























1400 


























1200 


























1000 


























800 



























Chart showing the seasonal incidence of croupous 
pneumonia. 



CROUPOUS PNEUMONIA 131 

Croupous pneumonia occurs with the greatest frequency between the ages of 
forty and fifty years, but it is also very common between fifty and sixty. The 
mortality is in direct proportion to the age of the patient. It affects males far 
more frequently than females, the proportion being as high as 88 per cent, of the 
former to 12 per cent, of the latter (Kerr). This high proportion in men is 
probably too high for the average, but it serves to emphasize the fact stated, and 
is approximately correct. The reason probably lies in the greater exposure of 
men to cold and wet and to their abuse of alcohol. 

The relative frequency with which croupous pneumonia affects the right and 
left lung, as based on many thousand cases collected by Meltzer in Russia ; Jiirgen- 
sen, Moellmann, and Brach in Germany, and West and Pye-Smith in England, 
is for the right lung, 51.4 per cent.; left, 39.4 per cent., and for both lungs, 9.2 
per cent. 

In 495 cases examined at autopsy, and collected by Fowler, Osier, Kerr, and 
Steven in this country and England, the disease was unilateral in 83 per cent. It 
is unilobar in the proportion of about 50 per cent. The disease affects a lower 
lobe in nearly 75 per cent, of the cases. 

Prevention. — At the present time we have no means of directly preventing 
development of this disease. It is hardly necessary to state that the sputum 
of the patient should be received into a spit-cup containing some suitable disin- 
fectant, or into a cloth which should be speedily burned. A patient suffering 
from croupous pneumonia should not sleep in the same bed with a person who is 
in health, and should be isolated as much as possible. 

Pathology and Morbid Anatomy. — In studying croupous pneumonia it must not 
be forgotten that the disease is, at least in some cases, a general infection with 
the Micrococcus lanceolatus, the morbid changes being chiefly manifested in the 
lungs, just as in typhoid fever they are chiefly manifested in Peyer's patches. The 
pneumococcus is found in the blood during the progress of this disease with great 
frequency, now that proper methods for its discovery are employed. Thus, 
Prochaska has found it in the blood in 38 out of 40 consecutive cases, Rosenow 
has isolated it in 77 out of 83 cases, and has discovered it in the blood as early as 
twelve hours after the initial chill. On the other hand, the mere presence of the 
pneumococcus in the blood of a patient does not necessarily mean that pneumonia 
is present, for it has been found in the blood in cases of tonsillitis, otitis, arthritis, 
and in pulmonary edema. Parker and many others have even described cases 
of purulent peritonitis due to this organism. Trevisanello demonstrated it in 
pure culture in the herpes of pneumonia but in weakened virulence. The possi- 
bility of spread of the disease from such lesions is obvious. 

Engorgement Stage. — The first change taking place in the lung in croupous 
pneumonia is a hyperemia of the intervesicular tissues of the lobe or lobes about 
to be consolidated. This engorgement rapidly becomes more marked, and is 
accompanied by the exudation into the air vesicles and later the smaller bronchi of 
white cells, red blood cells, and plasma. From the plasma fibrin forms and causes a 
solid exudate, so that all that part of the lung which is affected may, in the course 
of a few hours, be devoid of air and impervious to its passage, except in those 
bronchial tubes which are of some size. 

Stage of Red Hepatization. — The lung is now said to be in the stage of red 
hepatization (Fig. 35), since the exudate is red from blood-coloring matter, and 
the consistency of the organ to touch and on section resembles that of fresh liver; 
hence it is said to be hepatized or liver-like. 

When a cross-section is made of the solidified lung the surface is seen to be granular 
because of the protrusion of the exudate from the air spaces. In some instances 
the cut surface is found not to be uniformly solid, probably because the process is 
less marked in some places than in others. This appearance of the lung on section 



132 



DISEASES DUE TO A SPECIFIC INFECTION 



is also largely modified in young children and in greatly enfeebled individuals, 
in whom the degree of solidification may be much less marked. If the exudate 
is examined microscopically, it will be found to contain not only shreds of fibrin, 
red and white cells, and desquamated epithelial cells from the walls of the vesicles, 
but large numbers of pneumococci as well. That the amount of extravasation 
is in many cases extremely large is shown by the fact that a lung may increase in 
weight by six or seven pounds. The leukocytes of the exudate constantly increase 



in number during this stage. 



Fig. 35 




Lung ; croupous pneumonia, stage of red hepatization. The centre of the microscopic field is occupied 
by an air vesicle containing a mass of exudate composed of a network of fibrin, red blood cells, and a 
few leukocytes. 

Stage of Gray Hepatization. — Following the stage of red hepatization there 
ensues the stage of gray hepatization. At this time the acute inflammation in 
the lung has passed by and the system is beginning the task of clearing away the 
results of the disease. This is made possible by liquefaction (autolysis) of the 
fibrin and dead cells, probably caused by enzymes from the leukocytes in addition 
to fatty degeneration of the cells. During this stage of resolution the exudate 
is gotten rid of by absorption and expectoration. Finally, the air cells are freed 
from the exudate with which they were filled, the epithelial lining is reproduced, 
and recovery results. 

Unusual Changes. — In rare instances the normal process of resolution is not 
followed, and in its place organization of the materials which have been extravasated 
takes place to some degree, new connective tissue is proliferated into the air vesicles 
from their walls, and fibrous bands containing bloodvessels extend throughout 
the lungs. Simultaneously a similar growth takes place in the interstitial tissues, 
and so the lung gradually becomes consolidated by overgrowth of fibrous tissue, 
i. e., organizing lobar pneumonia. 

Flexner and others have urged the view that unresolved lobar pneumonia is 
due to the fact that, owing to some disproportion between the leukocytes and other 
constituents of the exudate, or other causes as yet undiscovered, the normal process 
of autolysis is not carried out, and so the exudate undergoes organization instead 
of resolution. 

In other instances which are far more rare the process of resolution is supplanted 
by the development of abscess or gangrene of the lung, which conditions are 



CROUPOUS PNEUMONIA 



133 



Fig. 36 



probably due to secondary infection of the lung by the streptococcus pyogenes, 
or staphylococcus pyogenes, or other bacteria capable of producing such lesions. 
Sometimes the process of fatty change and death of the extravasated cells is so 
rapid that on section of the lung the vesicles exude a purulent matter looking like 
true pus, which indeed it may be, but this in no sense is an abscess of the lung. 

Associated with the changes in the lungs we find adjacent organs involved 
by direct extension of the inflammatory process or by the infection itself. The 
most common of these is inflammation of the bronchi (bronchitis), which 
is practically always present. After bronchitis in frequency comes inflammation 
of the pleura, due to direct extension from the underlying lung and to infec- 
tion of the pleura by the specific organism 
of the disease. Nearly always this is mani- 
fested by the formation of a plastic fibrinous 
exudate on the serosa and an abnormal 
amount of fluid in some part of the pleural 
cavity, which fluid is often serous and not 
infrequently purulent. (See Pleuritis.) 

Sometimes the pericardium is similarly 
affected, and even the endocardium may 
be infected by the specific germ. (See Peri- 
carditis and Endocarditis, under Complica- 
tions.) 

Reference is made elsewhere to the men- 
ingitis which sometimes develops. 

It is a great mistake to view the lesions 
just described as representing all the path- 
ology of croupous pneumonia. It is true 
that these changes are the most evident, 
but it is not to be forgotten that the toxemia 
of the malady exerts a very great influence 
in producing symptoms and lesions during 
life which are not so readily seen, but are 
equally important in their influence on the 
patient. The muscular fibres of the heart 
and the epithelial cells of the kidneys un- 
dergo albuminous degeneration, and similar 
changes occur in the liver. When the heart 
is opened after death we frequently find its 
cavities, particularly those of the right side, 
almost filled by firm clots, part of which 
may have formed so long before death as to 
be of the " chicken-fat" type. The liver is 
often found to be greatly engorged with blood, 

because of the impeded circulation in the vena cava, produced by the difficulty 
with which the right side of the heart empties itself. The bronchial lymph nodes 
also show by the swelling of their cells and by their distended sinuses that they 
have endeavored to prevent the entrance of the micrococcus and its toxins into 
the general system, for in them may be found broken-down cells, red cells, pneu- 
mococci, and phagocytes containing cells or organisms. 

My colleague, Coplin, has shown that definite changes take place in the inter- 
costal muscles in the course of pneumonia and pleurisy. 1. Granular degeneration 
or cloudy swelling of the muscle fibres, which is probably a part of the general 
action of the toxic bodies circulating in the blood. 2. The muscle fibres are dis- 
sociated, edema is present, but there is little fibrin-containing substance. Groups 




Antemortem heart-clot from a case of 
pneumonia, extending into the vessels. 
(Comrie.) 



134 DISEASES DUE TO A SPECIFIC INFECTION 

of muscle fibres and bundles show changes that cannot be differentiated from 
the hyaline degeneration described by Zenker as occurring in the muscles of the 
abdominal wall in typhoid fever. 3. In addition to the changes already described, 
leukocytes become abundant, bacteria are often present, and, finally, if the in- 
flammatory process is chronic, there is an overgrowth of fibrous tissue and fatty 
infiltration of the muscle. 

Incubation. — The incubation period of croupous pneumonia, that is the time at 
which the chill of onset occurs after exposure to another case, is forty-eight 
hours. 

Symptoms. — Before describing the symptoms met with in cases of croupous 
pneumonia, it is essential to emphasize the fact that in no other infectious disease 
are the manifestations of illness so variable. These variations depend not only 
upon the virulence of the infecting germ and the susceptibility of the patient, 
but upon his habits, age, and general state of health. In some cases the malady 
develops as a frank, open inflammation of the lung. In others, it is so insidious 
as to be overlooked, except by the most careful physician. In certain cases the 
course of the disease is markedly sthenic, in others profoundly adynamic. In 
still others the progress is so mild that the patient is never seriously ill, and in 
some instances it springs like a tiger upon a seemingly healthy man and destroys 
him. 

The symptoms of croupous pneumonia may be divided into three stages for 
readiness of description — namely, those of onset, those of the well-developed 
stage, and those of convalescence. 

Stage of Onset. — The patient, usually an adult, is seized after, or without, a 
brief period of general malaise, with a chill, followed by a well-developed fever. 
The chills may be repeated and may vary from a slight feeling of creepiness to 
a severe rigor of sufficient force to shake the patient severely, and to last for over 
an hour. The pulse is quickened, but not as much so as we would expect from 
the sharpness of the onset, and at first may be small, but soon becomes full and 
bounding if the patient has been previously in good health; the respirations are 
also markedly increased in rate per minute. More or less severe pain may be 
felt in the chest on the affected side. The degree of pain, however, varies greatly, 
some patients bitterly complaining of it, while others seem to have little or no 
suffering, probably because in the latter cases the inflammation of the lung is so 
deeply situated that it does not extend to and involve the visceral layer of the 
pleura. It is important to bear in mind the fact that this pain not infrequently 
is referred by the patient to another part of the body. I had a case admitted not 
long since to my wards, on the statement of a well-known physician that she 
had appendicitis, when she was really suffering from a pleuropneumonia of the 
right lower lobe. Children are very prone to refer the pain to the epigastrium. 

If the patient is very feeble it sometimes happens that the onset of the malady 
is insidious and no pain felt. This is especially apt to be true when the disease 
complicates chronic alcoholism, renal disease, or other grave malady. 

The temperature usually makes a sharp and decided rise, immediately after 
or during the chill, to 103° or 105°, and in some cases even higher than this, and 
remains high throughout the disease, the variation in the morning and evening 
temperature not being more than a degree or a fraction thereof. (See Fig. 37.) 

The face is usually flushed, particularly over the cheek bones, and it is a note- 
worthy fact that this flush is usually most marked upon the cheek of the same 
side as the lung involved. The expression of the face is apt to be somewhat 
anxious, the skin dry and hot, and a moderate degree of cyanosis may be seen 
in the capillaries of the lips and finger-tips, and about the nose. 

Violent headache may or may not be present. A more or less active delirium 
may also develop at this time, and the patient may be quite restless unless the 



CROUPOUS PNEUMONIA 



135 



pain in the side makes it more comfortable to lie quietly in bed. An incessant 
unproductive cough is often an early symptom of onset. 

The physical signs of the disease in the thorax in the stage of onset are not, 
as a rule, well marked. Inspection may reveal some impairment of expansion 
upon the affected side; palpation may evince some increase in vocal fremitus; 
auscultation will show in many cases fine crepitant rales, increased bronchial 
breathing or tubular sounds, increased loudness of vesicular breathing for a few 
hours, and often some exaggeration of the normal respiratory sounds on the sound 
side. Indeed, this increase in the harshness of the breath sounds over the normal 
side, due to the increased activity on the part of the healthy lung, to compen- 
sate for the impairment of the diseased lung, may mislead the beginner in physical 
diagnosis into thinking that this is the lung diseased. Percussion may also reveal 
some impairment of resonance over the affected area. 

Fig. 37 



BOWELS 


=> 






















> 
























> 




















> 












= 














- 








URINE 


-t 






















« 
























I 




















s 


























s 












a~ 










































































































































































































































































































































































































106 

105° 

101° 

~ 103 
cc 
I 
< 

lx- 

^ 102 

LU 

tx 

3 


















































































































































































































































































































































































































-* 






L 5- 




-= 




















«j-i 




-f- 




























'- 














o" 


-S 












































































































































































































































































































































































































' 




































<" 




js._ 








^ 






_2 




- s - 


"<" 


_s_ 










Jr 


K 


1 




































-t 


< 


; 


< 






< 




< 




< 




< 


UJ 




2 


3- 


























■S-| 


E 












| 


i 


-i- 


~s 


5- 


2- 


-s 


| 


•£ 


-s- 




-f 


s 


5 


1 




1" 


2- 




I- 


:-: 


1 


->o_ 


1 


s : 


-s 


: !- 




































































"2^ 


s 






:s: 


^" 






































































































































































































>- 














< 


























































































































































~£' 
















































































































■p 




-2- 




1 
















































































































I 






































































JL 


ri 




£> 




a> 










.0 




Q 






< 
























































































































































































s 


















































































































































< 101 
111 

£ 

H .1.00° 
99° 

98° 
97 
















































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































^ 




:? 
























"w 


















.... 




_U|. 






"S 




-3- 










V- 




"IS" 




IS 






X 




"S J 
















*3 


^ _ 












5 


















































































































































































































»■ 




-S 






s 




£- 


















: 


.E 


_S. 




■ 2= - 


■SK 




-; 
























































































































































M 


lO 












°- 






















































































-G^ 
















































































































































































































































































































































































































s- 






































































































































































































































































































































































































DAY OF 

DISEASE 


CO 










^ 












lO 












o 






o 






00 




PULSE 


f. 


fa 

V 


t4 


t4 


t& 


t4 


t 


& 

%> 


f4 


f& 


#& 


t4 


t4 


•$$ 


&> 




>f<^ 


f 


^ 
^ 


St 
f-4 


3# 


\>>' 


^ 


P 




<$ 


f# 


^ 


>*^ 


RESP. 


■5) 


% 




H 


■p 


?4 


% 




?% 


% 


% 


H 


£*' 


f 


/•5i 


$ 


& 


#'%' 
/'"#' 


?4 




H 


DATE 


c-. 










o 

CO 












T-l 












C3 












■* 





A chart of croupous pneumonia in a girl of six years, showing the little effect produced upon the 
temperature by sponging, and the characteristic crisis on the sixth day. 



Developed Stage. — The developed stage of the disease is characterized by 
certain conditions and physical signs, some of which are almost pathognomonic 
of the malady. The peculiarity of the pulse is that it is quite slow as compared 
to the rapidity of the respirations. Usually when high fever is present the pulse 
rate is as high as 110 or 120., or even higher, while the respirations are about 24, 
but in pneumonia of the croupous type the pulse rate is sometimes only 90, while 
the respirations are as high as 30 per minute. Sometimes, however, the respi- 
ratory rate mounts to as high a point as 40 or 50 per minute, while the pulse 
reaches 110 to 120, the relative proportion being 1 to 3, while in health it is usually 
about 1 to 4.5. 

A second peculiarity of this stage is the rusty or bloody sputum, which is still 
more characteristic in that it is sticky and tenacious, and therefore difficult to 



136 DISEASES DUE TO A SPECIFIC INFECTION 

expectorate, and so adherent that even when a spit-cup is filled with it the vessel 
can be held nearly upsidedown without losing its contents. 

A third characteristic of croupous pneumonia at this stage is the development 
of single or multiple fever blisters, or spots of herpes, upon the lips or about the 
edges of the nostrils. 

Dyspnea may or may not be present. If present it depends upon the fact that 
so much of the lung is involved that respiration is difficult, or it is due to feeble- 
ness of the heart from engorgement of its right ventricle by the blood which can- 
not pass readily through the diseased lung; or, again, it may be dependent upon 
actual impairment of the power of the heart as a result of the action of the toxin 
of the disease upon its muscular tissues and nerve centres. Dyspnea in croupous 
pneumonia may, therefore, be due to pulmonary, cardiac, or toxic causes. Cyano- 
sis may be very marked, and not uncommonly the jugular and other superficial 
veins can be seen to be full and distended. 

A peculiarity of the dyspnea of pneumonia is the fact that the patient does 
not seem capable of resting quietly, but continually moves about making exer- 
tions which seem scarcely compatible with so much shortness of breath. 

Delirium of an active type is common in this stage, and it may be difficult 
to keep the patient in bed, particularly if he is an alcoholic. 

During the second stage of croupous pneumonia the pulse may become hob- 
bling or dicrotic, the heart sounds tumultuous, and the dyspnea severe. In other 
instances the pulse seems voluminous, but nevertheless is very easily compressed 
to the point of extinction, while the sounds of the heart reveal the fact that that 
viscus is laboriously endeavoring to fill vessels which, because of their relaxation, 
fail to offer the normal resistance to its action. In still other instances, if the 
heart is markedly affected by the toxemia of the disease, the heart sounds will 
be feeble and difficult to differentiate, and the pulse be very small and easily 
extinguished by pressure. In still other cases auscultation over the area of the 
pulmonary valves at the third left interspace will reveal accentuation of the pul- 
monary second sound or a murmur due to incompetency of these valves under 
pressure, while later on the labored action of the heart is shown not only in the 
signs named, but also in the pulsating jugular veins, which are distended and full, 
indicating great venous engorgement, as the result of the obstruction of the flow 
of blood out of the right ventricle, or because of incoordination of the auricular 
and ventricular contractions, as the result of the formation of a heart clot or from 
toxemia. 

The physical signs of croupous pneumonia in the well-developed stage are quite 
characteristic in typical cases. Inspection shows an even greater impairment of 
expansion on inspiration on the affected side than in the stage of onset, and pal- 
pation reveals, when the patient speaks, a distinct increase in vocal fremitus 
over the part of the lung which is diseased. Auscultation gives a harsh inspiratory 
sound, prolongation of expiration, and a large number of fine crackling or crep- 
itant rales in the same area, so fine that they may not be heard by the careless 
examiner. They sound very much as does that noise which is produced by moisten- 
ing the tip of the forefinger and thumb with saliva, pressing them together, and 
separating them, or, again, as does the sound made by the hair which grows above 
the examiner's ear when it is rubbed between the finger and thumb. Ordinary 
vesicular breathing over the area diseased is absent, and in its place is heard 
bronchial breathing, which is caused by the air in the bronchial tubes, pro- 
ducing a sound which is transmitted through the consolidated lung unmuffled 
by the vesicular murmur usually present. Auscultation while the patient speaks 
will also show a distinct increase in vocal resonance. That is to say, the sound 
of the voice will be transmitted through the chest-wall with a greater degree 
of clearness than in health. While auscultation is being performed in cases which 



CROUPOUS PNEUMONIA 137 

have a delicately developed chest, as in youths and children, it is often noted that 
the movement of the anterior chest- wall under the ear is not uniform, but undu- 
lating, one part expanding at an appreciable interval before the other. 

Percussion, a most valuable aid in the diagnosis of this disease, reveals, if the 
lesion in the lung is near the surface, marked impairment of resonance amount- 
ing to dulness, but it is a fact well worth remembering that if the lesion in the 
lung is deep-seated, and not near its surface, the percussion note over the area 
diseased may not be impaired or dull, but hyperresonant, or, as Samuel West has 
said, "boxy" in character. Usually hyperresonance is demonstrable all over the 
lung, except where it is consolidated, and is also to be found upon the healthy 
side of the chest, owing to the increased amount of air which is in these parts to 
compensate for the area of consolidation; but careful examination will reveal the 
fact that the hyperresonance over the consolidated area, or in its immediate neigh- 
borhood, has a different tone from that in the healthy and compensating lung, 
the "boxy" note just named. I have frequently been able to determine the pres- 
ence of deep-seated pneumonia by the presence of this sign. By the aid of care- 
ful auscultation and percussion it is usually, but not always, possible to definitely 
determine the exact area of the lung which is involved. 

While in the majority of cases these positive signs of croupous pneumonia may 
be found in a more or less well-developed form, it is not to be forgotten that nega- 
tive signs may be as valuable in making a diagnosis. That is to say, there may 
be absence of any one or all of the signs just enumerated, and a total absence of 
vesicular breathing. In such cases, therefore, the physician must exercise care 
lest the loud and exaggerated breath sounds of the healthy part of the chest mis- 
lead him into thinking that that portion is the one which is diseased. 

In certain instances, in which the action of the heart is very labored, its sounds 
distant, and the pulse is small and insufficient, careful examination may reveal 
a pericarditis with effusion, which, by its pressure, interferes with the movement 
of the cardiac muscle. This question as to whether there is pressure by peri- 
cardial effusion is by no means readily determined, because it frequently happens 
that there is a marked degree of cardiac dilatation present at this time, which 
naturally increases the area of cardiac dulness downward and to the right. Further, 
as it is the right ventricle which is most apt to be engorged, the area of cardiac 
dulness may be abnormally great in this direction. Again, it not infrequently 
occurs that the compensatory fulness of the healthy lung, if the disease is on the 
left side, pushes the heart downward and to the left, or, on the other hand, if the 
right lung is diseased, the unusual expansion of the left lung causes an extension 
of pulmonary resonance to the right, and so increased area of cardiac dulness 
is very effectually masked. 

Patients suffering from croupous pneumonia should always be turned on the 
side when the back is to be examined, as it is dangerous, because of the state of 
the heart, for them to sit up in bed. 

The urinary flow during an attack of croupous pneumonia is usually dimin- 
ished, so that the passage of about twenty ounces of urine in twenty-four hours 
may be taken as the average. This urine is usually highly concentrated, and 
contains, as does the urine in most febrile diseases, an increased amount of urea 
and an excess of amorphous urates which are deposited on standing. It also con- 
tains, very constantly, a moderate amount of albumin, but the chief peculiarity 
is its scanty content of chlorides, which may be entirely absent. If the albumin 
be large in amount, or casts are present, the probability is that the kidneys were 
diseased before the onset of the pneumonia. 

During the course of croupous pneumonia the function of the alimentary canal 
is rarely seriously disturbed, although loss of appetite because of the fever may 
be a marked symptom. The most important change in any part of the digestive 



138 DISEASES DUE TO A SPECIFIC INFECTION 

system, if it may be so called, is seen in the tongue, the state of which is note- 
worthy, because it gives some idea of the general state of the patient. It is, of 
course, prone to be dry and somewhat coated, caused by the rapid breathing 
through the mouth, and because of the fever; but if it be exceedingly dry and red, 
narrow and pointed at the tip, it possesses a more positive significance as to the 
general state of the patient than if it be broad and moist. 

Sometimes when pneumonia is very severe and particularly when toxemia is 
marked, an excessive degree of tympanites develops, which is of evil significance, 
in that it shows a diminution in vitality and causes interference with the action 
of the lungs and heart by pressure. I have seen this most commonly when the 
disease has affected those addicted to the excessive use of alcohol. 

The nervous symptoms of pneumonia are quite various and depend more upon 
the previous habits of the patient, the location of the lesion, and the degree of 
toxemia than upon any other causes. Delirium varies in degree from mind wander- 
ing, as the patient is about dropping off to sleep, to active mania, during which 
it may be very difficult to keep the patient in bed. The severity of the delirium 
depends largely upon the age of the patient and his habits. Alcoholic patients 
nearly always have delirium in a well-marked degree, and in this class of patients 
it is grave from a prognostic point of view in direct proportion to its constancy 
and severity. 

The type of the delirium also varies very greatly in the strong and in the weak. 
In those who are adynamic from some previous disease or from bad habits, it is 
often of a low, muttering type, resembling that sometimes seen in toxic cases of 
typhoid fever, while in other instances it may be violent, as already described. 

It is a noteworthy fact that delirium is particularly prone to affect those who 
suffer from pneumonia at the apex of the lung, and I have frequently seen in 
children, who had pneumonia at the apex> a delirium in which there seemed to be 
a constant fear of falling, so that the child clutched its mother every time it was 
moved. Holt's experience, on the other hand, leads him to believe that the por- 
tion of lung involved has little influence upon the production of nervous symptoms, 
and without doubt the recent advances in the study of pneumococcus infection 
tend to show that the toxemia and not the portion of lung involved is responsible 
not only for the marked nervous manifestations, but also for the dyspnea and 
great acceleration of the respiration. A peculiarity of the delirium in many alco- 
holic cases is that they labor under the delusion that they are lying in a coffin, 
and in their constant efforts to escape greatly exhaust themselves. This form of 
delirium is exceedingly grave from a prognostic stand-point. Delirium is also very 
much more apt to be marked in those patients who suffer from toxemia than in 
those in whom a very considerable area of the lung is involved, but who have, 
nevertheless, comparatively slight signs of poisoning by the toxin of the pneumo- 
coccus. 

Very rarely, in young children, the onset of the disease is characterized by 
convulsions instead of by the ordinary chill. 

Insomnia is a very constant symptom of croupous pneumonia, and may become 
so persistent as to require medicinal measures for its relief, particularly if it be 
accompanied by great restlessness. 

The skin in an ordinary case of croupous pneumonia is usually hot and dry, 
but if the toxic. element in the case is very marked, it may, as death approaches; 
become cold and clammy and even bedewed with sweat. In toxic cases, too, 
it is not infrequently somewhat jaundiced. If this jaundice is associated with 
hemoglobinuria the prognosis is almost certainly fatal. On the other hand,, in 
some instances jaundice occurs apparently as the result of the action of the toxin 
upon the liver, and this type is not so grave. 

Profuse sweating nearly always occurs at the time of crisis. The frequency 



CROUPOUS PNEUMONIA 139 

with which herpes appears about the mucous membranes and skin of the mouth 
and nose has already been mentioned. 

Stage of Resolution. — As the disease approaches the period of crisis, and 
sometimes not until this event has taken place, it will be noted that the rapidity 
of respiration as compared to the rapidity of the pulse more nearly approaches 
the normal ratio. 

The first change which can be noted in the physical signs in the chest is the 
development of fine moist rales, which indicate the early stages of resolution. 
These rales, when they are first heard, are fine and crepitant, and closely resemble 
those heard in the stage of onset; for this reason they are called rales redux. 

The rales in the chest become more and more coarse and moist in character 
as convalescence is carried on, and the speed with which nature in an otherwise 
healthy individual clears away the exudate is quite extraordinary, although usu- 
ally for several weeks after a sharp attack of croupous pneumonia, involving the 
surface of the lung, impaired resonance on percussion and some prolongation of 
expiration with harsh inspiration can be demonstrated. 

The critical fall of temperature is often preceded by a sharp rise, but when the 
fall occurs it takes place with extraordinary speed, the patient being afebrile or 
with a subnormal temperature within a few hours, or even within one hour (Fig. 
35). Sometimes this critical state is accompanied by a profuse sweat, and even 
collapse may develop, with urgent dyspnea, due to vasomotor palsy and vascular 
relaxation. 

When the fall is quite gradual, extending over a day, it is called a protracted 
crisis; this very commonly occurs in children. 

Often the day after crisis the temperature returns to slightly above normal, 
and sometimes an apparent crisis fails to reach the normal and the fever rises 
again. Such a pseudocrisis is rarely seen after the fifth day. 

The critical fall of temperature, as has already been stated, usually occurs 
on about the eighth or ninth day of the disease, but it may occur as early as 
the third day (Fig. 38). In feeble persons and in children the disease sometimes 
ends by lysis. 

Complications. — The complications of croupous pneumonia are quite numerous. 
Of these the most frequent is undoubtedly pleurisy. Indeed it may be said that 
in almost every case of croupous pneumonia a certain amount of inflammation of 
the pleura exists. As an illustration of this fact, the statistics of Kerr are of value. 
Out of 171 cases which came to autopsy from croupous pneumonia, no less than 
118 showed acute pleuritis. Of these, 74 were acute fibrinous pleuritis, 38 sero- 
fibrinous pleuritis, and 6 acute empyema. In Osier's 103 autopsies pleuritis was 
present in all but 2 cases. The pleuritis is due to the extension of the inflammatory 
process to the visceral layer of the pleura and to infection of the pleural mem- 
brane by the pneumococcus or by some other organism which is associated with it. 
(See Pleurisy.) The inflammation of the pleura manifests itself by an excess of 
pain in the area involved, by a friction sound on auscultation, and later, it may 
be, by the outpouring of a considerable amount of fluid which may be serous or 
purulent. When the fluid is serous it is often absorbed with a rapidity only equalled 
by the absorption of the croupous exudate in the lungs. In other instances it 
persists and actually increases in quantity, relief only being obtained when the 
physician performs paracentesis. In 4523 cases of croupous pneumonia, occurring 
in twelve large hospitals in the United States and England, pleural effusion is 
stated to have occurred in 233 cases, a percentage of 5.15. 

In still other cases the effusion is purulent from the beginning, and in this way 
an empyema is formed. Like all collections of pus, recovery can only be reached 
in the majority of these cases by giving vent to the accumulation. The presence of 
the pus is usually manifested by a return, or maintenance, of the febrile movement 



140 



DISEASES DUE TO A SPECIFIC INFECTION 



seen in the early stages of the disease, accompanied, it may be, by the ordinary 
manifestations of septic poisoning, such as chills, sweats, and irregular tempera- 
ture. On the other hand, all evidences of the 
presence of pus may be absent, owing to the 
non-absorption of toxic matters through the 
pleural membrane. In 10,076 cases of croupous 
pneumonia collected principally from the official 
reports of hospitals in the United States, Eng- 
land, and Germany, empyema is stated to have 
occurred in 208 cases, a percentage of 2.06. 

In all cases in which speedy recovery from 
croupous pneumonia does not take place and 
where marked impairment of resonance persists 
upon the diseased side, pleural effusion or em- 
pyema should be strongly suspected, and the 
tests for the purpose of determining these 
complications be instituted. Sometimes the 
presence of a pleural effusion is not suspected 
because it produces no symptoms until, by the 
increase in its quantity or the taking of moderate 
exercise by the patient, it produces dyspnea by 
interfering with respiratory movements. (See 
articles on Pleural Effusion and Empyema.) It 
is a noteworthy fact that if the empyema be 
due to the pneumococcus, the prognosis is more 
favorable, both as to complete recovery and to 
speediness of cure, than if it be due to some 
other infecting micro-organism. 

Hydropneumothorax has .occasionally been 
recorded as a complication, but it is very rare. 
Gangrene and abscess formation in the lungs 
are two very important and serious lesions which, 
fortunately, are not of common occurrence in 
connection with cases of croupous pneumonia. 
Eisendrath has analyzed 96 recorded cases of 
pulmonary abscess, gangrene, and bronchiectasis 
following croupous pneumonia. When the totals 
are computed as to percentage of recovery, 
the result is quite striking, especially in the 
more acute cases. Of 25 cases of acute single 
abscess, 96 per cent, recovered and 4 per cent, 
improved; of 28 cases of acute gangrenous ab- 
scess, 71.4 per cent, recovered, 7.2 per cent, 
improved, and 21.4 per cent. died. Of 14 cases 
of chronic simple abscess, 42.8 per cent, recov- 
ered, 21.4 per cent, improved, and 35.8 per cent, 
died ; while in 26 cases of chronic putrid abscess 
with bronchiectasis 50 per cent, recovered, 15.3 
per cent, improved, and 34.7 per cent. died. 

Norris gives the incidence of pulmonary abscess 

as 0.5 per cent, in 14,214 cases of pneumonia. 

Eisendrath found, from his review of the subject, that the symptoms usually 

came on after the crisis and consisted in a ppstcritical rise in temperature, which 

then became remittent in type. The sputum becomes purulent, and there is 



















Fie 




38 




















If 


■* a 


Sa 


Sa 


5a 


— es 

<»a 


«a 


U 


3a 


2a 










1 










































































































7 $ 1 ' 
























































































































































6$ 
16$ 

16$ 

21$ 

16$ 

16$ 

6$ 

5$ 

24 



































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































Chart showing day of crisis in acute 
croupous pneumonia, based on 216G 
cases in hospitals in the United States, 
England, and Germany. The black 
area shows the proportion (percentage) 
which have their crisis on any given 
day. The percentages for third and 
fourth days are taken from Aufrecht's 
statistics alone, as they could not be 
ascertained in all the other cases. 



CROUPOUS PNEUMONIA 141 

a distressing cough, accompanied by expectoration of pus in large quantities. 
If the abscess cavities do not communicate with a bronchus there is but little 
expectoration. There is in all cases emaciation, loss of appetite, and a rapid 
decline in strength. If the abscess becomes chronic there may be. recurrent attacks 
of fever, with profuse expectoration. 

Physical examination in these cases is rather disappointing. The lesions are 
most frequently in the lower lobes, and this is of some aid in diagnosis. There 
are no typical physical signs, owing to the fact that the cavities, be they due 
to abscess, gangrene, or bronchiectasis, may be near the surface, or quite deeply 
situated, and may or may not communicate with a bronchus. Dulness, decreased 
respiratory murmur, decreased vocal resonance, and decreased fremitus are present 
in the majority of cases, but bronchial breathing may be heard. The most reliable 
sign is the presence of large, moist rales, not infrequently metallic in character. 
Another striking feature is the variability of the physical signs, so that dulness 
and then tympany may alternate at the same spot. Clubbed fingers develop quite 
early, as do also symptoms produced by pressure on the heart, liver, and spleen. 

Gangrene must be suspected when there occurs a rise of temperature, a few 
days after the crisis, and the breath becomes fetid. The sputum is also fetid and 
divides itself into three characteristic layers. (See Gangrene of the Lung.) 

The frequency of hemoptysis in cases of gangrene is due to the fact that the 
vessels are apt to pass freely through the cavity, owing to the more rapid 
destruction of tissue. 

In bronchiectasis following pneumonia the sputum may be fetid at times, but 
the odor is not so penetrating as in gangrene and there are no elastic fibres. There 
is usually a history of long-continued expectoration of large quantities of pus. 
This, however, is not characteristic, for the same history may be true of chronic 
simple abscess. 

Pericarditis occurs as a complication of pneumonia in about 1 per cent, of the 
cases. In the majority of instances it is of such mild degree that it does not jeopar- 
dize the patient's life; but in other instances, when the effusion which follows 
it is profuse, it may, by mechanical pressure, produce great cardiac disability. 
When the accumulation is extensive, a definite increase in the area of cardiac 
dulness is usually demonstrable. Not rarely, however, the presence of this com- 
plication may be unsuspected during the patient's life. Thus, Thayer was only 
made acquainted with the presence of pericarditis in one of his cases of croupous 
pneumonia when the autopsy disclosed a thick layer of pyogenic membrane over 
the visceral pericardium, with a large quantity of pus in the pericardial cavity. 
Statistics seem to show that pericarditis varies in frequency in from 5 to 
16 per cent, of all cases, but in 21,383 cases of croupous pneumonia collected by 
me, principally from the official reports of hospitals in the United States, England, 
Germany, and Austria, pericarditis is stated to have occurred in only 266 cases 
of croupous pneumonia, a percentage of 1.24. (See Pericarditis.) This closely 
corresponds with Norris' statistics of 43,722 cases with an incidence of 1.1 per 
cent. 

Endocarditis is a rarer complication than pericarditis; occurring in about 0.5 
per cent, of cases. In a considerable proportion of cases the pneumococcus is 
responsible for the lesion. It often affects the aortic valves, and it is generally 
of the ulcerative type. In 14,510 cases of croupous pneumonia collected from 
several series of cases reported by German, English, and Swedish physicians, 
and from official reports of hospitals in the United States, England, Germany, 
and Austria, endocarditis is stated to have occurred in 106 cases, a per- 
centage of 0.73. Norris in 105 cases found it recorded five times, while 
Sears and Larrabee, in Boston, found it nine times in 940 cases. Aufrecht, 
in 1500 cases, met with endocarditis only once. Out of a total of 5738 cases 



142 DISEASES DUE TO A SPECIFIC INFECTION 

of croupous pneumonia von Brach found less than 0.2 per cent, complicated 
by endocarditis, and less than 0.5 per cent, of them complicated by pericarditis. 
Preble, from an exhaustive study, places the average at 1 per cent, in all cases and 
5 per cent, in fatal cases, and these figures are probably correct. Osier found 
16 instances. of endocarditis in 100 fatal cases. Preble believes that while pneu- 
monia is more common in males than in females, endocarditis due to this infection 
is more common in females. (See Endocarditis.) 

Two apparently distinct types of meningitis are rarely found as complications 
of croupous pneumonia; one appearing at the onset of the disease, the other 
during the active or postcritical stage. The former variety is seen most fre- 
quently in children, and is probably symptomatic; it is rarely fatal, and therefore 
its pathology is somewhat uncertain. On the contrary, meningitis developing 
during the course of the well-developed infection is generally the result of menin- 
geal infection and is very frequently associated with endocarditis. True pneu- 
mococcic meningitis is, however, rarely met with. Roily, in Leipzig found it only 
five times in 1050 cases of croupous pneumonia. (See Cerebrospinal Meningitis.) 

Numerous cases are on record of croupous pneumonia in children which at 
the onset simulated meningitis, cerebrospinal meningitis, and even hemiplegia. 
But the subsequent appearance of local physical signs, the pulse and respiration 
ratio, and the crisis, marked by a sudden fall in temperature about the eighth 
day, have confirmed the diagnosis of croupous pneumonia. The favorable ter- 
mination in many of the reported cases has not permitted an adequate pathological 
investigation, although meningitis due to the pneumococcus is well recognized. 

Disturbance of the nervous system over and above the signs of meningeal irri- 
tation or true meningeal inflammation may occur. Hemiplegia in croupous pneu- 
monia was recorded by Huxham; later it was described by Charcot, Lepine, 
and Vulpian as hemiplegie pneumonique. It may occur early in the course of the 
disease, or may not develop until the period of convalescence. Such a paralysis 
has been observed in cases as early in life as the eighteenth month and as late as 
the seventy-sixth year. 

Pierre Boulloche has collected 56 cases of paralysis resulting from croupous 
pneumonia. In this analysis the type of paralysis was found to be nearly always 
hemiplegie. In advanced years death nearly always ensued upon this complication, 
while in the young the mortality was very much lower, recovery being the rule. 
In 1 case occurring at the age of fifty-eight years, hemiplegia, with aphasia, 
developed during the course of the disease, but ended in recovery. 

In some instances the paralysis is monoplegia, and this is well illustrated by a 
case described by Boulloche in a patient thirty-two years of age, who from the 
onset of the disease, was delirious and who presented a typical right-sided croup- 
ous pneumonia. Paralysis of the right arm and right side of the face was dis- 
covered upon the sixth day of the disease. Movements of the right leg were 
entirely retained. There was aphasia, but no loss of consciousness, neither was 
there any disturbance of sensibility; twelve days later the fever had subsided, 
the aphasia had diminished considerably, and the muscles of the face were less 
drawn. Sensation in the pharynx returned and a day later the aphasia disappeared. 
The facial paralysis passed off; the relative strength of the two arms showed only 
a decrease of 10 degrees in the affected side, and at the expiration of twenty days 
the monoplegia had entirely disappeared. 

Transitory aphasia is a complication reported by Chantemesse. This observer 
has found that aphasia usually occurs about the second or third day of the disease, 
that it is ordinarily preceded by headache and giddiness, even to the verge of syn- 
cope; in some cases numbness or a sensation of pricking in the right side of the 
face and right arm is experienced; in other cases it may set in abruptly without loss 
of consciousness or become manifest after a typical apoplectiform seizure. The 



CROUPOUS PNEUMONIA 143 

characteristics of the speech impairment do not differ from those dependent upon 
an organic lesion of the third frontal convolution upon the left side of the brain. 
The paralysis may involve the entire right side of the body, but usually only the 
inferior portion of the right side of the face, the right half of the tongue, and the 
right superior extremity are affected; as a rule, sensation and the reflexes are not 
altered. In pronounced cases the paralyzed parts may be the seat of increased 
redness and an edema, which is more or less circumscribed and increased by heat. 
The phenomena persist commonly for from a few hours to a few days, and seem 
in no way to influence the primary disease. 

It is doubtful whether the clinical picture and pathology of these cases of transi- 
tory aphasia differ in any particular from many of the cases already described as 
hemiplegic. They probably represent the cases in which no lesion is found post- 
mortem. 

Softening of the brain has occurred in some cases. In one case, reported by 
Suckling, it was due to thrombosis of the basilar artery, and thrombosis of the 
circle of Willis; with plugging of the superficial arteries of the left hemisphere. 
While these lesions have been found as the causative agents in producing hemi- 
plegia, there are also cases on record in which the autopsy has been negative. 
In other words, hemiplegia with lesions and hemiplegia without lesions occurs. 
In the former case hemiplegia results from either meningitis or softening, or is 
due to thrombosis or embolism. In the second class the paralysis is like that of 
diphtheria — that is, of the toxic type. It is important to remember that it is pos- 
sible for hemiplegia to develop in pneumonia without there being any relationship 
between the two conditions. 

The fact that these marked nervous manifestations sometimes come on early 
in an attack of croupous pneumonia emphasizes the importance of examining the 
chest in all cases of paralysis, not only because pneumonia is competent to produce 
hemiplegia or other localized palsy, but also because these conditions are quite 
competent to produce secondary pulmonary lesions. In other words, pulmonary 
lesions may be the cause of hemiplegia, and hemiplegia may be the indirect cause 
of croupous pneumonia. 

Neuritis, occurring chiefly as a sequel to croupous pneumonia, has been de- 
scribed by several observers. These cases resemble those described by Boulloche 
as paralysis with muscular atrophy, coming on during the period of convalescence. 

Until Weichselbaum isolated the pneumococcus from the pus aspirated from 
the synovial sac of joints involved during the course of croupous pneumonia, 
the occurrence of arthritis was considered a coincidence, but since 1888 arthritis 
and osteoarthritis have been recognized as being not rarely due to a pneumococcus 
infection. Herrick has collected 52 cases from the literature of the subject, includ- 
ing some of his own, but it is interesting to note that in 2292 cases of pneumonia 
collected by me, treated by various Swiss and German physicians, only 2 cases 
of arthritis occurred. 

In regard to the frequency with which different joints are involved in this com- 
plication, the following quotation from Herrick's paper is of interest: "In 23 
of 52 cases the upper extremities alone were involved; in 18 cases the joints of 
the lower extremities alone; in 11 there was involvement of joints of both the 
upper and lower extremities. These figures show a slight preponderance in favor 
of limitation to the upper extremity, but so slight that little or no significance 
can be attached to it. In fact, the knee seems to be the joint oftenest affected, 
being involved in 22 of the 52 cases, in 3 of which both knees were affected, so that 
out of a total of 84 joints the knee makes up 25, or about 30 per cent. The involve- 
ment of other joints was as follows : the sternoclavicular, eight times; the shoulder, 
twelve times; the elbow, nine times; the wrist, eight times; the metacarpo- 
phalangeal, twice; the hip, three times; the knee, twenty-five times; the ankle, 



144 DISEASES DUE TO A SPECIFIC INFECTION 

three times; the metatarsophalangeal, three times. The arthritis was monarti- 
cular in thirty-two instances, or 61 .5 per cent, of the cases. The joints thus solitarily 
involved were: shoulder, ten times; knee, nine times; wrist, five times; elbow, 
twice; sternoclavicular, four times; and the hip, ankle, metacarpophalangeal, 
and metatarsophalangeal, each once. Of the remaining cases there were involved : 
two joints, nine times; three joints, four times; four joints, once; more than 
four, three times." These figures bring out the fact that the larger joints are 
more often affected than the smaller ones. 

The process in subacute cases is sometimes highly destructive to the joint. 

It is a noteworthy fact that the prognosis as to life is grave, the mortality amount- 
ing to 65 per cent., chiefly because this lesion is associated, as a rule, with affec- 
tions of the serous membranes elsewhere, and particularly in the endocardium. 

Venous thrombosis is an exceedingly rare complication of pneumonia. Steiner 
could find only 38 cases recorded, and reports 3 of his own. In 27 of these the 
thrombosis occurred during convalescence. In 1 case it occured at the time of 
crisis and in 4 during the course of the disease; and in the cases collected by him 
the lower extremities were always involved. The left lower extremity was involved 
in 16 cases; the right in 10, and both legs in 7. The more frequent involvement 
of the left extremity is attributable in this disease, as in typhoid fever, to the greater 
length and obliquity of the left common iliac vein and its passage beneath the right 
common iliac artery. Adding Steiner's 3 cases to the 38 which he found in the 
literature, making 41, we find that recovery occurred in 25, death in 9, and that 
no definite information is given of 7. 

Gangrene of a limb due to arterial thrombosis or embolism has been recorded 
by Zuppin, Benedict, Grimm, and Nielsen. 

Parotitis, while a rare complication of croupous pneumonia, may occur, and 
not infrequently goes on to suppuration. Most of the cases so far reported have 
not been due to the pneumococcus, but to the staphylococcus or streptococcus. 

Otitis media is quite a common complication of croupous pneumonia in children, 
the infection taking place through the Eustachian tube. 

A relapse in croupous pneumonia is practically never met with, but an extension 
to adjacent parts of the lung and recurrence is very common. 

Varieties of Croupous Pneumonia. — Croupous pneumonia varies much in its char- 
acter with the condition of the patient that is attacked. I have already men- 
tioned the type which occurs in persons who are addicted to the excessive use of 
alcohol. In other individuals the disease is accompanied by such marked symp- 
toms of adynamia that the patient seems to be suffering from typhoid fever, so 
far as his general symptoms are concerned. This form is known as typhoid pneu- 
monia, in that it is typhoid in character; but this term does not necessarily imply 
that typhoid infection is associated with that by the pneumococcus. On the other 
hand, it sometimes happens that patients suffering from typhoid fever also have 
a pneumococcic infection of the lung, and this, of course, is another form of so- 
called typhoid pneumonia. True croupous pneumonia also occasionally, although 
rarely, complicates malarial fever, acute articular rheumatism, and pulmonary 
tuberculosis. Sometimes, too, it occurs as a sequel to the administration of ether 
as an anesthetic. This is probably due primarily to the chilling and irritation of 
the lung by the drug, and secondarily to the inhalation of pneumococci from the 
mouth, where, as already stated, they are almost constantly present even in healthy 
persons. 

Diagnosis. — Croupous pneumonia is to be carefully differentiated from acute 
tuberculous pulmonary infection, from lobular or catarrhal pneumonia, from 
infarction of the lung, accompanied by bloody expectoration, due to cardiac 
disease, from pleurisy with effusion, and from chronic inflammation of the pleura, 
with marked thickening of that serous membrane. Finally, it is to be separated 



CROUPOUS PNEUMONIA 145 

from hypostatic congestion due to cardiac feebleness arising in the course of acute 
diseases or chronic ailments. 

The differentiation from acute pneumonic phthisis may be quite impossible 
until the development of profuse sweating, a feeble and rapidly acting heart, 
and the appearance of yellow elastic tissue and tubercle bacilli in the sputum 
takes place. From pulmonary infarction it is to be separated by careful examina- 
tion of the heart, which may reveal valvular lesions, and by the fact that in infarc- 
tion the onset of pulmonary disorder is instantaneous and the sputum contains 
bright blood. From pleural effusions it is differentiated by the development of 
the physical signs of that condition. (See Pleurisy, with Effusion.) Hypostatic 
congestion of the lungs is discovered by the character of the sputum, which may 
be blood-stained, although it is usually serous, by the fact that the lesions are 
usually bilateral, and also by the fact that the heart is primarily very w T eak. 
Catarrhal or lobular pneumonia is recognized by the absence of the typical rusty 
sputum, by the history of the presence of some primary disease prior to the 
onset of the pneumonic consolidation, and by the wide distribution of the lesions 
and the more diffuse physical signs. 

An important aid to the diagnosis of croupous pneumonia is the increase in 
the number of the polymorphonuclear white cells, the so-called leukocytosis of 
croupous pneumonia. In this disease, in most instances, the increase in these 
particular white cells causes a leukocytosis of from 18,000 to 30,000. A count 
below 10,000 may mean a mild attack but more often is found in a case of unusual 
severity in which the patient is not reacting well to the infection. In the latter 
cases the prognosis is bad. 

The blood serum of these cases is capable of causing agglutination of the pneu- 
mococcus and the degree of agglutinative power seems to be greatest about the 
time of crisis, but there are technical difficulties about the test which render it of 
little value in diagnosis. 

It is of the greatest importance that the severe pain sometimes described as 
being in the belly at the onset of pneumonia is not mistaken for that due to ap- 
pendicitis. Cases frequently occur in which pain due to thoracic disease is thought 
to be abdominal, particularly if the base of the lung is involved. The presence 
of pain or pressure over McBurney's point, of some fixation of the abdominal 
muscles, and of a high leukocyte count may be so misleading as to lead the 
physician to operate for disease of the appendix. 

It is characteristic of croupous pneumonia that the chlorides in the urine are 
greatly decreased. 

The physician should always be on his guard lest he overlook a "central" or 
deep-seated pneumonia, which presents no marked physical signs. 

Prognosis. — The prognosis in croupous pneumonia is always to be governed 
by the recollection of the fact that its mortality in adults is usually high, and 
again by the condition and habits of the patient. It is to be remembered that 
the prognosis in a case of croupous pneumonia is grave in direct proportion to 
the years of the patient. In young children, unless it is complicated by some grave 
accident, the disease has a very low mortality. By far the greater number of 
children recover, whereas in advanced years the disease is exceedingly fatal (Fig. 
39). As an illustration of how low the mortality may be when young, healthy 
persons are affected by the disease and come under skilful treatment early in its 
course, Osier states that in 40,000 cases occurring in the German army the mortality 
was only 3.6 per cent. 

If the mortality percentage is based upon the total number of deaths from this 
disease, it may be stated to be as high as from 25 to 40 per cent. ; but if, on the 
other hand, those cases which would naturally fall victims to its ravages are ex- 
cluded, the mortality is probably only about 10 per cent., if we accept the large 
10 



146 



DISEASES DUE TO A SPECIFIC INFECTION 



statistics of Townsend and Coolidge, who excluded patients over fifty years of 
age and those who were delicate or suffering from some other disease primarily 
present. In private practice the mortality varies from 6 to 18 per cent. Statistics 
are of little value because all forms of pulmonary consolidation are apt to be 
reported as pneumonia and because they fail to deal with the primary state of 

Fig. 39 



UJ 

CD 
< 

z 

LU 

o 

cc 

UJ 

a. 


CC 

< 

£ LU 

> <3 
in < 

CC U- 

uj O 

Q 

Z 

D 


5- 

UJ Q 

> z 

h- < 

LU m 

m 


Z o 

UJ CM 
UJ Q 

<: z 

h- < 

UJ o 

CO - 


Z o 
LU n~> 
LU Q 

£ z 

i- < 

UJ o 

ca <m 


Z o 

LU <*• 
LU Q 

^ z 

h- < 

LU o 
CO <*> 


Z o 

LU "■> 

LU Q 

£ z 

f- < 

UJ O 
CQ "* 


Z o 

LU f> 
LU o 

<: z 

i- < 

LU o 
CQ "> 


Z o 

LU f» 
LU Q 

^ z 

1- < 

LU o 
03 vo 


57 


























Mil 








































• 






56 




























1 i 








| 


































y 


7* 










55 

•31 




























i 1 








































i 


r 


































































































oS 




































































i 


















52 
































































1 




















51 




































































i~ 




















50 


































































/ 






















19 


































































' 






















48 
































































j 
























47 




























































/ 


























M 












1 
















































1 


























15 












i I 










































/ 




























44 












1 












































/ 




























IB 


























































~1 






























42 


























































T 






























41 


























































/ 






























40 
























































J 
































3U 






















































1 
































38 
























































/ 
































37 






















































1 


































3li 






















































( 


































35 




















































I 




































3i 


















































j 


1 




































33 
















































1 






































32 
















































/ 








































31 
















































rf' 








































30 














































/ 










































29 














































t 










































28 












































i 












































27 








































i 














































26 










































1 














































25 










































' 














































24 






















































































23 






































/ 


A 












































22 






































1 
















































21 






































~tt 
















































20 






















































































19 






































f\ 
















































IS 
























































































17 




































i 




















































16 
































/' 




















































15 






























/I' 






















































14 






























A \! 






















































13 
































( 






















































12 
































J 
























































11 






















/ 


'; 


r i/ 
























































10 




























h 


























































9 




























/ 


























































8 




























i 


























































7 




























T~ 




























































6 


























/ 






























































5 










- 
















/ 




















































! - 








— 


1 




















/ 




















































:; 
























i 






























































2 






















i 
































































1 


















f 
































































































































1 





Chart showing the morbidity and mortality of croupous pneumonia at different ages, based on 868 
cases in the Presbyterian Hospital, New York, and Guy's Hospital, London. Solid line, morbidity; 
dotted line, mortality. 



the patient. Thus in alcoholic patients, diabetic patients, or those suffering from 
nephritis the proposition is far more grave than in patients in whom the disease 
is primary, not secondary. 

Aside from advanced years, the other causes which render the prognosis espe- 
cially grave are renal disease, with secondary cardiovascular lesions, alcoholism, 
and diabetes, Indeed, these three states contribute a very large proportion of 



CROUPOUS PNEUMONIA 147 

the number of cases which suffer from this malady, and also the largest proportion 
of deaths in the statistics. 

It is stated by some authors that any history of previous ill health distinctly 
increases the danger from croupous pneumonia. While this may be true in certain 
cases in which vitality is greatly depressed, it is also a fact that oneumonia in 
chronic invalids frequently runs a comparatively mild course unless the cause of 
their ill health be renal or cardiac disease, whereas it may speedily produce death 
in robust, powerful, muscular men, who frequently succumb to its ravages far more 
rapidly than more lightly built and apparently delicate individuals. Indeed, the 
physician of experience dreads the onset of this disease in powerful, well-developed 
men much more than when it attacks those who are less given to active exercise 
and feats of physical strength. Stout persons also seem much more susceptible 
to the lethal influences of the disease than those who are lean. This probably 
depends upon two causes : first, the heart and lungs may be overweighted by fat, 
and second, such persons usually contain in their tissues a large amount of serum, 
in which, perhaps, specific micro-organisms find an opportunity to grow and to 
prepare their toxic product in large quantity. 

Cases of croupous pneumonia characterized by moderately high fever do not 
possess the unfavorable outlook of other diseases which suffer from hyperpyrexia; 
that is, a temperature in the neighborhood of 106°. On the other hand, it not 
infrequently happens that cases running a temperature course varying from 101° 
to 102° are more severe as to toxemia than those which range in the neighborhood 
of 103° or 104°, or even 105° for a short time. If, with the drop in temperature, 
which occurs at crisis, the general condition of the patient does not markedly 
improve, the prognosis is bad. If in place of the ordinary rusty sputum it is of 
the color of prune-juice, it is usually considered that the disease is malignant. 
On the other hand, as stated by Sir William Jenner, the brighter the sputum, the 
less the weight, the better the prognosis. 

An important prognostic point in any given case is the degree of toxemia which 
is present. In other words, the prognosis depends not so much upon the area of 
lung which is involved as it does upon the quantity of toxic material which the 
infecting micro-organisms seem to be producing. Again and again death occurs 
in apparently otherwise healthy individuals who present a small area of consolidated 
lung and almost no typical signs of pneumonia, but who are apparently overwhelmed 
by great toxemia. 

An absence of leukocytosis in a case of croupous pneumonia usually posesses 
an evil import, since it seems to indicate a degree of toxemia with which the system 
of the patient finds it difficult to deal. 

A very valuable prognostic sign is the ratio of blood-pressure to pulse rate. 
If the blood-pressure, in an otherwise healthy patient, expressed in millimeters 
of mercury is well above the pulse rate per minute the patient is doing well. 
If the pressure so expressed and the pulse rate are identical numerically the 
patient is in great danger. If the pulse rate is greater than the blood-pressure 
expressed in millimeters of mercury he will almost certainly die. Thus a pressure 
of 130, pulse rate 90, is equivalent to safety. Pressure 110 and pulse rate 110 is 
equivalent to great danger. Pressure 100, pulse rate 120, is usually followed by 
death, if maintained. 

Treatment. — The treatment of a case of croupous pneumonia varies greatly 
with the condition of the patient who is suffering from the disease. When it 
attacks the stout and robust, the only duty of the physician, in a large number of 
instances, is to watch the patient's symptoms; to insist upon rest in bed in a 
well-ventilated and quiet room, and to administer a sufficient quantity of 
Dover's powder, or morphine to relieve pain, if that symptom is excessive. If, 
on the other hand, the patient is one who has been addicted to the use of alcohol 



148 DISEASES DUE TO A SPECIFIC INFECTION 

in excess, whiskey or brandy should be given him in amounts varying with the 
quantity which he has been accustomed to ingest daily. Not only does his sys- 
tem require the effects produced by this drug, but its use is also necessary to 
prevent the rapid development of delirium tremens, which is a most fatal compli- 
cation in these cases. An active stimulation is also usually required in many cases of 
croupous pneumonia in which the patient is just recovering from some other severe 
infection, such as typhoid fever. 

It is, however, a fatal mistake to think that every patient suffering from this 
disease should be stimulated. The physician . should always bear in mind the 
important rule not to meddle with the course of the disease unless symptoms 
are so pressing as to require interference. There can be no doubt that one of the 
best stimulants in many cases of croupous pneumonia, accustomed to alcohol, 
is alcohol, in some form which will agree well with the stomach. The dose of 
this drug in the form of whiskey or brandy must depend upon the needs of the 
individual. Rarely will any patient require more than 8 to 12 ounces in the twenty- 
four hours, and many will do best on much less than this. Valuable adjuvants to 
alcohol are the aromatic spirit of ammonia, given in the dose of 30 minims, well 
diluted, every two or three hours; and should any sign of acute cardiac failure 
develop, Hoffmann's anodyne, in the dose of 1 or 2 drachms, in water, every hour 
or two, is an invaluable remedy. 

For a condition of acute cardiac weakness, the value of strychnine should 
also be borne in mind. Under these circumstances it is often invaluable, and if 
need be may be given in full dose, frequently repeated, by a hypodermic needle, 
until the patient rallies. Usually -^ to ^V grain, repeated once or twice, at an 
interval of two or three hours, approximates the proper dose. At the present time 
it has become fashionable for physicians to administer strychnine as a cardiac 
stimulant throughout the whole course of pneumonia. This is an abuse of a good 
remedy. Strychnine is not a direct cardiac stimulant. It increases the activity 
of the heart by rallying the nervous system and acting as an indirect whip to 
the circulation. If its use is persisted in it soon loses its so-called stimulant effects, 
and is apt to produce a condition of nervous irritation, particularly in the aged, 
which may be quite distressing. Its constant use deprives the physician of a 
valuable remedy for meeting critical moments in the course of the disease. 

The value of digitalis for the purpose of combating cardiac failure in acute 
croupous pneumonia has been questioned. It is a well-known fact that digitalis 
loses a large amount of its power over the heart in the presence of high fever; 
and fever is nearly always a marked symptom in this disease. It is also coming 
to be a well-recognized fact that digitalis is of little value in those cases in which 
the heart muscle has undergone degenerative change, and the toxemia of pneumonia 
often produces such alterations in the muscle fibres of this viscus. In cases in which 
there is marked vascular relaxation and cardiac dilatation, I have known it to do, 
good when given in a few large doses, particularly if strychnine and atropine were 
simultaneously administered. Although it is a drug which contracts the blood- 
vessels, the vasomotor dilatation or relaxation of advanced pneumonia is often so 
marked that digitalis seems to be unable to raise the arterial pressure, and I am 
convinced that in many instances death occurs more largely because of the relaxed 
condition of the bloodvessels than by any direct effect of the disease upon the 
heart. When I* use digitalis, therefore, I am in the habit of prescribing 5 or 10 
drops of a physiologically tested tincture every eight or six hours, and the same 
quantity of tincture of belladonna every three or four hours, in order that the bella- 
donna may increase the tone of the vessels. This treatment, however, is rarely 
instituted before the fifth or sixth day, or at the approach of crisis. 

If cardiac failure is the result of cardiac dilatation due to the obstruction of 
the flow of blood through the lung, digitalis may be advantageous, but when 



CROUPOUS PNEUMONIA 149 

the cardiac weakness is due to toxemia it is probably of little value, and if a clot 
has formed in a cardiac cavity it is manifestly useless. Sometimes when the fever 
is high and digitalis fails to act, it is well to aid its effect by quieting the heart 
through the application of an ice-bag placed upon the precordium. I have also 
known the reduction of temperature by the local application of the ice-bag and by 
cool sponging of the body, with friction, to be followed by the manifestation of 
a distinct digitalis influence. If moderate doses of 5 to 10 minims of a physiologic- 
ally tested tincture, three or four times a day, fail to produce good effects under 
these circumstances, I feel quite confident that larger ones will not be of any value. 

Should sudden collapse come on, a hypodermic injection of strychnine and 
atropine should be given, and it may be wise to introduce under the skin, by 
hypodermoclysis, a pint of normal saline solution. The normal saline solution, 
under these circumstances, cannot do much good directly because the relaxation 
of the bloodvessels is so great that even if it is absorbed its influence will not be 
felt, but it forms a reservoir from which it will be slowly absorbed and so flush 
the kidneys. 

The value of saline infusion also depends upon the degree of toxemia which 
is present and upon the activity of the kidneys. If, in a given case, the urinary 
secretion is scanty and toxic symptoms develop, a pint of normal salt solution may 
be given by hypodermoclysis every six or eight hours for twenty-four hours with 
advantage. If, on the other hand, the pneumonia complicates renal disease, and 
there is any tendency to edema of the subcutaneous tissues, this method of treat- 
ment may be disadvantageous, in that it tends to increase the dropsy, and perhaps 
increase the tendency to pulmonary edema. As marked toxemia is usually asso- 
ciated with renal inactivity, this method of treatment should be borne in mind. 
Direct infusion of a saline solution into a vein is probably not advisable in the 
majority of cases, since it is usually absorbed with sufficient rapidity from the 
subcutaneous tissues. 

When the skin becomes relaxed and bedewed with sweat, atropine is often a 
life-saving drug. 

In cases in which the heart is laboring, where there is evidence of dilatation of 
its right cavity with pulsating jugulars and other evidences of venous stasis, free 
venesection may be practised with advantage, and sometimes gives wonderful 
relief; but in cardiac failure without these signs of venous obstruction, venesection 
is practically of no value whatever. 

The value of inhalations of oxygen gas is problematical. I always employ them 
because they seem to give comfort both to the patient and his friends. The oxy- 
gen should not be given through an inhaler, but be allowed to escape, through the 
opening of the rubber tube or glass nozzle, about the lips or nose of the patient, 
for the ordinary individual who is suffering from dyspnea in this disease will not 
permit one of his nostrils to be blocked or his mouth closed by such an inhaler, 
as his desire for ordinary air is too great. If the dyspnea is due to toxemia 
the oxygen is probably useless. If it is due to a large area of the lung being inca- 
paciated by consolidation, it is conceivable that oxygen can do great good. 

The treatment of the fever during the course of croupous pneumonia is not 
of as great importance as it is during the course of a more prolonged malady, like 
typhoid fever. Indeed, there is some evidence to show that fever within moderate 
bounds may be an effort on the part of the organism to protect itself from the 
infecting germs. If the temperature does not exceed 102.5° to 103°, antipyretic 
measures need not be instituted, although sponging the patient with tepid or cool 
water three or four times a day will control the temperature somewhat, allay 
peripheral nervous irritation, keep the skin clean, and often produce sleep. These 
spongings are, therefore, useful in the ordinary case of pneumonia with a tem- 
perature of 103° or more, but they are not to be carried out with the same vigor, 



150 DISEASES DUE TO A SPECIFIC INFECTION 

either as to the activity of the rubbing or degree of cold, as is employed in typhoid 
fever, for the temperature, as a rule, does not resist the cold, and if it is applied too 
freely the patient may be thrown into collapse by a sudden fall of fever. Nearly 
every case of acute pneumonia will be benefited if an ice-bag is kept applied to the 
head, and if the action of the heart is very rapid when the fever is high an ice- 
bag over the precordium, is often advantageous. 

The administration of antipyretic drugs to patients suffering from pneumonia 
is absolutely inexcusable. In the first place, antipyresis by drugs is rarely if ever 
needed. In the second place, there is overwhelming clinical and experimental 
evidence to show that the use of these drugs materially diminishes the vital resist- 
ance of the patient, decreases the ability of his blood to convey oxygen to his 
tissues, reduces its ability to destroy infecting micro-organisms, lowers vascular 
tone, depresses the heart, and is altogether evil in its influence, probably also 
diminishing the elimination of toxic materials by the kidneys, and certainly giv- 
ing these organs the additional labor of eliminating the antipyretic drug, which, 
perchance, may be irritating to them. 

Quinine is employed by some practitioners with the idea that it possesses specific 
as well as antipyretic power, and there is no objection to its use in small doses; 
large doses, which produce cinchonism or irritation of the stomach, are value- 
less, and may do harm by irritating the stomach, producing cerebral congestion 
and meningeal irritation, or irritating the kidneys. 

When croupous pneumonia is of the typhoid type and asthenia is marked, 
valuable results can be obtained very frequently by the hypodermic injection 
of 1 grain of camphor, dissolved in sterilized olive oil. This injection may be 
given once, twice, or thrice in twenty-four hours for one or two days, but ought 
not to be continued too long; first, because it rapidly loses its effects if used too 
frequently, and, second, because in these doses there may be some danger of 
camphor poisoning. Camphor is to be regarded as a remedy for an emergency, 
and is to be reserved for critical periods. 

Recently very large doses of camphor, as much as 30 grains a day, given hypo- 
dermically, have been advocated as a specific treatment of croupous pneumonia. 
I have proved these doses not to be poisonous, but have not Used this method 
in a sufficient number of cases to assert its usefulness. 

If great mental and nervous excitement is present and persistent, life can often 
be saved by the administration hypodermically of -g-, -§-, or ^ grain of morphine. 
This will often produce several hours of desired sleep, from which the patient 
awakens much refreshed and perhaps free of the delirium which before the admin- 
istration of the morphine was an annoying symptom, in that it produced physical 
exhaustion through the constant activity of his body and mind. 

The employment of nitroglycerin in the treatment of pneumonia is limited 
to those cases which have a very high arterial tension before the acute illness. 
The drug, under these circumstances, is of great value in that it diminishes the 
work of the heart by removing the vis a fronte. If, on the other hand, vascular 
spasm does not exist, the drug is useless, for it is not, as some have thought, 
in any sense a direct cardiac stimulant. A blood-pressure, theoretically high, is 
often induced by nature to aid in maintaining the circulation through fibroid 
vessels, and it is usually better to leave it alone. 

The question of the employment of circulatory sedatives in the early stages of 
acute croupous pneumonia is one which has been widely debated, particularly 
in this country. There are many excellent practitioners who consider that full 
doses of veratrum viride or aconite in the earlier stages of croupous pneumonia 
are advantageous. Statistics, or, to speak more correctly, wide personal expe- 
rience on the part of many physicians, seems to justify the use of this drug in some 
cases, namely, in those instances in which the physician sees the patient during 



DIPHTHERIA 151 

the first hours of the attack, and if the patient is a strong, sthenic individual, with 
a full, bounding pulse, and great flushing of the face. Under these circumstances 
the relaxation of the general vascular system produced by the veratrum viride 
and the quieting of the excited heart seems distinctly advantageous. Whether 
such treatment in any way aborts, or jugulates, or diminishes the violence of the 
subsequent attack is difficult to determine. In a few instances of acute croupous 
pneumonia and acute pleurisy, seen in the very early stages, I have noted good 
results from such treatment. But in the vast majority of instances the physician 
does not see the patient for nearly twenty-four hours, by this time the disease is 
well started on its way, and the symptoms of great circulatory excitement have 
usually passed by, so that circulatory sedatives are distinctly contra-indicated. 
The use of chloral as a nervous sedative in the course of croupous pneumonia is 
usually inadvisable. 

The diet should be liquid and consist of milk, with a little pancreatin and bicar- 
bonate of soda, to aid in digestion, and of animal broths and gruels made of wheaten 
grits, oatmeal, rice, or barley ; the digestion of these starchy foods being aided by 
the administration of taka-diastase or pancreatin. I am quite convinced that we 
too infrequently resort to these cereal fluids in the treatment of diseases of this 
nature, since they possess much nutritional value and, if their digestion is aided, 
agree with the vast majority of patients, and enable us to change the diet so that 
the patient does not become tired of any one particular kind of food, which is a 
great advantage. 

Care should be taken in cases of croupous pneumonia that the patient receives 
an adequate amount of water to drink, so that the kidneys may be well flushed 
with fluid in each twenty-four hours; but it is important that only small amounts 
of fluid be taken at a time, as distention of the stomach may cause fatal cardiac 
embarrassment. The bowels should also be moved each day in the early stages of 
the attack by full doses of calomel, and in the later stages by salines, or, if the 
patient is too weak for the use of these purgatives, by a rectal injection of water 
or of glycerin and water. 

The administration of expectorants in croupous pneumonia is useless until 
the stage of resolution is reached. Even then they are probably of little value in 
clearing up the exudate in the vesicular portions of the lung. But the chloride 
of ammonium, the oil of sandal-wood, guaiacol, and terpin hydrate often prove 
useful at this time in aiding in removing the symptoms of chronic bronchitis which 
exist, a state which results in the formation of a good deal of thick, tenacious 
bronchial mucus, which the patient may have difficulty in expectorating. 

Excessive cough in all stages of croupous pneumonia is best controlled by the 
administration of Dover's powder, codeine, paregoric, or the newer drug, heroin. 
In the stage of resolution cough sedatives should not be administered unless the 
physician is certain that the cough is in excess of the needs of the patient in getting 
rid of the materials in his chest which should be gotten rid of in this way. 

Meningeal symptoms are to be treated by the application of cold to the head, 
and sometimes it is wise to apply a blister to the nape of the neck. 

DIPHTHERIA. 

Definition. — Diphtheria is an acute infectious disease, which chiefly affects 
children under puberty. It is due to the Klebs-Loeffler bacillus, and is char- 
acterized primarily by an acute local inflammatory process which affects, as a 
rule, the pharynx, larynx, or nasal mucous membrane, and which is peculiar in 
that it is associated with the development of a false membrane due to a fibrinous 
exudate. From the spot upon which this condition develops the general system 
becomes affected, not by the micro-organism of the disease, but by the poisons or 



152 DISEASES DUE TO A SPECIFIC INFECTION 

toxins produced by the specific organism at the site of primary infection. Other 
infections may occasionally cause the production of a false membrane, but the 
discovery of the presence of the Klebs-Loeffler bacillus determines that the affection 
is diphtheria. All cases in which a false membrane develops on a visible mucous 
membrane should be considered to be cases of diphtheria and treated as such until 
proved to be non-diphtheritic, because in this way the spread of the disease is 
prevented and the use of the specific remedy, antitoxin, will save life if the disease 
is present and do no harm if it is not. 

In the great majority of cases the disease primarily affects the pharyngeal 
mucous membrane, or the mucous membranes immediately adjacent thereto, 
and from this area spreads to the nose or larynx, where the results of its develop- 
ment are very fatal. The specific inflammation and false membrane may, however 
develop on any exposed mucous membrane, and even upon the true skin if the 
epiderm be removed intentionally or by accident. 

It is possible for bacteriologists to find the Klebs-LoefHer bacillus in cases of sore 
throat in which there is no false membrane and no systemic symptoms of diph- 
theria, and in some of these instances even local disturbances may be absent 
because of the resistance offered to this infection by some persons. These cases 
are not to be considered instances of diphtheria, although they are entirely capable 
of conveying the disease to others and hence are "carriers." 

On the other hand, cases are not rarely seen in which the physician finds a 
shaggy false membrane on the throat associated with signs of great systemic 
toxemia, and in which the bacteriologist fails to find the specific micro-organism 
of diphtheria. This condition is called diphtheria by the physician and pseudo- 
diphtheria by the bacteriologist. The streptococcus is probably responsible for 
cases of the latter type, while in other patients the pneumococcus causes a similar 
effect. These instances are met with most commonly as complications of scarlet 
fever or more rarely of measles, and also occur as manifestations of severe 
tonsillitis or angina. 

History.— Diphtheria has been recognized for many centuries as a disease, but 
it was not until the clinical observations of Bretonneau, of Tours, that its separate 
identity was established under the name of "diphtherite." He classed all cases 
of "putrid sore throat," "cyanche maligne," and "suffocative angina" under this 
one heading, and much more recently those cases heretofore called "membranous 
croup" have also been very properly put in the class called "diphtheritic." This 
sweeping classification is not scientifically justifiable, as has just been pointed out, 
but from a clinical stand-point it is proper because in the majority of instances the 
false membrane is due to this cause. 

Distribution. — Diphtheria is a disease which occurs in nearly all parts of the 
world, but is much more prevalent in the temperate zones than elsewhere. It 
occurs in epidemics and in sporadic cases, and is endemic in nearly every large 
city. While common in cities, it is even more common in country districts. No 
special influence upon its development is known to be exercised by bad drainage, 
although such drainage may, by diminishing vital resistance, very greatly increase 
susceptibility to the malady. 

It is a disease of the poor rather than of the rich, and when it occurs in the well- 
to-do it is usually sporadic and its source can often be traced to some single expos- 
ure. The reason for this does not lie so much in greater susceptibility of the poor 
as in greater exposure to the infection, for when the children of the well-to-do are 
attacked they succumb as readily as their otherwise less fortunate fellows. 

Diphtheria occurs much more frequently between the ages of two and five 
years than at any other time of life (Fig. 40). 

Etiology. — Diphtheria is due, as has already been stated, to a specific bacillus 
first described by Klebs in INN:}, and later isolated by Loeffler. This micro- 



DIPHTHERIA 



153 



organism is from 1.5 to 3.5 or rarely 4.5 micromillimeters in length, and from 0.3 
to 0.8 in breadth. It usually appears singly, in groups of two or three, but true 
chains are said not to occur; the organisms may lie side by side or at an angle. 
They are slightly curved with straight, rounded ends, sometimes branched, and 
commonly beaded or barred. They do not give off spores, and flagella are absent. 
They may contain highly refractive bodies which cause them to stain irregularly. 
The best stain is that of Loeffler, the oval bodies in the organism staining more 
highly than the rest of the bacillus. They are grown best in Loeffler's blood serum 
but develop in all the laboratory media. The organism is non-motile and almost 
purely aerobic. 

All cases of diphtheria are due to the entrance into the body of this specific 
bacillus originally derived from some patient ill with the disease. The transfer 
is made in a multitude of ways. Sometimes it is by the clothing, by books, by food- 
stuffs, or drinks, or drinking- vessels, by pencils, or by the coughing of an individual, 
who may have the bacilli in the throat, in such a way that the infectious agent is 
driven into the respiratory passages or mouth of the other person. Convalescent 
patients may in this manner act as disseminators of the disease long after they are 
apparently entirely well, and healthy persons with the bacilli in the mouth may also 
carry the infection. 

Fig. 40 



PERCENT 


en cc 

UJ < 

Q Ul 

z >- 


M CO 

h as 
<- >- 


m co 
i- < 

^ UJ 

CM > 


"* CO 

1- < 

K UJ 

co >- 


m co 

r- UJ 

* >- 


ID CO 

?■< 

r- UJ 


f* CO 

^ UJ 

to > 


oo co 

1- UJ 


01 CO 

r- uj 

co >- 


2 CO 
1- UJ 


■~ CO 

^ UJ 

o >- 


CM 

•- CO 

?< 

r- UJ 

r- >- 


m 

>- co 

o 5 

t- UJ 
CM >- 


*- CO 

^ Ul 

co >- 


12 


— 














































1 












































































































































































































































































































































































11 








































1 
























































































































































































































































































































































































10 
































V 




















































































\ 




















































































\ 






















































































v 




















































































\ 




















































9 








































\ 




















































































\ 


















































































































































1 




















\ 
































































































































8 










































\ 




















































































v 






















































































i 




















































































\ 




















































































\ 










































7 










































^ 


























































1 






1 
















\ 


















































































\ 
















































































































































































































6 
































































































































































































1 
































































































































































































S, 
































5 
























































< 




















































































3 


























































































































































































































































































4 


































































































































































































































































































































































































































3 






























































































































































































































































— 
































































iV 




































































































2 




















































































— 
















































































































































































































































































1 










































1 



















Showing the age incidence of diphtheria, based on 3360 cases collected from various sources. 



Thus it is entirely possible for a nurse who has been in charge of a case of diph- 
theria to carry in the crypts of the tonsils the specific micro-organism, to have 
no sign of the disease, and yet infect a child or adult whom she may care for soon 
after leaving the first case. It is evident, therefore, that while the infection is not 
carried by the air, as in smallpox, it is very easy for a patient who sneezes or coughs 
to distribute the infectious agent broadcast by its falling on neighboring sub- 
stances which act as agents of conveyance. These are some of the causes that 



154 DISEASES DUE TO A SPECIFIC INFECTION 

result in the rapid spread of the disease in tenement houses, schools, and other 
public places where children are congregated. 

As the specific bacillus possesses great vitality, the relationship between cause 
and effect may not be readily discovered. Thus, if the bacilli fall on a garment 
they have been found to remain capable of producing the disease six months 
later, and they have been found in the throat many months after perfect health 
has been established. So, too, the dust of the room may carry the infection, and 
even the hair or beard of the physician may do likewise, if the patient expels any 
secretion upon it. Finally, as already intimated, milk may act in this manner, and 
cheese made from contaminated milk may even convey the bacillus. Pet animals, 
such as cats and dogs, also act as distributors, and rodents, such as rats and mice, 
may do likewise. 

While not all the diseases of birds, cats, and calves characterized by the forma- 
tion of a false membrane are communicable to man, the possibility of a true diph- 
theritic infection, in domestic animals, cannot be denied. 

There are a number of causes existing in the patient which exercise a predis- 
posing influence in connection with this infection. Some of these are at present 
obscure and probably depend upon a lack of antibodies in the blood and tissues, 
but others are equally active, readily recognizable and in many cases remediable. 
There can be no doubt whatever that chronically enlarged tonsils, overgrowth 
of the so-called pharyngeal tonsil and chronic catarrh of the nasopharynx very 
materially increase the susceptibility of a child to diphtheria. For this reason 
these conditions should not be allowed to exist in otherwise healthy children. 
Further than this the crypts of the tonsils when diseased may harbor the Klebs- 
Loeffler bacillus, until a time when the system of the patient is favorable for its 
growth and then develop rapidly, or on being expelled cause the malady in another 
individual. 

None of the pathogenic organisms seems to possess a greater degree of variance 
in virulency than the one under discussion. In some instances it fails to exert 
any malign effect beyond a local influence, and even this may amount to nothing 
more than a sore throat. In other cases it attacks the patient with a virulence 
which is perfectly terrifying. 

It is not probable that sex has any influence as a predisposing cause. Statis- 
tics vary, however, some showing that a greater number of cases occur among 
boys than among girls. That these differences are merely fortuitous is exemplified 
by the fact that of 22,005 cases collected by me from various sources 11,006 oc- 
curred among boys and 10,099 among girls, a difference of only seven cases. 

Pathology and Morbid Anatomy. — In studying the pathology and morbid anatomy 
of diphtheria it is essential to remember that the disease is primarily local and 
secondarily systemic; that the local area of infection is the site at which the 
specific organism multiples and produces local changes by its growth, and at the 
same time elaborates a toxin which, being absorbed, acts on distant parts and so 
endangers life. The bacillus enters the blood stream in a relatively constant 
percentage of cases. 

Local Lesions. — The local change produced by the growth of the bacillus 
is now well understood, for a large number of researches in Europe and America 
have given us clear conceptions of it. Of these researches by far the most note- 
worthy is that carried out by Councilman, Mallory, and Pearce in Boston. 

The poison produced by the specific bacillus in the mucous membrane of the 
throat results in the death of the tissues and in this necrotic mass the bacilli then 
very rapidly develop. The epithelium in many cases manifests more or less pro- 
liferation, becomes hyaline and necrotic, eventually fragmenting and disintegrat- 
ing. The inflammatory exudate which permeates the mucosa and even the sub- 
mucous stratum is very rich in fibrin elements, and when brought in contact 



DIPHTHERIA 155 

with the necrosing structures forms a fibrinous reticulum entangling within its 
meshes the cells and bacteria. The membrane formed by the coagulation necrosis 
and hyaline degeneration of the cells may be so transparent as almost to escape 
detection during life (hyaline type), or it may be granular or fibrillar. The necro- 
sis may extend into the superficial epithelium only or penetrate the submucosa 
and cause ulceration, in some instances involving the parenchyma of the tonsil 
or even the submucous muscular structures. This necrotic membrane is subject 
to a number of important changes. It may disintegrate and form a mass of shreddy 
detritus on the surface or it may be thrown off by being elevated by the exudate 
which forms beneath it. In the latter process a very thick, false membrane formed 
of consecutive layers may be produced. The membrane always develops on a 
necrotic surface, but it may extend a short distance over the surrounding mucous 
membrane. 

The depth of the destructive process is not very great in the majority of cases, 
but in rare instances it has become deep enough to erode the carotid artery. In 
many, if not all, such instances other organisms play an important part in the 
spread of the necrosis and add to the intoxication their own poisonous products. 
It is important to bear in mind in diphtheria that the infection is "mixed" in the 
vast majority of cases; that is, the false membrane not only holds in its meshes a 
multitude of the specific bacilli but many other micro-organisms as well, many 
of which possess a power for evil, as, for example, the streptococcus. 

The membrane is closely attached to the tissues beneath and is stripped off 
with great difficulty except when it develops in the larynx and bronchi, where 
it is dislodged quite readily. 

The false membrane may develop on any mucous membrane or upon any wound 
or abrasion, but it most frequently appears on the tonsils. According to Lennox 
Browne, of London, the relative frequency of its appearance is as follows: 

Above the larynx, 84.1 per cent.: 841 cases. 

Fauces (including tonsils) alone 672 cases. 

Nose alone 2 cases. 

Fauces and nose 165 cases. 

Mouth or lips alone 1 case. 

Hard palate alone 1 case. 

Involving larynx, 15.9 per cent.: 150 cases. 

Larynx alone 4 cases. 

Larynx and fauces 100 cases. 

Larynx, fauces, and nose 46 cases. 

Cornwell in 600 cases in Philadelphia found the tonsils involved in 460 instances. 

The growth of the membrane, whatever its site, varies greatly in rapidity, in 
the area covered, and also in its thickness, but the virulence of the systemic in- 
fection is not always in direct ratio to the size of the diphtheritic patch. On the 
other hand, the degree of secondary infection depends largely upon the particular 
surface involved, and if it develops in the nasopharynx the toxemia is apt to be 
profound. In many severe cases the accessory nasal cavities are infected, particu- 
larly the antrum of Highmore. 

Visceral and Systemic Lesions. — The action of the toxin of diphtheria is 
chiefly expended upon the heart, the nervous system, and the kidneys. The 
heart suffers from an acute myositis or inflammation of its interstitial and muscular 
tissues, and this may be followed by conversion of the muscle fibres into hyaline 
masses. In a large proportion of the cases in which sudden death from heart- 
failure occurs the cause lies in the effect of the poison upon the nervous mechanism 
of the heart, possibly to a greater degree than its effect upon the myocardium. 
In some of these cases, however, death is due to thrombi in the heart cavities (see 
Sequelae), or, again, portions of these thrombi are swept out of the heart and produce 
embolism in the coronary arteries, in the pulmonary vessels or in the general 



156 DISEASES DUE TO A SPECIFIC INFECTION 

arterial system. As would be expected from the effects upon the heart, just de- 
scribed, the bloodvessels are also affected. An acute arteritis often occurs and 
affects particularly the intima. 

The nervous system is involved chiefly in its peripheral portions. The nerve 
trunks suffer from acute toxic neuritis and less commonly autopsy reveals hemor- 
rhage into the spinal cord and its membranes as a result of the vascular action of 
the poison. A much more common spinal lesion is, however, an acute anterior 
poliomyelitis, that is, involvement of the cells in the anterior horns of the gray 
matter. Sometimes the posterior nerve roots in the cord may be also affected. 
The special cranial nerves are also involved in many instances and loss of function 
in the oculomotor, vagus, hypoglossal and spinal accessory fibres takes place. It 
is, however, interesting to note that while paralysis, due to peripheral diphtheritic 
neuritis, may be absolute and widespread, it usually gets well unless the function 
of some vital part is so interfered with that death speedily ensues. The brain is 
very rarely affected. 

The kidneys are more or less affected in all cases of diphtheria. In some there 
is only a mild albuminuria produced by the irritative effect of the toxin upon the 
renal epithelium. In more severe cases an acute toxic nephritis develops. This 
nephritis primarily is parenchymatous, involving the Malpighian tufts and the 
tubules, but it speedily becomes diffuse. Hyaline degeneration also takes place 
in the renal vessels, as elsewhere in the body. 

The spleen is enlarged, markedly congested, and minute hemorrhages are to 
be seen beneath its capsule. The liver may be found, on cross-section to be dotted 
with small areas of coagulation necrosis. 

As the infection is most marked in the throat the cervical lymph glands are 
usually infiltrated and the poison may also cause enlargement of the lymphatics 
in the mediastinum and in the retroperitoneum. The inflammation of the lymph 
nodes, however, rarely ends in suppuration or extensive necrosis. 

The lungs are often the site of bronchopneumonia resulting from a complicat- 
ing pneumococcus infection, but true croupous pneumonia is a rare complication. 
When great dyspnea is present because of laryngeal stenosis compensatory emphy- 
sema may develop. In the laryngeal form the membrane may extend to the 
smaller bronchi. 

The blood is affected very deleteriously by the poison of diphtheria, so that 
a great diminution in the number of the red cells takes place with a corresponding 
fall in hemoglobin. A leukocytosis occurs except in the very malignant forms 
of the disease. Myelocytes are said to be present in severe cases. 

Symptoms. — After a period of incubation varying from two to seven days the 
disease has its onset in the form assumed by most acute infections, namely, with 
general malaise, chilliness, and fever, the temperature often reaching 102° or even 
103° in the first twenty-four hours. The severity of these symptoms varies greatly. 
In some cases they are so mild that the child is scarcely thought to be ailing, and 
the physician at his second visit is shocked on examining the throat to find distinct 
local lesions. In other cases the disease is fulminating in its onset. I have seen a 
small patch of membrane on a tonsil within twelve hours involve the larynx and 
necessitate tracheotomy, the membrane involving the external edges of the wound 
in less than twelve hours more. In nearly every case there is some complaint 
of sore throat, or of difficulty in swallowing arising from this cause. The pharyngeal 
mucous membrane is reddened and upon the tonsil or tonsils is seen a tiny patch, 
which is the beginning of the membrane, but which may be due to the exudate 
thrown out by a follicular tonsillitis. This membrane rapidly spreads and may 
extend to the pillars of the fauces, the pharynx, nasopharynx, and the uvula. It 
is grayish or light mouse color in hue, and in many cases speedily becomes shaggy 
and dirty looking. If the physician attempts to remove it it, is found to adhere 



DIPHTHERIA 157 

to the mucous membrane, and it can be taken off by only tearing it loose, so that 
a raw, bleeding surface is exposed over which a false membrane speedily reforms, 
for reasons given when discussing the pathology and morbid anatomy of the disease. 

There is nearly always some enlargement of the glands at the angle of the jaw. 

The degree of systemic disturbance depends in every case upon the virulence 
of the infecting bacillus and the rapidity with which the toxin is absorbed. 

Some patients who present on examination a large area of membrane suffer 
slightly in a comparative sense. The fever does not rise above 102° or 103°, the 
pulse does not go above 100 to 110, and the general state of the patient is favor- 
able. In other instances from the very onset the general systemic state is bad, 
even when the local changes may seemingly be slight. Even in severe cases, how- 
ever, the fever is not prone to be high, and often it never rises above 101°. 

The nervous symptoms consist in restlessness, sometimes in delirium, and rarely 
convulsions come on. As the disease approaches a fatal issue, the child becomes 
apathetic and it may be difficult to rouse it. 

. The circulation is feeble and irregularity of the pulse is a very frequent symptom. 
In White's exhaustive study of 946 cases this irregularity was present in 60 per 
cent. The younger the patient the greater the frequency of irregularity of 
pulse. Endocardial murmurs, systolic in point of time, occurred in 94 per cent. 

Albuminuria is a very constant symptom in these cases, appearing as early as 
the third day. The albumin may appear in considerable quantities, but the urin- 
ary flow is in many cases not greatly increased, although the presence of granular 
and hyaline casts shows that a true nephritis is present. Dropsy is uncommon. 

In cases which are not complicated or are treated by antitoxin, the membrane 
ceases to grow by the fifth or sixth day, and gradually separates at about the 
seventh or tenth day, leaving at its former site a bright red surface which bleeds 
easily. The nasal false membrane persists longer than this in the pharynx, 
and often comes away in one mass. 

After this period convalescence gradually goes on, the patient being profoundly 
weak and anemic and in great danger of sudden death from heart-failure if any 
sudden change in posture is made. A great many cases thought to be on the high 
road to recovery meet an unexpected fatal ending at this time. 

Special Forms. — There still remain to be described the special symptoms con- 
nected with those cases of diphtheria in which particular portions of the respiratory 
mucous membrane are involved, or in which the disease presents conditions which 
may be considered aberrant. In nasal diphtheria the false membrane may be so 
hidden by the swollen turbinated bodies that it is overlooked until it extends well 
forward into the nostril, when it may completely occlude the nares. Only a careful 
rhinoscopic examination will reveal this form in its early stages. Because of the 
importance of instituting treatment in all cases of this disease at the earliest pos- 
sible moment the nasal cavities should always be examined at the same time the 
throat is investigated, and any signs of nasal obstruction taken as of importance. 
A valuable sign of nasal diphtheria, but one which unfortunately does not 
manifest itself until the disease is well advanced, is a nasal discharge which may 
excoriate the upper lip. 

It is never to be forgotten that nasal diphtheria is a very malignant type of 
the disease in nearly every instance in which it occurs, and it is particularly prone 
to affect infants or very young children. 

Some practitioners confuse a condition of membranous rhinitis with this state 
and do not appreciate the gravity of nasal diphtheria although it is a state very 
prone to be characterized by profound toxemia. 

Laryngeal diphtheria manifests itself chiefly by the marked respiratory obstruc- 
tion which it produces very shortly after the pathological process begins in the 
mucous membrane of the larynx. Hoarseness on speaking, or crying, and a harsh 



158 DISEASES DUE TO A SPECIFIC INFECTION 

cough of a metallic sound, sometimes called "brassy," develop. Following these 
symptoms it is noted that there is slight inspiratory stridor which is accentuated 
at intervals by what seems to be associated laryngeal spasm. This is followed by 
persistent stridor, harsh breathing, and manifest unrest and respiratory anxiety. 
The child may grasp its throat with its hands as if endeavoring to remove the 
obstruction, and as it becomes livid, partly from mechanical failure of respiration 
and partly from toxemia, it often grinds its teeth and looks from side to side for 
relief, presenting at the same time signs of profound toxemia. Its pallid skin 
may be bedewed with sweat. As the disease advances the child becomes more 
and more limp, and struggles less and less for its breath. In children old enough 
and strong enough to cough violently in an effort to dislodge the membrane it 
often happens that they expel pieces of false membrane, and in some instances 
they may expel complete casts of the larynx. The fever in this type of diphtheria 
may not be at all high after the larynx has become infected, but, as would be 
expected, the pulse is usually exceedingly rapid and small. 

Laryngeal diphtheria rarely occurs without extension to the pharynx, so that 
at the time of death the membrane usually covers a wide area. When the pharyn- 
geal symptoms are very marked there is usually great enlargement of the cervical 
glands. 

Bronchopneumonia, due to the inspiration of septic material, is a frequent com- 
plication of this type. Like nasal diphtheria, laryngeal diphtheria has a very 
high mortality, partly because it causes suffocation and partly because it is 
associated with toxemia of a grave type. 

Diphtheria of the conjunctiva may occur as a complication or as a primary lesion. 

Complications and Sequelae. — The complications, involving the cervical glands, 
the lungs, heart, kidney, and nervous system, have already been mentioned. 
Nevertheless it is proper to say something more concerning them. 

Sudden heart-failure toward the close of the attack, or after convalescence is 
established, sometimes occurs on the slightest exertion. The child sits up to take 
a drink, or to grasp a toy, or becomes angry, and drops over dead. 

In other instances, instead of almost instantaneous cardiac failure with sudden 
death, a more gradual manifestation of grave heart disease is developed. A patient 
apparently on the high road to convalescence, except for the reddened throat and 
profound anemia, is found to have developed a weak pulse, which flags, and he 
presents unduly feeble heart sounds. Endocardial murmurs may be present. 
Sometimes the pulse is abnormally slow. In other cases it is too fast, and, with 
these circulatory symptoms, some epigastric distress or even vomiting occurs. 
The pulse becomes weaker and weaker and arrhythmia increases, the face is more 
and more pallid, and cardiac dyspnea with lividity comes on. Auscultation reveals 
fetal heart sounds or there may be a "delirium cordis." Death finally closes the 
scene at the end of twenty-four or forty-eight hours, in the presence of gradually 
deepening asthenia and a mind which is clear almost to the very last. Acute 
cardiac dilatation may occur. 

There are three causes for the types of heart-failure which arise as a result of 
diphtheria. When the heart fails in the course of an attack it is usually the result 
of cardiac thrombosis. When it occurs after an attack it is due usually to a toxic 
myocarditis or to the failure of the nervous supply of the heart through bulbar 
paralysis or paralysis of nerve fibres. Some statistics indicate that thrombosis 
is the most common cause of death after disappearance of the membrane. Of course 
all three of these factors may be present simultaneously. It is probable, however, 
that thrombosis is more frequently the cause of sudden death than is generally 
thought. Barbier in 71 autopsies on cases of sudden death in diphtheria found an 
antemortem cardiac thrombus in no less than 52 per cent. These thrombi were 
commonly found on the right side of the heart, usually in the right auricle. 



DIPHTHERIA 159 

Sometimes death is due to paralysis of the phrenic nerves, so that diaphragmatic 
paralysis ensues. 

The septic condition of the throat, the labored respiration, the decreased vital 
resistance of the patient, and the feebleness of the pulmonary circulation in severe 
cases very greatly predispose the patient to bronchopneumonia, and this complica- 
tion or sequel of diphtheria is the cause of death in a very large number of young 
children. 

Local or widespread paralysis often follows an attack of diphtheria, and if it 
involves vital nerves causes death. On the other hand, these palsies are note- 
worthy because of the fact that they usually recover. It is by no means uncom- 
mon to see a child so paralyzed that it can neither move hand nor foot or even move 
its head, that lies perfectly limp in its mother's arms, entirely recover muscular 
power. These palsies are not usually immediate sequences of an attack of diph- 
theria, but are all the more alarming because they may manifest themselves from 
one to three weeks after an attack. Again, it often happens that a very mild 
attack of the disease is followed by this distressing sequence, although as a rule 
severe cases usually have this result. The palate is the part most commonly 
paralyzed, and this results in difficulty in swallowing, regurgitation of liquids 
through the nose, and in a peculiar tone to the voice. When the throat is exam- 
ined the palate is seen to hang relaxed and motionless when the patient attempts 
to phonate, and it is also somewhat anesthetic, so that the contact of food is not 
well recognized. 

The time of onset of the paralysis varies somewhat with the parts involved. 
The form that occurs most frequently and which affects the muscles of the pharynx 
and eyes and extremities, or even that of the heart or the muscles of respiration, 
is a late palsy of the seventh to the twenty-first day of convalescence, whereas 
that form which affects the palate is more frequently met with at the end of the 
first week. 

True facial paralysis very rarely occurs except as a result of otitis media arising 
secondarily from the diseased state of the pharynx. 

Statistics as to the frequency with which paralysis accompanies or follows 
diphtheria vary. Hoppe-Seyler states it to be 27 per cent. Johannessen, for all 
Norway, 12.5 per cent.; the report of the Metropolitan Asylums Board of London, 
18.5 per cent. 

The collective investigation of the American Pediatric Society based on 3384 
non-hospital cases treated with antitoxin showed that 328 cases of paralysis oc- 
curred, which gives a percentage of 9.6. 

Hemorrhage from the ulcerative process in the nose may be sufficiently free to 
seriously exhaust the patient. When subcutaneous hemorrhages appear they are 
always a sign of very profound toxemia. 

When that practically constant sequel of diphtheria, profound anemia, remains 
persistently present and is but little improved under treatment, the possibility 
of renal disease being a serious sequel is to be recalled. 

Diagnosis. — There is no disease in which it is more important for the physician 
to make a correct diagnosis promptly than diphtheria, because if it be recognized 
in its earliest stage it can be cured by antitoxin in the majority of instances. On 
the other hand, there is no disease which is more difficult to prompt diagnosis in 
some cases. As diphtherial infection may be present without marked formation of 
membrane, all cases which manifest sore throat during an epidemic or, after expo- 
sure, should receive antitoxin as a preventive, and the throat should be swabbed 
and the secretion obtained examined bacteriologically for the bacillus. 

In every large city at the present time the health authorities provide tubes 
and swabs for the transmission of cultures from the patient to a laboratory. Usu- 
ally the swab is delivered in a sterile tube and the culture medium is placed in a 



160 DISEASES DUE TO A SPECIFIC INFECTION 

second sterile tube. The directions issued by the New York Board of Health are 
as follows: "The patient should be placed in good light, and, if a child, properly 
held. In cases where it is possible to get a good view of the throat, depress the 
tongue and rub the cotton swab gently but freely against any visible exudate. 
In other cases, including those in which the exudate is confined to the larynx, 
avoiding the tongue, pass the swab far back and rub it freely against the mucous 
membrane of the pharynx and tonsils. Without laying the swab down, withdraw 
the cotton plug from the culture-tube, insert the swab, and rub that portion of it 
which has touched the exudate gently but thoroughly all over the surface of the 
blood serum. Do not push the swab into the blood serum nor break the surface 
in any way. Then replace the swab in its own tube, plug both tubes, put them in 
the box, and return the culture outfit at once to the station from which it was 
obtained/' 

It is worthy of note that in some instances cultures made from the throat of 
suspected diphtheria carriers are negative, although nasal cultures are positive. 

A loss of valuable time is prevented during the bacteriological test by using 
antitoxin, but many hours need not be lost if the bacteriologist is skilful. Dr. 
Park, of New York, who has done such excellent work along these lines, has this 
to say in regard to this matter: "The examination by a competent bacteriologist 
of the bacterial growth in a blood-serum tube which has been properly inoculated 
and kept for fourteen hours at the body temperature, can be thoroughly relied upon 
in cases where there is visible membrane in the throat, if the culture is made during 
the period in which the membrane is forming, and no antiseptic, especially no 
mercurial solution, has lately been applied. In cases in which the disease is con- 
fined to the larynx or bronchi, surprisingly accurate results can be obtained from 
cultures, but in a certain proportion of cases no diphtheria bacilli will be found 
in the first culture, and yet will be abundantly present in later cultures. We 
believe, therefore, that absolute reliance for a diagnosis cannot be placed upon a 
single culture from the pharynx in purely laryngeal cases." 

Diphtheria is to be separated from tonsillitis with exudation from the follicles 
of the tonsils and from the diphtheroid false membrane produced by the strepto- 
coccus and by an organism closely allied but not identical with the Klebs-Loeffier 
organism, which is found in scarlet fever, typhoid fever, and measles. Sometimes 
this can be done only by the bacteriological test. 

In follicular tonsillitis the exudate may be scattered over the openings of several 
follicles, it is rarely as dark in hue as the true membrane, it can be wiped off with 
an applicator more readily than the membrane of diphtheria, and the tonsillar 
swelling is marked. The systemic symptoms are, however, of little value in differ- 
entiation, because tonsillitis is a disease characterized by very severe symptoms 
as compared to its gravity, for aching in the back and limbs, high fever, and great 
evidence of systemic depression are frequently seen during its course. Holt has 
pointed out the fact that the surfaces of the wound left after tonsillotomy may for 
a few davs closely resemble tonsillar diphtheria, and I have seen the free applica- 
tion of a strong solution of silver nitrate to the pharynx produce an appearance 
which might readily be mistaken, if examined in a poor light, for diphtheria. 

Reference has been made to diphtheroid conditions of the throat. These 
states are probably in a large number of instances due to the streptococcus 
pyogenes. The false membrane, if none of the true bacilli of Klebs and 
Loeffler are present, is usually more soft and creamy in its consistency, it is not 
so tightly adherent to the underlying mucous membrane, and is often very foul. 
Occurring as a complication of grave infectious diseases such as scarlet fever and 
typhoid fever, it is dangerous, but otherwise the mortality is not high, being about 
2.5 per cent., if we can take the New York City statistics as representative of all 
cases. 



DIPHTHERIA 161 

Prognosis. — At the present time it may be said that the prognosis of diphtheria 
depends entirely upon the promptness with which antitoxin is used. Without anti- 
toxin the death rate varies greatly in different epidemics. In some it reaches the 
appalling rate of 50 per cent., while in others it is not more than 30 per cent. It 
is very much more fatal in babies than in older children. Symptoms of evil prog- 
nostic import are grinding of the teeth, gallop rhythm of the heart sounds, epigastric 
pain, and vomiting. 

The cases manifesting laryngeal and nasal involvement are always grave as to 
prognosis. The physician should also be most guarded as to his prognosis as the 
disease passes its most active period, because everyone of experience knows that 
an attack of sudden heart-failure often occurs as the child, once more feeling 
strong, attempts to sit up. A rapid or gradual heart-failure may come on during 
convalescence. (See Sequelae.) 

The presence of much membrane and an afebrile temperature is evil in import. 
Marked pallor, or yellowish pallor, with duskiness of the lips not due to respiratory 
obstruction ; not due to membrane, but to toxemia, bodes death. Paralysis is usually 
not of serious import unless the respiratory or cardiac innervation is attacked. 

Prophylaxis. — As the intimate association of a person, or garments, bearing 
the specific bacillus with another individual who is susceptible to the disease is 
essential for its spread, it is evident that by proper quarantine and isolation per- 
fect prophylaxis is possible. All patients who have diphtheria should be isolated 
at once, and the attendant who nurses the child or adult who is affected should 
not associate with other persons until after a bath has been taken, the face and 
head well shampooed and the pharynx and nasal cavities well douched. Cultures 
from the throat of the nurse should be made before she proceeds to another case 
which is not diphtheritic. After the patient is convalscent, it is to be recalled that 
the specific bacillus may remain in the nasopharyngeal mucus for a long period 
and so isolation is still essential. The child should not play with other children 
for at least two weeks, and during this period should have its nasopharynx sprayed 
daily with some bland antiseptic wash such as Dobell's solution, alkathymol, or 
normal saline solution. Particularly in public institutions, the nasopharyngeal 
secretion should be examined bacteriologically during convalescence to prove the 
presence or absence of the specific infecting germ before the child is discharged. 
As illustrative of this fact the results of the New York Board of Health investi- 
gation are of interest. Out of 605 cases examined it was found that the bacilli 
were not present in 304 on the third day after the membrane disappeared, in 176 
they were present for seven days, in 64 for twelve days, and in 36 cases for fifteen 
days. Twenty-one days after the membrane was gone 12 showed bacilli, and 4 
cases showed them for twenty-eight days. Another set yielded 4 cases of bacilli 
for thirty-five days, and 2 for sixty-three days. 

It seems hardly necessary to add that the garments, bedding, and toys of all 
diphtheritic patients should be destroyed or thoroughly disinfected by steam or 
formaldehyde. The floors and walls of the room and the furniture should also 
be treated with formaldehyde, and it should be done as thoroughly as if the case 
had been one of smallpox. All discharges from the patient should be received 
in a vessel containing bichloride solution, or, if cloths are used, these should be 
burned. 

A very important measure in all cases in which the disease arises in a family of 
children is the use of immunizing doses of antitoxic serum for the protection of 
the well from the diseased. There is no doubt whatever that this is a most efficient, 
never-to-be-neglected measure. The dose is not less than 500 to 1000 units and 
the protection lasts about three or four weeks. Nurses as well as children should 
be protected by its use. 

The Schick test is a test used to determine the natural immunity of an individual 
11 



162 



DISEASES DUE TO A SPECIFIC INFECTION 



to diphtheria infection. Its field of usefulness is during an epidemic in an institu- 
tion or family where there are a considerable number of persons exposed. It con- 
sists in injecting jj part of a dose of diphtheria toxin that would be lethal to a guinea- 
pig, into the superficial layers of the skin. If the patient is susceptible to diph- 
theria a red spot develops at the side of the injection in about forty-eight hours, 
whereas, if it does not appear, it may be considered that the individual is relatively 
immune and less in need of antitoxin. 

When treating or examining the throat the physician and nurse may protect 
themselves from the discharges by looking through a pane of glass held before the 
face of the patient. 

Treament. — The treatment of diphtheria at the present time is more scientifically 
accurate in its basis and in its results than that of any other malady save malarial 
fever, in which we know not only the cause but the remedy for its removal. The 
keystone of the treatment is the liberal use of antidiphtheritic serum. 

It is not necessary in a work of this character to give massive accumulations of 
statistics to prove that this plan is based not only on scientific laboratory investi- 
gations, but upon bedside experience as well. 

The following figures, which are Baginsky's, show the decrease in mortality ac- 
cording to age: 

Before the introduction of antitoxin the mortality of diphtheria according to 
age was — 



to 2 years 
2 to 4 years 
4 to 6 years 



60.2 
51.2 
38.0 



6 to 8 years 

8 to 10 years 

12 to 14 years 



Since the introduction of antitoxin the death rate is — 



to 2 years 
2 to 4 years 
4 to 6 years 
6 to 8 years 



25.88 
17.12 
17.24 
11.39 



8 to 10 years 
10 to 12 years 
12 to 14 years 



22.9 

28.8 
18.5 



5.17 
10.0 
13.3 



The following chart of Park and Bolduan is another illustration of the life- 
saving effects of antitoxin. 



Fig. 41 



100 
90 

80 

ro 

GO 
50 
40 
30 
20 
10 



Chart showing the combined curve of mortality of diphtheria in 19 cities in America and Europe. 

The use of antitoxin began in 1894. 



'78 


'79 


'80J'81 


'd2 


'83 


'84 


'85 


'88 


'87 


'88 


'89 


'oo 


*91 


'92 


'93J'94 


'9.3 


'98 


'97 


'98 


'99 


'00 


'01 


'02 


'03 


'04 


'05 
























































































































































































































































































































































































































































































































\ 

















































































































The physician who fails to use antitoxin, when it is to be had, is guilty of a gross 
lack of professional knowledge or is atrociously careless of his patient's welfare. 



DIPHTHERIA 163 

There are several points to be borne in mind in regard to the use of antitoxin, 
namely (1) it must be employed early in the attack to get the best results, for it 
is manifest that after the disease has existed long enough to do permanent damage 
to the tissues no antidote can be satisfactory. No one would expect to give the 
antidote for arsenic two days after the poison was taken and expect good results. 
Nevertheless, when antitoxin has not been used early it must be given freely in the 
hope of its aiding the patient sufficiently to help him withstand the infection. 
(2) The antitoxin should be given liberally. A few large doses in the onset of the 
attack not only are of great value, but are really economical so far as cost is con- 
cerned. (3) It must be given in particularly large doses in cases of nasal and 
laryngeal diphtheria, because these are forms in which rapid absorption of the 
toxin of the disease and respiratory obstruction takes place and the malady must 
be most actively opposed. In these cases it may be useful to give it intravenously. 

(4) Whenever a person is exposed to diphtheria he should receive a moderate dose 
of antitoxin to protect him from infection. The dose should be about 1000 units. 

(5) When diphtheria is suspected to be present it is well to give antitoxin at once 
rather than run the risk of waiting for a sure diagnosis. In administering anti- 
toxin the following rules should be followed: 

1. The skin over the outer surface of the thigh or over the flank or lateral abdom- 
inal wall should be cleansed with soap and water and alcohol. 

2. The serum should be injected by means of a syringe or bulb, through a large 
hypodermic needle which is inserted through the skin where it has been cleansed. 
If the injection is made on the outer side of the thigh it is best given directly into 
the belly of the vastus externus muscle. 

3. The injection should be made slowly and quietly and the swelling which 
results should not be rubbed. 

4. At least 4000 to 5000 units of antitoxic serum should be given at the first 
dose and repeated in four to eight hours, according to the severity of the case. 

If the patient is seen as late as the second day the dose should be 6000 units, 
and if seen on the third day, from 9500 to 20,000 units if the membrane is large 
or the other signs severe. 

5. In nasal and laryngeal cases 6000 or more units for the first dose are usually 
necessary. 

The result of this plan of treatment is often magical. The symptoms of general 
systemic disturbance, such as a rapid pulse and fever, become modified, the mem- 
brane ceases to grow and loses its tenacious hold of the subjacent tissues, becoming 
not only loose but softened, and speedily disappears. 

The only disagreeable effects of using antitoxin in large doses are the subsequent 
development of some pain or soreness in the joints or the appearance of an urticarial 
rash; but even if these symptoms appear they are not serious and need give no 
alarm. "These symptoms of so-called serum sickness" are largely avoided by 
the use of antitoxin in the form of globulins, as it has been found that they depend 
upon a certain substance or substances in the serum, which are present in compar- 
atively small amounts in the globulins, which, in turn, contain most, if not all, of 
the antitoxic power. Besredka also claims that if a few drops of antitoxin or 
globulin solution are first injected, this small dose if repeated two or three times at 
half-minute intervals, desensitizes the patient so that the large dose may be injected 
with much less danger of serum sickness or anaphylaxis. 

It is impossible to determine beforehand what cases will, because of idiosyncrasy, 
suffer from anaphylaxis, save that asthmatics and patients of a marked lymphatic 
type seem more prone to it than others. Notwithstanding the startling 
effects in these cases it is to be distinctly understood and sharply emphasized 
that thejiumber of these accidents has been so infinitesimal as compared to the 
hundreds of thousands of injections given during the last ten years that no hesita- 



164 DISEASES DUE TO A SPECIFIC INFECTION 

tion should be allowed in the use of antitoxin in diphtheria except in the class of 
cases already referred to and under the conditions about to be named, for the 
danger of the disease is great and that of the injection is a negligible quantity. 
An important fact to be borne in mind is that the injection of antitoxin for the 
purpose of immunizing an individual who has been exposed to the disease or for the 
purpose of combating an attack of diphtheria already present produces after the 
lapse of several days a condition whereby the patient develops an increased 
susceptibility to the serum or, in other words, becomes sensitized to its effects, 
thereby producing a state in which, the severe symptoms already spoken of may 
ensue when a subsequent dose is given. This condition, called anaphylaxis, does 
not take place if the doses of serum are given every few hours or even every day 
for an indefinite period of time. It is only when an interval elapses between 
doses amounting to several days or more that the patient is in danger of anaphylaxis 
when an injection is given. In other words, a patient who has received an immu- 
nizing dose of antitoxin or a curative dose on one occasion is far more likely to 
develop evil symptoms after a dose given some time later than a patient who 
receives the antitoxin for the first time. The lesson to be learned from this in 
practical medicine is that when a patient gives a history that antitoxin has been 
comparatively recently used, the physician should be cautious in the administration 
of the remedy or prophylactic. When a second attack of diphtheria is actually 
present the danger to life is probably far greater from the disease than from the 
possible development of anaphylaxis, but the fact that hypersensitiveness to anti- 
toxic serum may have been developed by a previous injection must be carefully 
considered when the question of giving a dose for immunization arises. The 
rule would seem to be that where a child is thoroughly exposed to infection, an 
immunizing dose had better be given, but where the exposure is not so great as 
to lead the physician to the belief that infection is almost certain to occur, it may 
be well to avoid the use of an immunizing dose for the reasons given. The physician 
is placed in the difficult position of determining whether there is greater danger 
to the child of an attack of diphtheria or of the development of the symptoms of 
anaphylaxis, and each case must be decided upon its merits. In orphanages and 
hospitals a large number of children are gathered together, the certain mortality 
of an outbreak justifies the universal use of immunizing doses, since the danger 
of the disease is infinitely greater than the danger of anaphylaxis. In private 
practice, however, the question is quite different and must be decided in each 
instance on its own merits. 

So far no method has been devised by which these desperate symptoms of anaphy- 
laxis can be combated. Adrenalin has been used without any very good grounds 
for its employment, and without very much success. The drug which would 
seem to promise the most relief, so far as the pulmonary edema is concerned, is 
atropine in full doses. 

The local treatment of diphtheria consists in the application to the false membrane 
of peroxide of hydrogen by means of a spray or swab. This active disinfectant 
disintegrates the exudate and aids in its removal. The other local applications 
which have been used in the past are painful, injurious, or ineffective as compared 
to this agent. 

The systemic treatment, aside from the use of antitoxin, consists in the employ- 
ment of foods which are easily swallowed and which will maintain the vitality 
of the patient to the highest degree, such as gruels made of barley or rice, which are 
digested in great degree by the administration of 2 to 4 grains of taka-diastase. 

When the pulse Hags, small doses of aromatic spirit of ammonia or Hoffmann's 
anodyne (10 to .30 drops in water may be used) or brandy which is old enough to 
have a "bouquet" may be given. Full doses of strychnine should also be used for 
the same purpose. Perfect rest of mind and body should be obtained if possible 



GONORRHEAL INFECTION 165 

and great care taken during the illness and during convalescence that no sudden 
exertion, which may cause cardiac failure, is permitted. 

When obstruction of the larynx takes place the patient's life may often be saved 
by intubation or tracheotomy. In these cases the patient should be kept in a 
room the air of which is moistened by steam. 

The complications and sequelae are treated in the following manner : The anemia 
is to be controlled by the use of moderate doses of reduced iron. Large doses are 
unnecessary and tend to cause constipation and disordered digestion. A quarter 
grain three times a day is quite sufficient, given in a small chocolate-coated tablet 
or placed in a gum-drop. In some instances 3 to 5 minims of tincture of the chloride 
of iron is equally good; y^-g- grain of arsenous acid in a sugar-coated granule may 
be given simultaneously or in alternate weeks. This treatment is also advisable 
for the relief of the local or general paralysis, which is usually associated with 
marked anemia. In other instances the syrup of the hypophosphites may be 
used, and phosphorus is often of value in the dose of t ^-q grain three times a day. 
Another remedy of great value as a roborant is cod-liver oil. 

In regard to the use of strychnine, which is so largely used as a circulatory and 
nervous stimulant in all conditions of depression, it should be remembered that 
it is never a stimulant which in any way increases the nutrition of the part involved. 
It simply acts as an irritant stimulant. If there is reason to believe that a "whip" 
is needed to spur atonic nerves to greater effort, it may be used, but if there is any 
evidence of nervous irritation it is better not to employ it. Aside from the treat- 
ment already named there is little which can be done to benefit the paralysis. 

GONORRHEAL INFECTION. 

There are still some roues, and ignorant persons, who lie under the delusion, 
at one time prevalent, that an attack of gonorrhea is of little more gravity " than 
a bad cold." A considerable number of both classes learn by experience sooner 
or later that this is a most mistaken conception of the disease. It must not be 
forgotten that within the last few years it has been proved again and again that 
the gonococcus may find entrance into the general system from the urethra and 
there cause the most disastrous consequences. Further than this, while systemic 
dissemination of the gonococcus usually is secondary to venereal infection, it is 
to be remembered that gonococcal inflammation of any susceptible mucosa, as 
the conjunctiva, may afford a point of entrance. Heimann has reported a case 
of gonococcemia in which he thinks infection occurred through a wound, and 
Kimball believes the mouth or upper air-passages may constitute portals of entry. 
He has also reported a series of cases of gonorrheal pyemia due to volvovaginitis 
in children, some cases being only three months old. If it gains access to the joints, 
it may not only produce a temporary gonorrheal arthritis, but it may also cause a 
chronic arthritis which is usually multiple, and sometimes is so widespread that the 
patient is crippled hand and foot, finger and toe, for the balance of his life, the 
incapacity of the patient being even greater and more rapid in its onset than if 
he were suffering from rheumatoid arthritis. 

Symptoms. — The appearance of a joint suffering from gonorrheal inflammation 
does not differ materially from that of acute rheumatic fever. It is swollen and 
exquisitely tender. The skin about the joint is hot, but often it is not much reddened ; 
on the contrary, in some cases it presents a peculiar leaden hue. The temperature 
of the body in general is usually normal, but there is often, at the time of onset, 
some fever. In some cases there is a notable serous peri-arthritis. 

Gonorrheal arthritis, as a rule, attacks the large joints. It is most commonly 
multiple, but it may be single. I have seen not only all the large, but the small 
joints infected simultaneously. Even the sacro-iliac, maxillary, and sternoclavicular 



166 DISEASES DUE TO A SPECIFIC INFECTION 

joints may be involved. This is a noteworthy point when we remember that infec- 
tion of the maxillary joint almost never occurs in ordinary rheumatism. 

According to French statistics the knees are attacked more frequently than any 
other joint in the body — 83 times out of 119 cases; the ankle 32 times, fingers and 
toes 23 times, the hips 16 times, the wrist 14, the shoulder 12, and the elbow 11. 

It must be distinctly understood that gonorrheal arthritis has no relation whatever 
to acute articular rheumatism. The tendency on the part of many physicians to 
call all swellings of joints rheumatism is to be deplored. The mere presence of 
heat, swelling, and pain in a joint, with or without fever, does not necessarily 
indicate that rheumatism is the cause. 

Suppuration of a joint as a result of gonorrheal infection very rarely occurs, but 
ankylosis, due to thickening of the synovial membranes, ligaments, and periarticular 
tissues, and atrophic changes in the cartilages and in the ends of the bone are met 
with. In other words, gonorrheal infection of a joint may result in fibrous ankylo- 
sis, or in atrophy, or in overgrowth of bony tissue, as in rheumatoid arthritis. 

The fascia in different portions of the body may also be infected. This is particu- 
larly apt to occur in the plantar region and not infrequently stiffening and inflamma- 
tion of the tendo Achillis is met with. 

A second serious consequence of gonorrheal infection is the development of a 
gonorrheal endocarditis. As long ago as 1854 Brandes recorded two cases of gonor- 
rhea with arthritis and endocarditis, and in 1862 Traube reported another of 
gonorrheal endocarditis without joint infection. None of these cases were proved 
to be due to the gonococcus because this organism was not known at that time, 
but in 1893 Leyden proved the presence of the gonococcus in the heart. Since 
then many more cases have been reported in which the gonococcus has been isolated 
from the endocardium or the circulating blood. Perhaps the most noteworthy 
report was that of Thayer and Lazear in 1899. 

There is no special time in the course of the attack of gonorrhea at which the 
endocardial involvement takes place. Occasionally it has come in the stage of 
onset, but in most cases it occurs at about the fifth week. In others it is postponed 
for weeks, or even for months. In a case reported by Finley and McCrae a fatal 
endocarditis developed nine months after the onset of the urethral discharge, 
and when that discharge was no longer present, although a microscopic examination 
of the urethral mucosa revealed gonococci. 

While it is true that these cases are comparatively rare when we consider the 
frequency of gonorrhea, it is probable that they occur with more frequency than 
has been generally thought, and it is a noteworthy fact that in those cases in which 
the physician is skilful enough to examine the blood, or the endocardium, for the 
gonococcus, that it is found as a pathogenic micro-organism much more frequently 
than in those cases in which the physician does not possess such pathological 
training. With improvements in technique, general gonorrheal infection will 
probably be recognized as being by no means as infrequent as it has been thought 
in the past. 

Males are very much more frequently affected by systemic infection of this 
character than are females. 

Systemic gonorrheal infection follows not only the primary disease in the urethra 
or vagina, but has been met with in infants suffering from ophthalmia neonatorum 
due to the gonococcus. In some cases the infection is pure; in others it is mixed. 

Diagnosis. — The statement of a patient suffering from an acute arthritis, acute 
ophthalmia, or, indeed, an acute endocarditis, that he, or she, is also suffering 
from gonorrhea will do much toward making the diagnosis of the condition clear. 
But in the majority of instances the patient neglects to give this important informa- 
tion, and in a considerable number of cases denies gonorrheal infection of the 
genitalia, thinking that it can have no bearing upon the inflammation elsewhere, 



GONORRHEAL INFECTION 167 

and that therefore it is unnecessary to mention the fact that such a local infection 
exists. Not rarely patients will deny the existence of a local genital lesion, and 
it can only be discovered upon careful examination. It may be necessary in some 
cases to examine the secretions of the urethra or the vagina by staining and by 
the microscope. 

It may be said that in every male suffering from acute arthritis between the 
ages of fifteen and sixty the possibility of gonorrheal infection should be considered 
as having almost equal rank with the possibility of acute articular rheumatism, 
and the development of endocarditis should not be considered as indicative of one 
condition more than the other, although as a matter of fact endocarditis is, of 
course, infinitely more common in true articular rheumatism than it is in gonorrheal 
infection. On the other hand the mere discovery by the physician of a presence 
of a purulent discharge from the urethra does not by any means prove that the 
patient has gonorrheal arthritis. It is entirely possible for him to have acute 
articular rheumatism and gonorrhea, and again, it sometimes happens that gouty 
persons have a purulent discharge from the urethra which does not depend upon 
the gonococcus. Rarely, too, a purulent urethral discharge is found, in persons 
who are not gouty, which does not depend upon the gonococcus, but is due to 
another form of infection. 

A therapeutic test of some value lies in the fact that full doses of the salicylates 
usually cause remarkable improvement in the arthritis of rheumatism, and affect 
in no way whatever the arthritis of gonorrhea. Again, it is characteristic of true 
rheumatism to leave one joint as it affects another; whereas, in gonorrheal rheuma- 
tism it is rare for the inflammation to diminish in the joint primarily affected when 
other joints become involved. 

Prognosis. — The prognosis in gonorrheal rheumatism is favorable in the majority 
of instances, provided the infection is not very severe, and is not persistent. The 
physician, however, must be most guarded in expressing an opinion as to ultimate 
complete recovery, for, as already stated, some of the severest cases of chronic 
multiple arthritis are met with as the result of this infection of the joints. The 
prognosis is also influenced to some extent by the history of the patient. If he 
has already suffered from previous attacks of gonorrheal arthritis, the probability 
of complete recovery is not as good as in primary attacks. 

Endocarditis due to gonorrheal rheumatism is a very serious condition and 
often results in death. 

Treatment. — The treatment of gonorrheal arthritis consists, first, in the cure of 
the local area of primary infection as rapidly as possible. For this purpose the 
ordinary forms of treatment for gonorrhea are to be followed. The arthritis is 
to be relieved by the use of a splint and by the application of a 50 per cent, ichthyol 
ointment to the joint. If the inflammation is exceedingly acute an ice-bag may 
be employed, and if the effusion is considerable aspiration may be needed to relieve 
pressure. In some instances the best results are obtained by opening the joint 
and permitting free drainage. Should the physician place the limb of the patient 
suffering from gonorrheal arthritis upon a splint, it should not remain so fixed 
for any length of time, as ankylosis is particularly prone to ensue. The splint is 
used only for the relief of pain in the acute inflammatory stages. 

As already stated, the salicylates are useless in gonorrheal arthritis. Indeed, 
they are worse than useless in that they in no way influence the infection and they 
are apt to disorder the stomach. Rest in the acute stages and the treatment of 
the local infection is the most that can be done for the patient aside from local 
applications. Later, passive movements of the joints and the use of the iodides 
or of the syrup of the iodide of iron, if anemia is also present, must be resorted to. 
Endocarditis is to be treated as- is ordinary ulcerative endocarditis. 

The use of antigonococcic serum, derived from the blood of sheep, has proved 



168 DISEASES DUE TO A SPECIFIC INFECTION 

of very great value in the treatment of gonorrheal arthritis, but useless in orchitis, 
epididymitis and urethritis due to the same organism. This serum causes a distinct 
general and local reaction. The dose is 2 c.c. given every second or third day. 
Given at long intervals it may cause anaphylaxis. So, too, gonorrhea phylacogen 
may be used, beginning with 2 c.c. at a dose and increasing the dose every second 
day. 

ERYSIPELAS. 

Definition. — Erysipelas is an acute infectious disease due to the entrance into 
the skin in its deeper layers of the Streptococcus pyogenes, sometimes called the 
Streptococcus erysipelatis. The skin of the part affected becomes dusky red, and 
swollen. A peculiarity of the area of redness is that it has a sharp line of demarca- 
tion separating it from the surrounding healthy tissue, which is usually of its 
natural color and appearance. The line of demarcation can be not only seen but 
can be felt by the finger-tip, and if the affected area be punctured and the serum 
which then exudes stained with methylene blue the chains of streptococci can readily 
be found under the microscope. Erysipelas is sometimes called "St. Anthony's 
Fire." 

Frequency. — Erysipelas is found in nearly all parts of the world and is not infre- 
quently present in epidemic form in hospitals and other institutions in which large 
numbers of persons, with impaired health, are together in wards and dormitories. 
Under these conditions it spreads rapidly from patient to patient, particularly 
if wounds afford an entrance into the body. For this reason the outbreak of the 
disease in an institution should be followed by the immediate isolation of the 
patient and a thorough disinfection of the entire ward in which he has been lying. 
The disease occurs most frequently in the spring months, particularly in April, 
but is met with at all seasons of the year. 

Etiology. — As already stated the cause of erysipelas is the entrance into the 
deeper layers of the skin of the streptococcus in a form which cannot be separated 
from that which sometimes produces purulent infection in other parts of the body'. 
The anatomical and many of the clinical features of this disease may be produced 
by several closely allied bacteria, but the clinical manifestations of erysipelas are so 
constantly associated with the Streptococcus erysipelatis that the different infections 
may be ignored or grouped with this one. Two additional factors are nearly 
always active in the production of the disease, namely, a break in the skin or in a 
neighboring mucous membrane, so that the streptococcus gains access to the tissues, 
and, secondly, some cause, local or general, which diminishes vital resistance to 
such a degree that the tissues afford a favorable site for the growth of the micro- 
organism. Thus erysipelas may be due to the infection of a small pimple, by 
scratching it with the finger-nail, and it is not uncommonly met with in those who 
are suffering from renal disease, from diabetes, from alcoholism, or from some 
condition which distinctly decreases the ability of the body to protect itself from 
infection. 

Sometimes the resisting power is decreased by local causes, as by exposure to 
great cold, but it is very doubtful if this cause alone, with the presence of the strepto- 
coccus, is capable of causing the disease unless the general systemic vital resistance 
is impaired. 

The course to be followed in cases of early erysipelas is to examine into the state 
of the urine at once, and, even if this be found normal, to examine it repeatedly 
for evidences of renal disease or diabetes, since such causes render the patient very 
susceptible. Search for other causes of impaired health should also be made, 
because erysipelas is a malady which is particularly prone to attack those who 
are already ill, even if the primary illness is not apparent. Occasionally the physi- 
cian meets with a case in which there is no underlying dyscrasia which predisposes 



ERYSIPELAS 169 

to the disease. In these instances the patient may have repeated attacks, due 
apparently to general susceptibility to this infection, the streptococci remaining 
inactive in the tissues in certain cases for weeks at a time. Women during the 
puerperal period are especially susceptible to the infection. 

Pathology and Morbid Anatomy. — Primarily the lesion of erysipelas consists of a 
hyperemia; later, an exudate composed of cells and fluid appears in the layers of 
true skin, associated with a rapid growth of the streptococcus in the lymph spaces 
in the margin of and often beyond the inflammatory zone. In severe cases the 
lesion spreads with great rapidity and may affect not only the deeper layers of 
the skin, but the underlying connective tissue as well. The destructive action of the 
bacterial toxin may lead to the formation of sloughs, gangrenous erysipelas, or the 
polymorphonuclear leukocytes may accumulate in such numbers as to constitute 
pus, forming the so-called phlegmonous erysipelas. In rare instances the strepto- 
coccus, after entering the body through some dissolution of continuity in the skin 
or mucous membrane, is carried by the blood or lymphatic system to distant parts, 
causing a development of the disease far from the site of the primary lesion. 

The accompanying visceral lesion may be due to the absorbed toxin or to strepto- 
coccemia. The former may cause degenerative changes, such as focal, or even 
diffuse, necrosis in the liver, spleen, kidneys, or myocardium. The entrance of 
the streptococcus into the blood may be manifested in an endocarditis, pericarditis, 
nephritis, pleuritis, meningitis, arthritis, osseous or pulmonary infections, or other 
evidences of colonization of the germ in the various organs or tissues. 

The onset of erysipelas is associated with a leukocytosis of polymorphonuclear 
cells, except in malignant cases in devitalized persons. 

Incubation. — The period between the introduction of the streptococcus and the 
development of the disease varies greatly in different cases. Usually the period 
of incubation lasts from three to seven days. 

Symptoms. — In the great majority of cases erysipelas affects the skin of the face 
about the corners of the nose or near the ear. A tingling of the skin is felt which 
speedily becomes an intense burning, and is increased by rubbing or scratching 
the part. This reddened area spreads rapidly and is characterized at the end of 
twenty-four hours, or before, by the presence of a sharp line of demarcation, which 
marks the advancing line of inflammation, a margin which can often be felt as a 
slightly indurated and raised edge. Sometimes the inflammatory process projects 
well-defined areas of extension into the healthy skin. Palpation of the diseased 
skin also reveals the fact that it is hot and somewhat brawny and tender. The 
color of the part is not a bright red, but is dusky in hue. The swelling of the face 
when well developed is sufficient to render the patient unrecognizable, and the 
eye, or eyes, may be completely closed by the infiltration of the eye-lids. The ears 
when involved become swollen to an extraordinary degree and the skin seems 
very tense and indurated. Not infrequently blebs or blisters form over the inflamed 
area. 

After the early stage of onset it has been my experience that patients rarely 
complain very greatly of pain and burning. 

The amount of systemic disturbance varies very much in different cases. In 
those who have previously been in moderate health the local lesion and the degree 
of systemic disturbance may be so slight as to be scarcely noticeable. The patient 
may complain of a slight chilliness, the pulse may be slightly accelerated, and the 
temperature raised one or two degrees. In other cases in which vital resistance 
is poor and the infecting germ virulent in form, the symptoms just described are 
very severe in degree, so that rigors, high fever, a rapid pidse, delirium, and great 
prostration may be present. In still other cases, not so common, when by reason 
of great diminution of vital powers the general health has been greatly undermined, 
as in advanced diabetes or Bright's disease, the disease attacks the patient so 



170 DISEASES DUE TO A SPECIFIC INFECTION 

vigorously that he sinks beneath its onset without having enough stamina to resist 
the infection, and may pass into semi-coma or even convulsions followed by collapse 
due to the apparent exacerbation of the underlying malady by the secondary 
infection. In rare instances the part involved may become gangrenous and death 
may follow from sepsis and exhaustion. 

In cases of ordinary severity the fever lasts about five days and ends by crisis. 

One attack of erysipelas does not protect but rather predisposes the patient 
to another. 

Under the name erysipelas migrans a form of the disease is met with in which 
the disease spreads from part to part and, in the course of its wandering, may 
affect successively almost the entire surface of the body. 

Complications and Sequel ae.— When erysipelas attacks individuals who are greatly 
impaired in health the results are often grave, not only because the onset of erysip- 
elas is dangerous in itself, but because it is an indication in many cases of a grave 
disease, hitherto unrecognized, which may speedily cause the death of the patient 
by an exacerbation. Thus the development of erysipelas in cases of chronic 
Bright's disease not only means that the renal lesion has resulted in poor resistance, 
but in addition the task of eliminating the toxins of the new malady may so over- 
whelm the kidneys that they may cease to perform their function. 

Again in cases of greatly impaired health the inflammatory process goes on to 
suppuration and the deeper tissues become filled with pus, forming the phlegmonous 
form of the disease. In other instances septic embolism occurs in the lungs, brain, 
kidneys, liver, and spleen. 

A focus of erysipelatous inflammation also results sometimes in the production 
of ulcerative endocarditis or even purulent pleuritis or pericarditis, but these complica- 
tions probably are of less common occurrence than has been thought. In 1674 
cases of erysipelas collected by Anders from the records of five large hospitals 
and from private practice, endocarditis occurred only once, and pericarditis not 
at all. Pleurisy was present in 7 cases. Roger, of Paris, did not have a single case 
either of endocarditis or pericarditis in 957 cases, and only 1 case of pleurisy. 

In 2631 cases of erysipelas croupous pneumonia is said to have occurred in 17 
cases, and the catarrhal form in 2. Of these cases 957 occurred in the practice 
of Roger, of Paris, and the remaining 1674 were collected by Anders, and represent 
chiefly the statistics of five large American hospitals. 

Prognosis. — The prognosis in a 'case of erysipelas depends largely upon the general 
state of the patient. As already stated the presence of grave visceral disease, as 
of the liver or kidneys, renders it very dangerous, but in the great majority of 
cases, when it occurs in otherwise healthy persons, the outlook is very favorable. 
Anders' statistics give the mortality at 7 per cent, for hospitals and 4 per cent, for 
private practice. When it occurs frequently or develops in different parts of the 
body consecutively, it may cause death by exhaustion, but in nearly all these cases 
there is a chronic malady as a predisposing cause. 

Treatment. — The treatment of erysipelas is local and systemic. If the bowels are 
not active they should be freely moved by a dose of 2 grains of calomel followed 
in twelve hours by a saline purge such as a Seidlitz powder or a half-ounce of Rochelle 
salts. As soon as the bowels have been evacuated thoroughly the patient should 
receive 10 minims of the tincture of the chloride of iron, well diluted with pure 
water, every three or four hours, or 30 minims four times a day. The excess of 
water protects the stomach from being disordered by the drug and also aids in 
flushing the kidneys, the activity of which prevents the accumulation of toxic 
material in the body. The diet should be as easily digested and as nutritious as 
possible, in order that the vital resistance of the patient may be maintained, and 
such foods as eggs, rare meats, broths, and milk should be freely given if the diges- 
tion of the patient is capable of dealing with them. If it is not, the food should be 



SEPTICEMIA AND PYEMIA 171 

given in small quantities every two or three hours, and if necessary it should be 
predigested by a peptonizing tablet or powder. 

The local treatment is a very important factor in these cases. For many years 
I have used with excellent results an ointment of equal parts of ichthyol and lanolin, 
or lard, smeared over the inflamed area and the adjacent skin, and kept in contact 
with the skin by also smearing this salve on a mask of gauze or lint which is applied 
to the part so that the medicinal effect is continuous. By this means the pain and 
burning is almost entirely relieved and a very definite and distinct influence for 
good is exercised both in curing the inflammation and preventing its spread. 

In cases in which the general systemic state is very much impoverished and the 
vitality of the patient is impaired, sufficient quantities of a good whiskey or brandy 
should be given to sustain the flagging powers. Moderate doses of quinine (about 
3 grains t. i. d.) may also be useful at this time to support the system, but large 
doses are useless and produce headache and a disordered digestion without causing 
any benefit. If the fever is excessive it may be controlled by the use of an ice-cap 
and cold sponging with friction. The coal-tar antipyretics should never be used, 
as they decrease vital resistance. 

Antistreptococcic serum is sometimes useful but vaccine is useless unless it be 
autogenous. 

SEPTICEMIA AND PYEMIA. 

Definition and Etiology. — Septicemia and pyemia are terms which are dependent 
upon antiquated ideas of septic processes, and do not strictly represent the states 
they are now used to describe. Septicemia originally meant that putrid material 
was in the blood, and pyemia, that the blood contained pus. We now know that 
blood infection is due to the presence in it of bacteria (bacteriemia) or to the entrance 
into this fluid of poisons made by microorganisms not in the circulation (toxemia). 
The older terms are placed at the head of this article because they are still commonly 
applied. 

Pyemia, as it is understood today, is that state in which bacteriemia is present 
with associated septic foci, or, in other words, metastatic abscesses. As a rule 
these abscesses appear chiefly in the tissues which are not far removed from the 
seat of primary infection. But this is by no means always true, for a septic process 
in the foot may cause metastatic abscesses in the lungs, kidneys, or liver. 

Cases are not rarely seen in which the patient is unable to give any history of 
even a small abscess or minute break in the skin through which germs may enter 
the circulation, and yet a diagnosis of septicemia or pyemia may be made even when 
no point of entry can be found 

The obscurity of most of these cases depends upon our inability to find the portal 
of entry, which may be the genito-urinary organs, the cranial sinuses, the 
middle ear or mastoid, the mouth or pharynx, possibly the alimentary canal, 
the biliary passages or gallbladder, an unrecognized appendicitis or other point 
of slumbering infection which may or may not be recognized during life or deter- 
mined with certainty even at a postmortem examination. 

Pathology and Morbid Anatomy. — The results of septicemia are not seen in equal 
degree in all cases. In some they may be so slight as not to be readily recognized, 
except by careful bacteriological or microscopic examination. In other instances 
the secondary results are so patent that the most careless observer cannot fail to 
be impressed by their character. Thus it not infrequently is found that septic infec- 
tion is the cause of a severe inflammatory process in any one of the serous mem- 
branes, so that pericarditis, peritonitis, meningitis, or pleuritis may occur. Septic 
inflammation of these parts results either in a distinctly fibrinous or sero-fibrinous 
exudate or in one which is purulent. The synovial membranes and other con- 
nective tissues of the joints are frequently infected, so that septic arthritis develops. 



172 DISEASES DUE TO A SPECIFIC INFECTION 

Examination of the veins may reveal thrombi near or remote from the primary 
seat of infection, and these thrombi may be soft and even purulent. It is important 
that a clear distinction be made between simple or bland thrombi and septic 
thrombi. Emboli of the former type cause infarction when they plug terminal vessels 
and mechanically disturb the circulation, whereas septic emboli not only plug the 
vessel and so disturb blood supply, but as they contain bacteria they constitute 
new foci of infection. 

Very intimately associated with the subject of septicemia and pyemia, so called, 
are the subjects of vital resistance and terminal infection. By vital resistance 
is meant that power, or property, possessed by the living body of protecting itself 
from the various micro-organisms which are continually gaining access to the sys- 
tem. This power lies largely in the ability of the blood to exercise its so-called 
bacteriolytic, or bacteria-destroying, power, and to the ability of the cells of the 
body to destroy invading micro-organisms by phagocytosis, and to manufacture 
certain other antibodies by the action of which bacterial toxins may be antagonized, 
neutralized, or rendered inert. A number of valuable papers on the presence of 
bacteria in the blood have been published within recent years (see Rosenberger 
in the American Journal of the Medical Sciences, August, 1903, for early facts and 
references) . When, because of diminution of vital resistance the invading pathogenic 
micro-organisms obtain a foothold and multiply, we have developed an infection. 
When a patient suffers from some malady which saps his vitality and so causes 
the approach of death, even in a remote degree, these micro-organisms at once 
attack his debilitated body, and the patient now suffers from what is called a 
"terminal infection." Very commonly this terminal infection is the actual cause 
of death, so that it has been well said that death is " rarely due to the primary cause 
of the illness." 

Symptoms. — The symptoms of septic infection vary greatly with the particular 
organs which may be the seat of the primary or secondary lesions. The manner of 
their onset varies likewise. In some instances the earliest manifestations consist in a 
rigor or chill, more or less severe, followed by fever which varies in its degree with 
the severity of the infection and the vitality of the patient. The chill and fever 
are followed usually by a period of normal, or nearly normal, temperature, and this 
is again followed by chill and fever. In this way the dominant symptoms of the 
case may closely resemble the quotidian malarial infection, a resemblance which is 
still further emphasized by the frequent occurrence of a distinct sweat as the fever 
falls. These sweats may be very profuse. 

Not rarely the pus in the primary focus of infection changes its character, and 
becomes less healthy looking. It is thinner and more ichorous, that is, to use a 
word now rarely heard, it is no longer "laudable pus." The infection causes 
general malaise, rapid loss of weight, and loss of appetite with gastric distress and 
perhaps vomiting. Anemia is rapidly developed, the skin of the hands and face 
becomes not only pallid but develops a peculiar cadaveric hue, an appearance 
difficult to describe, but alluded to by those of experience as the "septic facies." 
Sometimes the skin may be slightly jaundiced. 

If the septic process develops secondarily in any special organ, localized symp- 
toms may at once appear, but it is noteworthy that they do not always ensue. 
Severe pain in the chest may betoken the presence of a septic pleurisy or pneumonia, 
or if the pain develops in the left side it is often due to septic infarction of the spleen. 
A physical examination of these organs may reveal the typical signs of these 
affections. 

As the case progresses pulmonary abscess, empyema, or suppuration of the kidney 
follows as the result of emboli in these organs. The pulse becomes more and more 
rapid, the general state more and more feeble, and the patient dies from general 
asthenia or from one of the acute complications just named. 



SEPTICEMIA AND PYEMIA 173 

There are other cases in which the onset of the systemic infection is not so pro- 
nounced, the chill, fever, and sweat being absent, but in their place a rapid extension 
of the local inflammatory process with the absorption into the general system of 
the poisonous products of the germ growth as well as the organisms themselves. 
In such cases the patient may speedily become not only feeble, but suffer from 
stupor and finally die unconscious within a few days of the beginning of the illness. 
These cases are usually those which, suffering from nephritis or diabetes, offer no 
vital resistance to infection, and die not only from this cause but by reason of 
rapidly increasing evidences of the primary disease as well. 

Still a third class of cases may be called subacute or chronic, and last for weeks. 
Not rarely these cases tax the diagnostic acumen of the physician to the utmost. 
A child was brought to me in July with the statement that in the previous March 
she had acute articular rheumatism, but no cardiac complications. The fever 
of the disease in onset had lasted but a short time, and in its place only a slight 
evening rise of temperature took place. The acute swelling of the joints disap- 
peared, but they remained tender, and the child was unable to walk. There was 
marked pallor, a septic hue of the skin, and a large boil on the buttock with smaller 
ones on other parts of the body. Occasional attacks of vomiting occurred. A 
diagnosis of chronic septic infection was made, and on the child's death, six weeks 
after, evidences of the correctness of this view were found in nearly every organ of 
the body, although in none of them were distinct purulent foci discovered. Circum- 
stances prevented bacteriological examination of the blood either before or after 
death. 

Diagnosis. — The presence of chill, fever, and sweat in any case should recall 
the fact that these symptoms may be due to sepsis as well as to other forms of 
infection. It must be recalled that a history of an infected wound is not needful 
to reach the conclusion that infection has occurred, for it may take place by a 
needle-prick, or through a small blister due to a badly fitting shoe, or through a 
break in the mucous membrane of the alimentary, respiratory, or genito-urinary 
tract. Typhoid fever often fails to cause death of itself, but a terminal septic 
infection following it may cause death. In other cases a fatal general infection 
follows gonorrhea, and in tuberculosis of the lungs the septic symptoms are due 
to the pyogenic organisms which are associated with the tubercle bacillus, rather 
than to that organism itself. So, too, gallstones with septic infection of the gall- 
bladder may afford the opening for infection. Finally, whenever a patient presents 
acute arthritis the physician should think first of sepsis rather than rheumatism, 
and when he has a chill, fever, and sweat which does not promptly yield to quinine, 
he should also think of sepsis or tuberculosis. 

Treatment. — The treatment of these states consists first in seeking and removing 
the cause and in the support of the vitality of the patient by every possible means, 
such as fresh air and sunshine, and good food which is easily digested and absorbed. 
Second, many cases are undoubtedly aided in combating infection by the use of 
tonic doses (5 grains t. i. d.) of quinine, with or without whiskey. In some instances 
well-diluted whiskey certainly seems to benefit the patient, and it is surprising how 
much can be taken without producing any signs of intoxication. Great care must be 
taken that doses large enough to be toxic are not given, for if they are, the toxemia 
of alcohol aids the toxemia of the infection. Full doses of tincture of the chloride 
of iron are valuable. The coal-tar products are never to be used, as they decrease 
vital resistance, increase sweating, and do not give any comfort or relief. 

If abscesses form they should be opened and drained as early as possible. 

When bacteriological tests reveal the presence of streptococci as the cause of 
the trouble, antistreptococcus serum should be used. Usually the patient is too 
ill to admit of the use of vaccines. If a specific germ is isolated, and the patient 
is not too ill to react, an autogenous vaccine should be employed. 



174 



DISEASES DUE TO A SPECIFIC INFECTION 



ACUTE RHEUMATIC FEVER. 

Definition. — This disease, also known under the name of acute articular rheuma- 
tism, or acute inflammatory rheumatism, is an acute, infectious, non-contagious, 
febrile malady characterized chiefly by acute inflammation of the synovial mem- 
branes and adjacent tissues about the joints of the extremities and by involvement 
of the heart valves, heart muscle and its surrounding serous membranes. It is to 
be distinctly separated from the various forms of septic arthritis. In other words 
it is a general infection with especially severe lesions in the parts named. 



Fig. 42 



a 
< 

i- 
z. 

LU 

o 
oc 

LU 
Q. 


UNDER 

10 YEARS 

OF AGE 


z ° 
Lu w 

LU Q 

£ z 

I- < 

m 2 


z ° 

LU " 

LU Q 

£ z 

I- < 

lu 
m w 


LU ^ 
LU Q 

<S Z 

H < 

LU o 

DO cn 


7 ° 

LU Q 

^ z 

I- < 

LU O 
CO ^> 


z ° 

LU Q 

$ z 

H -* 
LU o 
<B 10 


o 
cc 

LU 

> 

o 


39 








































































38 








































































37 








































































36 








































































35 








































































34 








































































33 








































































32 








































































31 








































































30 






































































29 








































































2S 








































































27 








































































26 








































































25 
































L 








































24 








































































23 








































































22 








































































21 
































I 






































20 








































































19 






































































18 








































































17 








































































16 






































































15 








'/ 






























































14 






































































13 






































































12 








































































11 








































































10 








































































9 








































































8 








































































7 








































































6 






































































5 






































































4 






I 
































































■■', 








































































2 








































































1 


















































































































I 


































































" I 























Chart showing age incidence of acute articular rheumatism, based on 432S cases. 



Distribution. — Acute articular rheumatism is a disease which is found chiefly 
in the temperate zone and rarely occurs in the tropics or in the far North. At 
present we lack reliable statistics concerning its frequency because in many countries 
its occurrence is not reported, and in those in which records of the frequency of 
rheumatism are preserved, so many cases are reported which are not true acute 
articular rheumatism that the statistics are valueless. Osier states A that hejsaw 
more cases in Montreal than in Philadelphia and Baltimore while connected with 



ACUTE RHEUMATIC FEVER 175 

hospitals in those cities. I was firmly convinced from my experience in English 
hospitals that the disease was more prevalent in England than in the United States, 
but when I came to the study of the statistics of the relative frequency of acute 
rheumatism in these two countries, I found that out of 74,808 medical cases in 
hospitals in London, there were 3822 cases of acute rheumatism, a percentage of 
5.1, and out of 73,839 medical cases in hospitals in different cities in the United 
States, there were 4153 cases of acute rheumatism, a percentage of 5.6. It would 
seem, therefore, that no marked difference in frequency exists in these parts of 
the world. 

Etiology. — The influence of season upon the occurrence of the disease is marked. 
It is more common in the cool, damp months of the year than at other times. In 
London its greatest prevalence is in September and October, whereas in Montreal 
it is most frequent in March and April. 

The influence of age upon the frequency of the disease is notable. It is met 
with in a very large proportion of the cases between twenty and thirty-five years 
of age and is very rare in children below five years. Between the ages of six and 
twelve years, however, it is not only common but has its greatest direct mortality. 
Thus' in 250 cases under twelve years recorded by Poynton, Agassiz and Taylor 
there were 59 deaths. Whereas in 99 cases over twelve years there were only 2 
deaths. After forty-five years it is also rarely met with, comparatively speaking 
(Fig. 42.) It must be remembered, however, that infection with the specific organ- 
ism of this disease is more frequent in adolescents than is commonly supposed, 
and it often causes very mild arthritic symptoms and yet makes a serious attack 
upon the heart. 

Males are more frequently affected than females, but this proportion is reversed 
when the patient is under twenty years of age, at which time females suffer more 
frequently. 

The question of the influence of heredity is still undecided. It is probable that 
it plays a very unimportant part in the causation of the malady. 

Of the immediate etiological factors we must include exposure to dampness 
and cold. These influences are not provocative of the disease unless the specific 
micro-organism is present, nor unless the exposure reduces the vital resistance of 
the joints so that the specific organism is enabled to multiply and induce its patho- 
logical effects. 

Acute rheumatic fever is a disease which is endemic, but it has periods in which 
it is distinctly epidemic. In other words, it is much more frequent in some years 
than in others. 

There can be no doubt that the infection usually gains access to the general 
system through the tonsils. 

The old theory of acute rheumatism being due to uric acid is now exploded. The 
excess of uric acid present in the urine in this disease is the result, not the cause, 
of the affection. 

Bacteriology. — A very large number of investigators have endeavored to 
isolate the specific micro-organism of this disease, but until recently no satisfactory 
proof that this had been accomplished was forthcoming. About twenty years ago 
Achalme asserted that he had done this, and later Triboulet and Wassermann 
made similar claims. Up to the present time it would appear that Poynton and 
Paine have come nearer to success in this line of research than any of their predeces- 
sors, and Meyer has also carried out studies which seem to prove the correctness 
of their conclusions. Still more recently Walker and Beaton have further confirmed 
the correctness of the views of Poynton and Paine. These last investigators believe 
it is impossible to separate this special organism, for which they advise the name 
Micrococcus rheumaticus, from the ordinary streptococcus. Meyer succeeded 
in obtaining it in a form which produced all the lesions found in the course of the 



176 DISEASES DUE TO A SPECIFIC INFECTION 

disease, and found the same organism in the sore throat, in the inflamed endocar- 
dium, in the pleura, and in the inflamed joints of persons attacked by this malady. 
More recently still Poynton has further endorsed his views. 

Beattie of Edinburgh also feels confident that the Micrococcus rheumaiicus has 
a close relationship to the streptococcus and is a specific organism. 

Rosenow (1913) by means of graded oxygen pressure isolated organisms from 
the joint exudate of 14 of 16 cases of articular rheumatism, the 2 negative cases 
being convalescent. He also found organisms in the blood in 4 of 7 cases. Three 
types of organisms were found in the series. One producing long chains and another 
resembling a micrococcus, when injected into animals, produce arthritis, endocardi- 
tis, and pericarditis but never a myositis. The third, a diplococcus from a case 
with muscular involvement, produces these three lesions but especially myocarditis 
and myositis. Each of the three, by cultural methods, can be converted into 
the other types. These findings indicate that acute articular rheumatism is due 
to streptococci having peculiar properties and that muscular rheumatism is due 
to closely related streptococci. For these Rosenow says the name Streptococcus 
rheumaticus may be retained to call attention to the lesions induced, but not with 
the idea that the organisms so called always produce rheumatism. His transmuta- 
tion experiments with streptococci and pneumococci of many different strains, 
in which he has converted each to one or more other types, including streptococci 
to pneumococci and vice versa, indicate that widely different lesions as pneumonia, 
arthritis, erysipelas, scarlet fever, tonsillitis, empyema and others are due to the 
same organism varying in properties under differing circumstances. 

It is a fact worthy of note that the introduction of many pathogenic micro- 
organisms into the body will result in endocarditis and arthritis, but these states 
are not true acute articular rheumatism. 

Morbid Anatomy. — The changes produced by an attack of acute rheumatic 
fever are not pathognomonic. On the contrary, the condition of the synovial 
membranes is one of more or less intense hyperemia with the effusion of fluid into 
the surrounding tissues and into the joint itself. The synovial liquid is turbid 
and contains leukocytes and some small flakes of fibrin. The secondary changes 
produced by the disease are vegetative endocarditis, acute pleuritis, and pericarditis, 
but there is nothing about these lesions which is peculiar to this specific infection. 
A mediastinopericarditis is not rare. (See Endocarditis.) In certain cases there 
can be no doubt that myocarditis of a grave degree is often present. Sometimes 
peritonitis occurs. Thus in 100 cases of Poynton, Agassiz and Taylor it occurred 
5 times. 

Symptoms. — The symptoms of acute articular rheumatism are usually sudden 
in onset. With or without premonitory signs of illness the patient awakes to find 
that one or more of his larger joints is acutely inflamed so that any movement causes 
great pain, and the part may be so sensitive to the touch as to prevent any thorough 
examination by palpation being made. 

The skin over the affected part is usually dusky red in hue, and quite puffy in 
appearance because of the presence of subcutaneous exudation, and the inflamed 
area is much more hot to the touch than adjacent tissues. Sometimes, however, 
no local redness is seen, but in its'place swelling and a peculiar sodden and livid 
hue of the skin. With the development of this arthritis a distinct febrile movement 
begins, and the fever may reach 102° or 103° on the first day in many cases. This 
level of temperature is not usually exceeded, but the variations in its course are 
very marked in that it is subject to great remission, particularly if the sweating 
is profuse. The fever ultimately falls by lysis. 

The tongue is coated, the bowels are usually confined, and the skin is hot and 
dry, or at times bathed in a profuse sweat. This sweat breaks out in paroxysms 
and is exceedingly acid, possessing a peculiar acid odor. It is probably an effort 



ACUTE RHEUMATIC FEVER 177 

at elimination, but it does not develop in all cases. The urine is nearly always 
scanty and concentrated, highly acid, and on standing deposits urates in excess. 

Acute articular rheumatism is characterized by the speedy spread of the arthritis 
to joints in other parts of the body. In some instances the involvement of a second 
joint is followed by diminution of the inflammation in the joint first affected, but 
in many instances the patient suffers from a progressively developing arthritis 
which soon involves almost all the larger joints. This fugitive character of the 
inflammation, wandering from joint to joint, is so very characteristic, that the 
presence of a monoarticular inflammation is a point against the disease being true 
rheumatism. The smaller joints, such as the fingers and toes, usually escape, 
but they are often apparently affected by reason of the fact that the swelling of 
the tissues extends from the large joint above so that it covers the smaller ones. 
In other instances, however, the joints escape severe infection, and the synovial 
coverings of the tendons suffer chiefly, so that parts near the joint may be swollen, 
and the swelling is purely periarticular. The vertebral and clavicular joints are 
very rarely affected. 

There is no form of acute arthritis which seems to give the same amount of 
severe pain as does that of this disease, and the close of the attack usually leaves 
the general system of the patient considerably shattered because of the severity 
of his suffering, his marked anemia, and the exhaustion caused by the sweats and 
the lack of sleep. The pain is also peculiarly trying because the state of the joints 
is such that movement is impossible and the patient gets bed-sore and bed-frantic. 

In some cases a subacute type of the disease develops in which all the symptoms 
in the joints at least, are very mild, but these cases are very prone to manifest 
cardiac complications later on. This is particularly true in children. 

One attack usually predisposes to another. It certainly in no way protects 
the patient from subsequent attacks. 

Duration. — The disease may run its course in a week or be continued over a 
very long period of time, lasting a month and causing great discouragement of 
both the physician and patient. In some instances, the arthritic state merges 
by degrees into one of chronic arthritis without fever, and the patient never fully 
recovers the free use of his joints, but this is fortunately very rarely the case. Even 
when the amount of inflammatory exudate seems very large gradual and complete 
absorption usually occurs. 

Complications. — The complications of acute articular rheumatism are the means 
by which it produces fatal results, and they are most frequently found in the heart 
muscle, in the cardiac valves, or in the pericardium. Indeed, cardiac lesions are 
almost as characteristic of acute rheumatism as is arthritis. The infection attacks 
the pericardium with great constancy, and even in those cases in which the arthritic 
changes are slight, it often plays the greatest havoc in the heart, so that we fre- 
quently see young persons with grave cardiac lesions who have presented such mild 
articular symptoms that the presence of rheumatism has been overlooked. Of 
842 cases of acute articular rheumatism, all of which were first attacks, valvular 
heart lesions were present in 420, or 50 per cent. Of these lesions, 390 were mitral, 
16 aortic, and 14 mitral and aortic. The following table arranged from the statis- 
tics of Church at St. Bartholomew's Hospital illustrates not only the frequency of 
cardiac complications but also the age incidence as well: 

Number of Number in which Percentage of 
Age. cases. heart was affected, heart affection. 

Under 10 years 25 20 80.0 

10 to 20 years 244 170 69.16 

20 to 30 years 241 124 51.1 

30 to 40 years 115 35 30.0 

40 to 50 years 41 9 21.39 

Over 50 years 17 7 41.03 

683 365 53.44 

12 



178 DISEASES DUE TO A SPECIFIC INFECTION 

The above table includes pericarditis as well as valvular lesions. 

It is generally recognized as a fact, that heart lesions arise less frequently in 
the old than in the young, and therefore the percentage of 41.03 given for cases 
over fifty in this table is probably excessive. 

These lesions are rarely lethal during their acute stage. They develop into 
subacute or chronic lesions, and days, weeks, or years after the patient has recovered 
from the acute illness become active agents in destroying life or incapacitating 
him for work. The reason for this lies in a continuation of the endocarditis, in a 
subacute or chronic form, for days or weeks after the acute symptoms have passed 
by, with the result that the valves become shrunken, and so are unable to perform 
their proper functions ; or they become glued together, and in this way their action 
is interfered with. Acute articular rheumatism with cardiac complications may 
therefore cause death many months or years after the acute attack. (See Endo- 
carditis.) 

Pericarditis is by no means as frequent as endocarditis. It is usually of the 
fibrinous or serofibrinous type, and occasionally it is purulent, particularly in the 
case of children. In rarer instances a myocarditis develops. 

It is of the greatest importance that the physician in charge of a case of acute 
articular rheumatism be continually on the lookout for cardiac complications. 
He can do something toward preventing these by following the directions given 
under Treatment, and by insisting upon absolute rest. The vast majority of 
cases of acute articular rheumatism manifest sometime during their course a more 
or less well-defined mitral murmur, and sometimes a pericardial friction sound. 
In many instances, instead of these lesions increasing in severity, they disappear 
with the subsidence of the joint symptoms. 

Pulmonary complications are not exceedingly common. Stephen Mackenzie 
found that pneumonia, or pleurisy, occurred in about 10 per cent, of 3433 cases. 
Not infrequently slight pulmonary congestion of the bases occurs. 

The nervous complications in acute articular rheumatism arise from three causes: 
the high fever, the profound toxemia, and the nervous irritation and exhaustion 
produced by many hours of suffering. Delirium is not commonly met with. An 
active, noisy delirium sometimes develops as a result of the administration of large 
doses of the salicylates. Such mental disturbance is said to not infrequently 
complicate the development of rheumatic pericarditis. Sometimes, too, excessively 
high temperature is associated with delirium. 

Meningitis occurs as a very rare complication. 

The relationship between chorea and rheumatism is not clear. There can be 
no doubt that they bear some relationship one to another, but whether rheumatism 
is to be regarded as an etiological factor in chorea is undecided. 

The skin lesions of acute articular rheumatism consist chiefly in the development 
of urticaria and erythema. Purpuric rashes sometimes appear, hence the somewhat 
old-fashioned term "purpura rheumatica; ,J but it is probable that these extravasa- 
tions under the skin are due to an associated infection rather than to the rheumatism 
itself. Another very interesting lesion occurring as a sequence of acute articular 
rheumatism consists in rheumatic nodides which vary in size from a small pinhead 
to a large pea, and develop chiefly on the hands and wrists and about the elbows and 
knees, and sometimes upon the back over the spine. They often last for months, 
and are seen more frequently in children than in adults. Indeed, they are so 
characteristic in children that they may be regarded as a positive sign that rheuma- 
tism has at some time been present. They are not, however, pathognomonic 
of rheumatism in all cases, for they appear in gouty and rheumatic subjects who 
have never suffered from the acute form of the disease (see below). 

Iritis is commonly met with, and it is probable that it is due to the presence of 
the Micrococcus rheumaiicus in the fine vessels of the muscle fibres of iris. This 



ACUTE RHEUMATIC FEVER 179 

organism may also induce the muscle soreness in some cases in which the joints 
escape. 

Diagnosis. — The diagnosis of acute articular rheumatism is by no means easy 
in all cases, but the presence of fever with progressive involvement of one joint 
after another is very indicative. The great difficulty lies in separating the various 
nearly related forms of septic arthritis from true rheumatism. If there is present 
a pre-existing septic focus from which septicemia may arise, the probability is 
that the malady is not the specific disease we are discussing. Thus, a multiple 
arthritis, with or without fever, often follows or complicates gonorrhea, and follows 
scarlet fever, typhoid fever, and dysentery, or any disease which, by providing a 
source of infection, exposes the joints to the invasion of micro-organisms. 

The chief conditions, aside from gonorrheal rheumatism and ordinary septic 
arthritis, that we must carefully exclude are acute osteomyelitis, which usually 
affects the femur, and which if it is not recognized early may destroy the patient's 
life; monoarticular inflammation, which is often due to syphilis, and acute gout, 
in which case the history of previous attacks of pain in the smaller joints will be 
present and the inflamed area will probably be in the ball of the thumb or in the 
joint of the great toe. In children an acute arthritis with little fever sometimes 
develops and soon suppurates. It is undoubtedly due to septic infection. Finally, 
let it be borne in mind that the mere presence of heat, pain, swelling and fixation 
in a joint should not be called acute articular rheumatism until all other possibilities 
are excluded. Perhaps no more frequent error occurs than the calling of all forms 
of acute arthritis "acute rheumatism." 

Prognosis. — Death very rarely ensues as a result of acute articular rheumatism 
without any complications. This is well shown by the following statistics. In 
8431 cases of acute articular rheumatism collected from the official reports of 
several American and English hospitals there were 127 deaths, which gives a 
percentage of 1.5. From the years 1880 to 1903, 1524 cases w r ere treated in the 
Pennsylvania Hospital with only 14 deaths, a mortality of 0.9 per cent. While, 
therefore, acute rheumatism rarely causes death during its presence in the active 
stage it is nevertheless true that no other acute disease causes death so frequently in 
after years because of secondary changes in the heart. 

The prognosis as to the development of a valvular lesion as a result of this infec- 
tion is unfavorable. The great majority of patients develop an endocarditis 
during the attack, particularly children, and in this class the lesion is often perma- 
nent. When rheumatic subcutaneous nodules are present the heart almost always 
suffers severely, probably because they afford sources of repeated infection. About 
50 per cent, of the cases which develop endocardial signs during the attack possess 
these signs permanently. Care must be taken to separate the soft murmurs due 
to myocardial disease from those due to valvular disease. A decision that the 
lesion is going to be permanent cannot be fairly reached until several months 
have elapsed after the acute illness. Taking a prolonged rest of weeks or months 
after the attack aids materially in making a favorable prognosis. 

Treatment. — The treatment of acute articular rheumatism is at times eminently 
satisfactory and at others equally disappointing. In a certain proportion of 
cases, in which treatment fails to produce good results, the condition is perhaps 
maintained by the presence of associated infections which help to produce the 
arthritis. While no true specific exists for acute articular rheumatism, the salicy- 
lates act in some cases with a degree of celerity which is most gratifying, and therefore 
they are always to be considered as the most important remedies when the physician 
is called upon to treat a case of this disease. The chief objects of the physician 
under these circumstances are the alleviation, modification, and shortening of the 
disease, and, second, the protection of the heart from the secondary affections of 
its endocardium, its muscle, and its pericardium. For the relief of the pain and 



180 DISEASES DUE TO A SPECIFIC INFECTION 

of the inflammatory processes in the joints the best remedy is the salicylate of 
strontium in the dose of 15 to 20 grains from three to six times a day. It should 
be given in capsules and followed by a copious draught of water or milk to prevent 
it from irritating the stomach. Sometimes a few swallows of the emulsion of sweet 
almonds may be taken to protect the stomach from irritation. 

If full doses of the salicylates, sufficient to produce distinct physiological symp- 
toms, such as fulness in the head and some deafness, do not produce signs of improve- 
ment in the course of five or six days, they will probably fail to cure, and had better 
be discontinued, as after this time they are apt to increase the discomfort of the 
patient, to disorder his stomach, and to increase the sweats. In their place the 
patient may receive 10 minims of the wine of colchicum root and 15 grains of iodide 
of potassium three times a day. While the salicylates are being given it is always 
advisable to give not less than 40 to 60 grains of sodium bicarbonate or bicarbonate 
of potassium in each twenty-four hours. The sodium bicarbonate seems to aid 
the stomach in withstanding the salicylates, and provides the body with a certain 
amount of alkali which is advantageous. 

Recently a preparation called "rheumatism phylacogen," which is practically a 
filtrate from a multiple culture of infectious organisms, containing an excess of 
the Micrococcus rheumaticus , has been introduced as a valuable remedy. It has 
been theoretically condemned. I have seen it produce excellent results when 
the salicylates have failed. 

Copious draughts of water are always to be given in rheumatism for the 
purpose of flushing the kidneys. 

For the prevention of endocarditis and pericarditis from four to six small fly- 
blisters may be placed over the precordium, and their influence as preventive 
measures is thought to be aided by the free use of the sodium bicarbonate just 
named. If pericarditis develops and the action of the heart is very excessive, 
small doses of aconite may be cautiously given to act as a cardiac sedative. But 
this drug is not to be used if the patient is markedly depressed. Sometimes an 
ice-bag placed over the heart acts equally well. 

The joints are best treated by anointing them with ichthyol and lanolin in equal 
parts, applying an excess of this ointment, and then wrapping them in cotton- 
batting. When the patient suffers pain because of the twitchings of his muscles, 
which in turn move his inflamed joints, some relief and comfort can be given by 
applying a splint to produce fixation of the joint. 

The acute inflammatory process in the joint is usually severe enough to make 
the patient content to remain in bed. But it not infrequently happens that as the 
pain in the joint diminishes the patient is most anxious to get about and return 
to his usual pursuits. Nothing can be more dangerous than the pursuance of such 
a policy. A very large proportion of cases of valvular heart disease are due to 
the fact that the patient has suffered from rheumatism, and has returned to his 
occupation before the endocarditis produced by the rheumatic poison has entirely 
disappeared. For a time he may be able to perform his customary duties, but the 
increased labor thrown upon his heart by exercise causes a delay in the healing of 
the lesions in his endocardium, and as a result he suffers from a degree of mitral 
stenosis or mitral regurgitation, or both, which sooner or later will make him a 
cardiac invalid. Even if these symptoms are not manifested for some time after 
the attack of rheumatism has been present, they may nevertheless become danger- 
ously active when with advancing years cardiac compensation is lost. The physician 
should therefore impress upon every patient, with acute articular rheumatism, who 
insists upon rising as soon as he feels well, the fact that he is taking his life in his 
hands by so doing. Even after all articular symptoms are passed by, the patient 
should remain in his bed for at least two or three weeks, and this advice holds good 
even if during the attack no signs of an endocardial murmur have been manifest. 



CHOLERA 181 



CHOLERA. 



Definition. — The word cholera when strictly applied is used to designate a disease 
which is characterized by profuse serous purging, cramps, vomiting, and extreme 
prostration, and which is due to an infection of the bowels by the specific micro- 
organism of this disease, called the Spirillum choleras asiaticoe, which, as it is often 
broken into short, curved rods, is frequently incorrectly termed the "comma 
bacillus." When it is desired to indicate that the true disease is present the term 
"Asiatic cholera" is used to distinguish the malady from other forms of serous 
diarrhea of a severe type, such as cholera morbus or cholera infantum. 

History. — Prior to 1817 cholera was confined to certain parts of India and never 
infected districts far removed from them. It is probable that the disease has 
occurred for many centuries, but it is a noteworthy fact that, unlike most epidemic 
diseases of pronounced characteristics and high mortality, no clear description of 
its presence was placed on record. Since 1817, when an epidemic of unusual 
severity broke out in India, it has been known to be constantly present in endemic 
form in some parts of that country, and it has from time to time been carried thence 
along well-travelled routes by pilgrims and travellers, or by their possessions, 
until many parts of the earth, removed thousands of miles from the original focus, 
have suffered from it. Seven distinct invasions of Europe have occurred since 
1817, and the last one from 1891 to 1895. The disease was first introduced into 
America by emigrants who landed in Quebec and New York early in the decade 
of 1830 to 1840. 

Distribution. — The geographical area of origin has already been described. The 
disease may occur in any part of the world to which the specific germ may be con- 
veyed. 

Etiology. — The cause of epidemic cholera is the spirillum which was first isolated 
by Koch. It is spiral-shaped or assumes the form of segments of a spiral, or short 
curved rods and S forms. 

The degree of curve varies greatly; sometimes the organism is almost straight, 
at other times it forms a partial circle. Bizarre forms also occur. It is active, 
motile, and flagellate. The bodies described by Hueppe as spores have not been 
so considered by other observers. 

Cholera is distinctly a water-borne disease in the vast majority of epidemics. 
The specific organism gains access to the body through contaminated drinking 
water or soiled food. In the Hamburg cholera epidemic of 1892, about 18,000 
persons were stricken, and of this number 8000 died. In the city of Altona, which 
is really a part of Hamburg, and which also derives its drinking water from the 
Elbe, there were only about 500 cases of cholera in a population of 150,000. Ham- 
burg had no filtration plant at the time, while Altona had a sand filtration plant. 
It is only by water and food that cholera can be transmitted, except that if choleraic 
stools are desiccated, and the dust is blown on food or into the mouth, it is conceiv- 
able that the infection may occur. Aside from the rarity with which this accident 
takes place, the fact that the bacillus speedily dies, when dried, militates against 
it being active under those circumstances. A more possible and indeed probable 
method by which the infecting agent may reach the food is its carriage by flies, 
for in the body of the common house-fly the specific organism may exist for twelve 
days. 

Hot weather favors the spread of the disease. As in all infectious maladies, 
all causes which decrease vital resistance, such as alcoholism, exposure, convales- 
cence from other diseases, and even profound mental depression, distinctly increase 
the susceptibility of the patient. 

Prevention. — It is evident from what has been said that there is no reason why 
cholera cannot be prevented, and it may be said of deaths from cholera, as it is 



182 DISEASES DUE TO A SPECIFIC INFECTION 

said of deaths from typhoid fever, that every one is preventable if proper care is 
taken to destroy all the specific organisms the moment they escape from the body 
of a patient suffering from the malady. That they are not destroyed in cholera 
is all the more to be condemned by reason of the fact that they escape only in the 
stools, whereas in typhoid fever the specific bacillus escapes by the feces, urine, 
the skin, and perhaps the saliva. The cholera spirillum is exceedingly susceptible 
to bactericides and particularly to acids, under favorable circumstances succumbing" 
to such weak acids as vinegar. 

All dejecta from cholera patients should be destroyed by heat or by the action 
of chlorinated lime, or formaldehyde, or of corrosive sublimate, contact with a 
solution of which should be complete and prolonged for at least one hour, for in the 
latter instance the mercury salt may combine with the albumin, or be decomposed 
by the gases in the stools. 

During the presence of an epidemic no food should be taken in the raw state, 
and it should be cooked immediately before it is eaten, in order that there may 
be no time for it to become infected after it is cooked. With these precautions 
the danger to physicians and nurses is reduced to a minimum. When there is a 
possibility of negligence, a valuable prophylactic is the use of dilute sulphuric 
acid in the dose of 5 to 10 drops in water three times a day after food. This does 
good, by reason of the fact that dilute acids kill the cholera spirillum, and again 
because this acid acts as an astringent remedy in diarrhea. Care should be taken 
during an epidemic that bad food and exposure are avoided, as this may prepare 
the way for infection. 

Through the researches of Haffkine in India, Kolle, and Strong in the Philippines, 
it would seem that it is possible to immunize human beings against cholera, but 
this plan of inoculation is of no value when the disease has once developed. 

During the years 1894 and 1895 Haffkine inoculated 3951 individuals with his 
anticholera vaccine. Of this number, 33, or a little less than 1 per cent., contracted 
the disease, whereas, of 9335 individuals who were uninoculated and similarly 
exposed to the infection, 210, or 2.24 per cent., were stricken. These observations 
were made in India. 

In July, 1902, an epidemic of cholera broke out in the prefecture of Nagasaki, 
Japan, and preventive inoculations were at once begun. Of 21,334 persons who 
were inoculated, 110 contracted the disease. In previous epidemics the number 
of persons affected ran well up into the thousands, but it is but fair to state that 
in this epidemic only 741 cases occurred in that prefecture among the uninoculated. 
As the number of uninoculated inhabitants is not stated, we cannot judge of the 
real value of the plan. 

Haffkine's conclusions as to the result of anticholera inoculations are as follows: 

1 . The inoculation produces an effect within four days. 

2. During these four days a difference in susceptibility shows itself in favor 
of the inoculated. 

3. After the expiration of the four days and during a period of at least fourteen 
months, a high degree of resistance to attack is observed in the inoculated. 

4. The proportion of deaths to cases is not influenced by the inoculation. 

The objection to Haffkine's prophylactic is the severe reaction it causes. 
Strong's prophylactic lacks this effect, but has not been sufficiently tested as yet. 

Pathology and Morbid Anatomy. — After death from cholera postmortem rigidity 
comes on very rapidly, and is persistent to such a degree that distortions of the 
limbs and body may be present. In typical cases the entire body appears shrunken 
and wasted and the dependent portions rapidly become livid. Not rarely a post- 
mortem rise of temperature takes place. 

When the body is incised the tissues are found to be devoid of their normal 
moisture, and the blood in the great vessels is thick and dark in hue. The stomach 



CHOLERA 183 

is empty, its mucous membrane is congested, and, in some instances, ecchymoses 
may be present. 

The chief changes are to be found, however, in the lower part of the small bowel. 
Its mucous membrane is boggy or sodden, and covered by a glutinous material 
which is readily detached. Not rarely the mucous membrane is stripped off in 
patches or shed in flakes. These changes may extend as high as the duodenum, 
and in the lower ileum Peyer's patches and the solitary glands are found to be 
swollen and congested. There may be present a diphtheroid exudate, which is 
adherent in part, and in part is fleecy or flocculent in appearance. Deeper ulcera- 
tions and perforations are exceptional. Hemorrhages may also be found in the 
mucous membrane at this place. 

Notwithstanding the active purgation, the large bowel in cholera is not as much 
altered as is the ileum, the only change, as a rule, being an acute catarrh of the 
mucous membrane. 

It is important to the student to recall the fact that cholera is characterized 
by changes in the small bowel, whereas dysentery is chiefly characterized by changes 
in the colon. 

The intestines are contracted, their coats thickened, and the peritoneum possesses 
a peculiar rosy hue. The mesenteric glands are enlarged and infiltrated. 

Granular changes in the large glandular viscera are present in a certain percentage 
of cases, and a complicating nephritis is occasionally seen. The kidneys may be 
enlarged and the vessels congested. Under the microscope the uriniferous tubules 
are seen to be filled with granular casts, but the tufts are not materially changed. 
The great loss of fluid by the serous discharges and the lessened absorption of 
liquids causes concentration of the blood and greatly interferes with the excretion 
of poisons by the kidneys. 

The liver is not enlarged but rather shrunken, and its cells show, under the 
microscope, cloudy swelling, with patches of fatty degeneration. The spleen is 
usually small. The heart is flaccid and the lungs shrunken. 

The cholera organism is found in immense numbers in the contents of the bowels 
and in the discharges of patients suffering from this disease, but, unlike the typhoid 
bacillus, it is not usually widely disseminated through the body (Figs. 43 and 44). 

Symptoms. — The symptoms of cholera develop in from a few hours to ten days 
after infection has occurred. The average period of incubation is usually three to 
six days. 

The earliest symptom, aside from a feeling of depression, is the onset of watery 
diarrhea, which may be associated with pain. The patient suffers from the tveakness 
and depression characteristic of ordinary watery diarrhea, and if the passages are 
very profuse there may be great feebleness and even collapse. In the majority of 
cases, however, the onset of the disease is more abrupt than that just described. 
With almost no indication of impending illness the patient is seized by active vomiting 
and purging, by severe cramps in the extremities and trunk, and passes into collapse. 
The stools, as soon as all the ordinary intestinal contents have been washed out, 
are rice-water in character, that is, on standing they separate into two layers, the 
upper clear and opalescent, the lower full of flakes of mucus and exfoliated necrotic 
mucosa. 

The amount of serum lost by the purging is very large, and it is expelled with 
considerable force. Because of the large quantities of fluid lost by this means 
the urine becomes scanty and suppressed. This loss of fluid, combined with the 
changes in the kidneys, results in uremia, which, of course, aids greatly in increasing 
the toxemia of the disease. The vomiting is not only violent, but persistent retching 
may greatly exhaust the patient. The cramps in the muscles are due to the rapid 
abstraction of fluid from their tissues and perhaps, in part, to the toxemia of the 
disease. 



184 DISEASES DUE TO A SPECIFIC INFECTION 

In about half the cases recovery begins to take place at this stage by a gradual 
modification of the symptoms, but if the patient is too ill to recover, the second 
stage, or that of collapse and profound asthenia, now develops. This stage may 
last from a few hours to two days. As it proceeds the patient becomes so feeble 

Fig. 43 






* :.t 






4 fife. «* ® *&& 






e 






Cholera spirilla in the fundus of a gland of Lieberkuhn in the small bowel, in a case of 
Asiatic cholera. (Kast and Rumpler.) 

that the respirations become shallow. The fluid stools pass from the bowel invol- 
untarily, escaping rather by relaxation of the sphincter than by the conscious 
act of the patient. Feeble attempts at emesis may still persist, and the cramps 
may be more severe than before. 

Fig. 44 




Cholera spirilla in the intestinal contents. (Kast and Rumpler.) 

As the exhaustion deepens the pulse becomes a mere thread at the wrist, and 
may even be imperceptible in the great vessels. The heart sounds become more 
and more indistinct, and occasionally soft murmurs are heard. 

The face bears the Hippbcratic expression, the ?wse is pinched and pointed, the 



CHOLERA 185 

eyes sunken and surrounded by dark rings, the mouth is partly open, the teeth 
covered with sordes, the skin of the entire body is livid and often bedewed with a 
cold sweat. The voice is whispering, the thirst excessive, and the mind clouded. 
Toward the close of life stupor or coma mercifully relieves suffering. Finally, 
with a continued fall of bodily temperature, death takes place. 

When the stage of reaction develops, before these grave symptoms threaten 
death, the pulse becomes a little stronger, the passages are less frequent and less 
copious, and the respirations grow deeper. Bodily heat is gradually restored, 
and the patient recovers, unless some of the complications mentioned farther on 
ensue. 

Variations from the Ordinary Course. — The patient may have so mild an infection 
as to be but slightly ill and never forced to go to bed. In other instances the 
serous diarrhea is excessive, but the urine is not suppressed, and the general debility 
does not become marked. These cases are sometimes called cases of "cholerine." 
They may speedily recover or rapidly proceed to the fully developed malady. 
In still another class the toxemia of the disease exceeds all other symptoms. The 
diarrhea may be absent, and the patient, overwhelmed by the poison, sinks into 
unconsciousness and death. This is called "cholera sicca." 

The degree of stupor varies greatly. In some patients the mind, at the well- 
developed stage of the disease, is remarkably clear; in other instances it is, almost 
from the first, stupid from toxemia. 

In some instances high fever develops. This is a very unfavorable sign. In 
others an urticaria or erythema is seen. 

Complications and Sequelae. — Aside from the grave complications of urinary 
suppression followed by uremia, the profound infection may result in localized 
gangrene of the toes and fingers. Edema of the lungs often causes death, and infec- 
tious arthritis and parotitis may develop. Profound weakness and feebleness may 
persist for a long time in convalescence, and secondary nephritis may ultimately 
cause death. 

Diagnosis. — The diagnosis of cholera is not difficult if the well-developed type 
of the disease is present, but in the early stages, or in the aberrant forms just 
described, the determination of the cause of the illness may not be easy. True 
cholera is to be separated from cholera nostras or cholera morbus, but in the presence 
of an epidemic of Asiatic cholera this may be impossible without bacteriological 
tests, for severe cholera morbus may not only be manifested by purging and vomit- 
ing, but by collapse as well, and even cramps may appear in the more severe types. 
Cholera must also be separated during an epidemic from the profuse watery purging 
sometimes met with in cases of Bright' s disease, when the purging is due to an 
effort at elimination. Various poisons may also cause choleraic diarrhea, notably 
antimony. Indeed, it is impossible to separate acute antimonial poisoning from 
cholera during an epidemic of the latter disease, because the symptoms are identical. 
Nothing but a chemical analysis, on the one hand, or a bacteriological test, on the 
other, can determine this question. 

It is important to remember that while the presence of the spirillum of cholera 
is characteristic of cholera, that inability to discover it in the discharges is not 
positive proof that cholera is not present, because in rare instances it may be 
temporarily undemonstrable. A very valuable method of diagnosis is the test 
of agglutination of cholera bacilli by the blood of the patient in a manner similar 
to that of the Widal test in typhoid fever. 

Prognosis. — The prognosis in cholera, whenever the symptoms are well developed 
is always grave, for the mortality in most epidemics is about 50 per cent. In the 
old and very young the outlook is worse than in a well-developed person in the 
prime of life. 

There are three facts aside from the severity of the disease which increase the 



186 DISEASES DUE TO A SPECIFIC INFECTION 

gravity of the prognosis very materially, namely, alcoholism, renal disease, and 
disease of the liver. In addition, it must be remembered that any pre-existing 
disease which decreases vital resistance increases the gravity of the case. 

In respect to the disease itself, it may be said that abruptness of onset, early 
hebetude, and rapid development of signs of collapse are the three facts that promise 
evil tendencies. If to these is added renal inactivity, pulmonary edema, or 
an abnormally low temperature, the case is to be regarded as almost hopeless. 
Contrariwise, there are several signs of good omen, namely, the presence of a good 
pulse and the maintenance of bodily heat, the return of a fecal color to the stools 
and the absence of the great emaciation and wasting which severe cases usually 
manifest. 

Treatment. — The three most important details in the treatment of cholera are 
the control of the diarrhea, the maintenance of strength, and the conservation 
of body heat. All persons who have any tendency to diarrhea, during a cholera 
epidemic should at once be treated by astringent mixtures, which should be increased 
in their efficiency by the addition of a few drops of sulphuric acid. By this method 
of treatment the development of cholera can be probably prevented in a considerable 
number of persons. The use of an astringent and acid substance like sulphuric 
acid is far more advantageous than the employment of opium, because the acid 
is destructive to the micro-organism, and it does not interfere with other functions 
of the body as does opium. If the diarrhea is already active 10 to 15 drops of 
aromatic sulphuric acid, with double that quantity of spirit of camphor, should be 
administered, well diluted with water or with brandy, every three hours, and 
counter-irritation in the form of a mustard plaster, or sinapisms, or capsicum drafts 
should be applied over the abdomen. If these cannot be obtained a turpentine 
stupe may be used with advantage. 

It seems scarcely necessary to add that even in mild cases the patient should be 
kept in bed and the greatest possible amount of rest enforced. If vomiting is 
an active symptom it may be necessary to avoid all medication by the mouth and 
give stimulants hypodermically. Under these circumstances 2 grains of camphor 
dissolved in sterilized olive oil may be given by means of the hypodermic needle 
every eight hours. Such a method of treatment will usually do much toward the 
maintenance of active circulation, but should the circulation fail the physician 
must employ not only the camphor injections named, but give atropine and strych- 
nine hypodermically, and more important still, for the purpose of compensating 
for the loss of much fluid by the bowel, hypodermoclysis should be resorted to. 
It is best to employ "concentrated sterile saline/' one ounce of which when added 
to a quart of pure water makes normal salt solution. But if this cannot be obtained 
ordinary common salt in the proportion of a drachm to the pint may be injected 
by hypodermoclysis. This fluid should of course be first sterilized by boiling, 
and the injection should be made slowly, the fluid being at the temperature of 100°. 
It is quite remarkable how rapidly the thirsty tissues will absorb this fluid, which 
not only compensates for the loss by purging, but also aids in overcoming suppres- 
sion of urine by supplying the bloodvessels with fluid. There can be no doubt 
that hypodermoclysis is a most valuable life-saving measure in the treatment of 
this disease. 

Rogers has shown that in the stage of collapse there is a loss of one-half to two- 
thirds of the blood serum and of the chlorides as well. To avert this loss intraven- 
ous injections of hypertonic salt solution, Locke's modification of Ringer's formula, 
should be resorted to. (This is on the drug market of the world under the name 
Concentrated Sterile Saline, P. W. & Co.) If this formula cannot be quickly 
obtained use two drachms of sterile sodium chloride to the pint of freshly distilled ' 
water. This fluid should be injected whenever the blood pressure is as low as NO 
mm. of Ilg. in Europeans or when the specific gravity of the blood is above 1056. 



YELLOW FEVER 187 

The specific gravity can be obtained by mixing glycerine and water in different 
proportions so that small bottles contain solutions varying in specific gravity from 
1050 to 1070. A drop of blood from a capillary tube is dropped in each bottle. 
If it sinks in one bottle and floats in another it is evident that its specific gravity 
is greater than the first and less than the other. Thus if it sinks in the mixture 
at 1056 it has a specific gravity in excess of normal; then intravenous injections 
should be given. 

To destroy the toxin in the intestine Rogers gives a solution of calcium perman- 
ganate, which is somewhat less astringent than the potassium salt and at the same 
time stronger, as it is divalent. This drug is given to drink ad. lib. in a solution 
of 6 grains or more to the pint. It is usually advisable to dilute it further at first 
until the patient gets accustomed to the taste, and then gradually increase its 
strength as much as possible. In addition, the potassium salt is given in pills, 
being more conveniently used in this form, as it is much less hygroscopic than the 
calcium permanganate: 

Potassium permanganate 2 grains. 

Kaolin q. s. 

Make a pill and coat with salol or keratin, so that it will pass through the stomach 
and dissolve in the small intestine, where the action is desired. Two pills are 
given every quarter of an hour for the first three hours, and then two every half 
hour until the stools become green and less copious, which usually occurs within 
about twelve hours. The pills are then discontinued, but a course of eight pills 
is given at the beginning of the second and third days under treatment, to prevent 
relapses. In children smaller amounts must be given. Any pills which are vomited 
are replaced by others. 

If the temperature at the stage of reaction rises above 103.5 or 104° active anti- 
pyresis by cold bathing or cold rectal injections is to be resorted to. To combat the 
collapse, hypodermoclysis is used and camphor, pituitrin, adrenalin, digitalis, stro- 
phanthus or caffeine given to stimulate the circulation. 

To aid in the restoration of renal activity a hot compress may be placed under 
the loins. 

As a rapidly acting diffusible stimulant in conditions of marked collapse Hoff- 
mann's anodyne in the dose of a drachm every hour may be given hypodermically 
or by the mouth with shaved ice. A drachm of spirit of camphor may also be used 
with advantage for this purpose. Aromatic spirit of ammonia may also be given 
by the mouth, but is not so valuable. 

YELLOW FEVER. 

Definition. — Yellow fever is an acute infectious disease occurring chiefly in 
tropical or semi-tropical regions, and characterized by fever, yellow discoloration 
of the skin, black vomit in some cases, and a tendency to oozing hemorrhages 
from the mucous membranes. The early development of albuminuria is also a 
noteworthy symptom. 

History, Etiology, and Prevention. — The earliest history of yellow fever records 
its occurrence among the followers of Columbus, and before that time it never 
attacked Europeans. It is, therefore, a disease indigenous to the Western Hemi- 
sphere. As early as 1648 the inhabitants of St. Kitts, and in 1655 those of Jamaica, 
were attacked by it. 

Since then yellow fever has devastated North and South America many times. 
It has extended its ravages all the way from Quebec to Montevideo, and on the 
western coast of the Western Hemisphere has been almost equally widely distrib- 
uted. In the latter part of the eighteenth century it destroyed 10 per cent, of 



188 DISEASES DUE TO A SPECIFIC INFECTION 

the population of Philadelphia. On more than one occasion it has brought military 
expeditions to defeat by the frightful mortality which it has caused among the 
troops. During the French expedition to Hayti, in 1802, 22,000 out of 25,000 men 
died from it in one season, and the various attempts which were made by Spain 
to subjugate Cuba were practically frustrated by the mortality from yellow fever 
among the Spanish troops. Davidson states that out of a population of 9000 
persons at Gilbraltar in 1800 only 28 escaped infection. In 1878 the financial 
loss in the Mississippi Valley produced by a single epidemic amounted to over 
$15,000,000. Out of a population of 19,500 in Memphis there were 17,600 cases 
and 6000 deaths. 

For one hundred and fifty years Havana was recognized as the focus in which 
yellow fever was practically constantly present, and from this focus many portions 
of the civilized world were again and again infected. It was not until the United 
States Army took possession of Havana and its medical officers instituted sani- 
tary measures that any real attempt was made to discover the means of propaga- 
tion of yellow fever or to limit its development in that city. When the brave, 
skilful, and scientific labors of these officers were completed one of the most bril- 
liant medical discoveries in the history of the world was announced. 

Under proper sanitary directions the death rate in "Havana fell from 91 and a 
fraction, under Spanish rule in 1898, to 33 and a fraction in 1899 under American 
rule, to 24 § in 1900, and to 22 and a fraction in 1901, but there was not a simul- 
taneous diminution in the frequency or mortality of yellow fever. Indeed, at that 
period there was an actual increase in the disease notwithstanding the fact that 
all other maladies were decreasing. It was under these circumstances that a 
commission was appointed by the Surgeon-General of the United States Army 
for the purpose of studying yellow fever. The chairman of the commission was 
the late Dr. Walter Reed, a major in the United States Army, and associated with 
him were acting assistant surgeons James Carroll, Jesse W. Lazear, and Aristides 
Agramonte. 

The medical profession should never cease to do honor to the members of this 
commission, who faced one of the most horrible and fatal diseases with the 
greatest bravery, and thereby have succeeded in saving the lives of hundreds of 
thousands of individuals. Dr. Lazear, who was one of the most enthusiastic 
members of the commission, allowed himself to be bitten by an infected mosquito. 
He was not infected by this bite, but several days after he was accidentally bitten, 
and lost his life from the consequent attack of yeltow fever. Another member, 
Dr. Carroll, allowed himself to be bitten, was also attacked by the disease, and 
narrowly escaped death. 

The fact that Ross and others had proved that the transmission of malarial 
fever was by the moquito, and that Dr. Carlos Finlay, a physician of Havana, a 
graduate of the Jefferson Medical College, of Philadelphia, had asserted as long- 
ago as 1881 that a certain species of mosquito in Havana was guilty of trans- 
mitting yellow fever from person to person, led the Army Board to direct their 
attention to the investigation of this question, and they soon found that if & female 
mosquito of the species Stegowiyia calopus were allowed to bite a yellow fever 
patient during the first three days of the disease, and then, from twelve to twenty 
days later, permitted to bite a non-immune, the latter almost invariably developed 
yellow fever. I repeat : If the mosquito bites a non-immune earlier than the twelfth 
day after biting a patient suffering with the disease it is not transmitted. The 
male insect does not bite. The female bites most viciously about dusk and about 
dawn. This insect is found everywhere around the globe between 38 degrees 
north and 38 degrees south latitude. 

That the disease is never carried by fomites was also proved by these investi- 
gators, who had a number of young non-immunes* sleep for twenty consecutive 



YELLOW FEVER 189 

nights in a room which was hung with articles soiled by black vomit, bloody fecal 
discharges, and urine, from fatal and other cases of yellow fever. These persons 
also packed and unpacked these articles night and morning from boxes in which 
they were placed. Other non-immunes actually slept in garments and between 
sheets that had covered fatal cases of yellow fever, but in not a single instance 
was the disease contracted, although as soon as these non-immunes were exposed 
to mosquitoes several of them developed yellow fever. 

The practical result of proving that the mosquito is the cause of the transmission 
of the infection has been the complete clearance of Havana of yellow fever. All 
cases of yellow fever were protected by mosquito netting so that mosquitoes could 
not carry infection from them to others. All pools and gutters containing water 
upon which mosquitoes could breed were removed, and the destruction of mos- 
quitoes was carried on actively, with the result that it was possible in a year to 
diminish the number of deposits of mosquito larvae in the city of Havana from 
26,000 to 300. As a result, the death rate from malaria fell from 344 in 1900 to 
151 in 1901, and up to July, 1902, it was only 47; while the diminution in the 
number of mosquitoes caused so great a decline in the prevalence of yellow fever 
that by September 28, 1901, new cases ceased to occur in Havana. After that 
time, according to Dr. Gorgas, of the United States Army, from whose reports 
much of this information is taken, not a single case originated in that city 
until the latter part of 1905, when relaxed vigilance allowed the disease again to 
reappear. 

The conclusions of the commission are so important that they are given ver- 
batim : 

1. The mosquito — Stegomyia fasciata calopus — serves as the intermediate host 
for the parasite of yellow fever. 

2. Yellow fever is transmitted to the non-immune individual by means of the 
bite of the mosquito that has previously fed on the blood of those sick with this 
disease. 

3. An interval of about twelve days or more after contamination appears to be 
necessary before the mosquito is capable of conveying the infection. 

4. The bite of the mosquito at an earlier period after contamination does not 
appear to confer any immunity against a subsequent attack. 

5. Yellow fever can also be experimentally produced by the subcutaneous in- 
jection of blood taken from the general circulation during the first and second 
days of this disease. 

6. An attack of yellow fever, produced by the bite of the. mosquito confers 
immunity against a subsequent attack of the non-experimental form of this disease. 

7. The period of incubation in thirteen cases of experimental yellow fever has 
varied from forty-one hours to five days and seventeen hours. 

8. Yellow fever is not conveyed by fomites, and hence disinfection of clothing, 
bedding, or merchandise, supposedly contaminated by contact with those sick 
with this disease, is unnecessary. 

9. A house may be said to be infected with yellow fever only when there are 
present within its walls contaminated mosquitoes capable of conveying the para- 
site of this disease. 

10. The spread of yellow fever can be most effectually controlled by measures 
directed to the destruction of mosquitoes, and the protection of the sick against 
the bites of these insects. 

11. While the mode of propagation of yellow fever has now been definitely 
determined, the specific cause of this disease remains to be discovered. It has 
later been shown that the organism causing this disease is ultramicroscopic in size 
and it passes through the pores of a Pasteur-Chamberland B. filter. 

Attention has already been called to the fact that the infectious agent of 



190 DISEASES DUE TO A SPECIFIC INFECTION 

yellow fever is conveyed by mosquitoes from patient to patient. It is there- 
fore essential that all cases of yellow fever should be kept under mosquito netting 
so that they may not be bitten by mosquitoes, and it is also wise for those 
who are well to protect themselves at night from mosquitoes by similar means. 
For screening those who are ill, a gauze of not less than twenty meshes to the inch 
should be used, otherwise the mosquito may pass through it. An active crusade 
against all mosquitoes and the destruction of their breeding-places should also be 
instituted, and it is important to bear in mind that these breeding places are not 
sunlit streams but shaded cisterns, old bottles, vases in cemeteries and rain gut- 
ters that do not drain themselves thoroughly. Swampy places should be drained 
and all high grass cut down. Stickle-back minnows placed in pools feed on the 
larvae and crude petroleum may be distributed over the surface of the pool for 
their destruction. 

Pathology and Morbid Anatomy. — One of the most marked changes produced 
in the body by the infection of yellow fever is that which takes place in the blood, a 
decided anemia developing. Many of the red cells are crenated and some of the 
white cells are granular. Free hemoglobin, hemin, and hematin are found in it 
owing to the destruction of the red corpuscles. 

The heart is soft and flabby, and minute ecchymoses in its muscular tissue may 
be present. The pericardium may contain an excess of blood-stained fluid, and 
its membrane may be dotted with petechias. 

The stomach shows changes with great constancy. It usually contains black 
fluid due to altered exuded blood; its mucous lining is congested in patches and 
is marked by ecchymosis or even softened. When placed under the microscope, 
sections of the stomach show the bloodvessels engorged and their walls under- 
going fatty degeneration. The intestinal canal also contains broken-down blood 
passed from the stomach, and its contents may be acid. Fatty degeneration of 
Peyer's patches and the glands of Lieberkuhn is present. 

The liver is often pallid or yellow in hue, and its cells also may undergo fatty 
change. Councilman states that associated with these signs of fatty degeneration 
areas of necrosis can be demonstrated in every case that comes to autopsy. 

As in many acute and severe infections, the kidneys show signs of acute diffuse 
nephritis with fatty degeneration of the cells lining the tubules. 

Small hemorrhagic spots are sometimes found in the meninges of the brain 
and cord, and fatty degeneration of the cells of the solar plexus has been described. 

Symptoms. — A very noteworthy fact in connection with the symptomatology 
of yellow fever is that in a majority of cases its onset is most abrupt. There may 
be, for a few hours before the well-defined symptoms show themselves, a sense of 
malaise and headache or vertigo. The first symptom of prominence is the appear- 
ance of a rigor, or rigors, which may be moderate or severe, but Bemiss states 
that chills are rare. In addition the patient suffers from severe lumbar and mus- 
cular pains, headache and eyeache, and marked pallor. There is often epigastric 
distress. In children the disease may be ushered in by cojivulsions. 

After the stage of onset the skin of the face becomes flushed and turgid; the 
mind may wander, but as the disease develops it is usually remarkably clear and 
alert, so that the patient watches those about him with the same degree of atten- 
tion as is often seen in acute peritonitis. The expression is anxious. The tem- 
perature rapidly rises so that it reaches its acme of from 103° to 107° by the end 
of twenty-four or thirty-six hours. 

If the case is a very mild one the febrile movement may cease as early as the 
end of the first day or on the morning of the second day, but usually the acme 
of the temperature is maintained for from two to three days, during which time 
there may be slight morning and evening variations. In cases which are moder- 
ately severe the fever usually begins to fall after this time and reaches a point 



YELLOW FEVER 191 

near the normal in from twenty-four to seventy- two hours. That is, the fall is 
by lysis. 

After the temperature has reached normal, that is when the stage of remission 
about to be described has become well marked, a secondary fever develops which, 
like that of the stage of onset, lasts from two to three days and falls by lysis. In 
cases which are likely to be fatal this fall may not occur. 

The respiration and pulse rate are at first increased in frequency and the indi- 
vidual pulse beat is increased in volume, but these circulatory conditions speedily 
undergo a marked change with the approach of the period of remission. On the 
second or third day, even if the temperature remains as high as before, the pulse 
rate begins to fall, or falls even while the temperature is still rising, so that a pulse 
rate which early in the onset was as high as 110 may now be as low as 75. 

After the fever begins to fall owing to the beginning of convalescence the pulse, 
as in many cases of ordinary catarrhal jaundice, may fall still farther till it reaches 
45 a minute. It is the slowing of the pulse in the stage of onset, while the tem- 
perature is still high, that is particularly worthy of note. 

The tongue is covered with a white fur save at its edges, which are red; the 
bowels are constipated, and there may be epigastric distress followed by the vomiting 
of acid mucus. 

The urine is scanty and it may be distinctly albuminous as early as the third 
day. This early albuminuria is considered by yellow-fever experts to be a very 
important aid to diagnosis. 

Hemorrhages usually do not develop before the third day and begin as a bleed- 
ing of the gums and epistaxis. Menorrhagia may develop. Hematemesis is seen 
as a rule only in severe cases. 

By the third day a very marked remission in the symptoms may occur. The 
pains and aches, the rapid pulse, the high temperature, and the flushing of the 
face all become modified. The gastric symptoms abate, but the conjunctivae may 
begin to be jaundiced and the skin of the body may also begin to show a yellow hue. 
This is the critical period of the disease, for the patient is now "at the parting of 
the ways." One path leads to rapid recovery with marked amelioration of all 
the symptoms; the other leads, after a remission of from twelve to forty-eight 
hours, to a recurrence of all the dangerous symptoms in an aggravated form. 

If the way is evil there is precordial and epigastric distress, persistent vomiting 
of clear liquid with flakes of brown, reddish-looking material, which speedily in- 
creases in amount until the well-known black vomit presents itself. The urine is 
more scanty and more albuminous than ever, and the general state of the patient 
is that of profound illness. The temperature in some cases rises as it did in the 
stage of onset, but it may, and this sign is of grave import, fall below normal. 
Even yet it is possible for recovery to occur by a gradual amelioration of all the 
symptoms, but usually the symptoms continually get worse. The grave depres- 
sion increases, the yellow skin develops a greater degree of yellowness, and petechia? 
are formed. The vomiting of black material is more severe and profuse, and 
hemorrhages may occur from other mucous membranes than that of the stomach. 
The scene closes with hiccough, profound asthenia, subsultus tendinum, the Hip- 
pocratic face, and in exhaustion and coma, due in part to the direct effect of the 
infection and in part to the uremia produced by the intense renal lesions. 

While these may be considered the symptoms of yellow fever in many cases, 
in others they are very different. In the so-called apoplectiform type the patient 
is seized with vertigo, stupor, unconsciousness, and convulsive attacks. He speedily 
becomes more and more deeply depressed, his circulation fails, the bowels and 
bladder are involuntarily emptied, and with the development of multiple hemor- 
rhagic extravasations he dies. 

In another severe type the symptoms are algid, the patient speedily passing 



192 DISEASES DUE TO A SPECIFIC INFECTION 

into profound collapse with a subnormal temperature and profuse hemorrhages, 
death coming on in a few hours. In still another type the violent vomiting, purg- 
ing, and collapse may cause the case to resemble one of cholera. 

Diagnosis. — It is stated by all physicians of experience that in some cases it is 
almost impossible to make a diagnosis of yellow fever in its early stages, chiefly 
because it has few pathognomonic signs, and these are of value only when asso- 
ciated and not when they appear singly. Again, many cases of yellow fever pursue 
a very aberrant course, so that several days elapse before the diagnosis can be 
made. 

Yellow fever must be separated from dengue, pernicious malarial fever, from 
malarial hemoglobinuric fever, and from relapsing fever. The differentiation of 
yellow fever from dengue has given rise to much bitter controversy, and even at 
the present time physicians of wide experience with both maladies are by no 
means agreed about the separation of these diseases in their early stages. 

Guiteras asserts that there are three notable symptoms of yellow fever which are 
of service in this connection. First, the facial expression of the yellow-fever patient 
is characteristic because in no other disease is it so flushed, the eyes so injected, 
nor the conjunctiva so icteroid after a few hours of illness. Second, the develop- 
ment of albuminuria as early as from the first to the third day, which may be 
transient and slight, or persistent and profuse. The third differential point is the 
change in the pulse already noted as occurring on the second or third day of the 
disease, during the continuance of fever. 

The jaundice of dengue rarely appears as early as the third day. 

The history of the patient as to exposure, the presence of the estivo-autumnal 
parasite in the blood, and the enlarged spleen of malarial infection point to per- 
nicious malarial fever. A porter-colored urine, the blood infection, and the en- 
larged liver point to hemoglobinuric fever, while the discovery of the spirillum of 
Obermeier in the blood will demonstrate the presence of relapsing fever. (See 
Relapsing Fever.) While all these facts may aid greatly in distinguishing yellow 
fever, it is not to be forgotten that the absence of some of them does not prove 
that the yellow fever is not present. Thus in some cases the albuminuria does not 
appear very early, in others the failure to discover the estivo-autumnal parasite 
may be due to the lack of skill of the observer or to the well-known difficulty of 
its discovery even by the most practised observers. Again, it is possible for the 
malarial parasite to be present when yellow fever is present, the two diseases exist- 
ing simultaneously. 

Prognosis and Mortality. — In a disease which is so variable in its manifestations, 
prognosis must always be guarded. If the febrile, gastric, and renal symptoms 
are mild in the stage of onset, the outlook is more favorable than if they are severe. 
If the period of remission is not well marked and hemorrhagic tendencies are well 
developed, the prognosis is bad. The great majority of cases terminate by the 
ninth day but death rarely occurs before the third day. 

The mortality varies very greatly in different epidemics, as already shown in 
the discussion of the history of the disease. Sometimes it is as low as 15 per cent., 
again as high as 85 per cent. It is apt to be lower in private than in hospital prac- 
tice. Some authors have made the interesting statement that the mortality is 
in inverse ratio to the morbidity. The average mortality may be stated at about 
30 per cent. Thus, in 25,220 cases of yellow fever occurring in the West Indies, 
Central and South America, Mexico, and the United States, 8020 cases were 
fatal, a percentage of 31.8. 

Treatment. — In the treatment of yellow fever it is essential that the patient 
shall have a plentiful supply of fresh air and sunshine, with absolute rest and 
proper sanitary surroundings. Bad hygienic surroundings always greatly increase 
the mortality of the disease. 



YELLOW FEVER 193 

As soon as the patient is suspected to be suffering from yellow fever, he should 
be put to bed and required to remain there until convalescence has been com- 
pleted, for physical and mental unrest distinctly predispose the patient to a fatal 
issue. During the whole period of the disease the patient should not be allowed to 
sit up in bed, since sudden cardiac failure may occur. All the food and medica- 
tion should be given to the patient when in the recumbent position, and the con- 
tents of the bowels and bladder emptied into a bed-pan. The patient should be 
lightly covered, and the use of heavy blankets or quilts should be discouraged. 

Cleanliness of the mouth should be carefully maintained, since otherwise soft- 
ening and ulceration of the gums not infrequently occur. 

Active medication for the treatment of the disease itself is unwise. The physi- 
cian should give remedies only when they are very distinctly indicated, as for the 
relief of a failing heart, with the hope of increasing the activity of the kidneys, 
and for the prevention of profound asthenia. In some portions of the world where 
yellow fever frequently occurs, it is customary to employ hot mustard foot-baths 
and even hot packs during the early stages of the disease, but they are unwise 
after the malady is once well developed. For the relief of the fever cool sponging 
with alcohol and water, or even with ice-water, may be employed, an ice-bag 
being applied to the head. The employment of the coal-tar products is never 
advisable, and they are particularly contra-indicated when the depression is 
marked. Many practitioners have employed emetics in the early stages of yellow 
fever, but these are certainly not required unless it is known that the patient's 
stomach is overloaded with food, when 10 to 20 grains of ipecac may be given. 

Many years ago former Surgeon-General Sternberg advised the employment 
of bicarbonate of soda, corrosive sublimate, and water in the treatment of yellow 
fever, but, although this method of treatment has been widely employed, it has 
now largely gone out of use, although large quantities of bicarbonate of soda are 
given freely by many practitioners as a matter of routine. 

As in most infectious diseases, the bowels, if constipated, should be moved 
by means of calomel, which in turn may be followed by one of the saline purges 
or by castor oil. Purgation may be resorted to every twenty-four or forty-eight 
hours, in order to keep the bowels thoroughly evacuated. To aid the purgatives 
and for the purpose of washing toxic materials from the large intestines, copious 
irrigations of the colon with normal salt solution are advisable. The patient 
should be urged to drink freely of water in order to flush the kidneys, and alkaline 
mineral waters, such as Vichy, Apollinaris, or Seltzer, or plain water, to which 
bicarbonate of soda has been added in small quantities, may be used with advan- 
tage to neutralize the acidity of the gastric contents and to act as diuretics. 

For the arrest of excessive vomiting, cocaine has been highly recommended, 
but there is no reason to believe that it exercises any better anti-emetic prop- 
erties in this disease than in other diseases in which vomiting is present. One or 
2 minims of creosote or carbolic acid are equally valuable. 

For the purpose of stimulating the heart and circulatory system, digitalis in 
the dose of 5 minims of the tincture, or strychnine in the dose of ■£$■ of a grain, or 
caffeine in the dose of 1 or 2 grains, may be given three or four times a day, and 
if collapse is threatened the strychnine may be given hypodermically with atropine, 
or Hoffmann's anodyne may be given by the mouth or by the hypodermic needle. 
Strong black coffee may also be employed by the mouth or by the rectum, for the 
purpose of rallying the patient. 

For persistent hiccough, sipping very hot water is often advantageous. 

From the beginning to the end of the attack it is the duty of the physician to 

carefully watch the condition of the kidneys by making daily examinations of 

the urine, since uremia is one of the greatest dangers which can beset the patient. 

After the kidneys have once become so inactive that the urine is exceedingly 

13 



194 DISEASES DUE TO A SPECIFIC INFECTION ' 

scanty it is often absolutely impossible to stimulate them to activity, whereas 
much can be done, if from the very first, renal activity is maintained. For this' 
purpose calomel may be given as a diuretic in the dose of 2 or 3 grains every few 
hours for one or two days at a time, or one of the diuretic potassium salts, such 
as the citrate or acetate, in large amounts of water. Hypodermoclysis with nor- 
mal salt solution may be employed. Renal congestion may be overcome by the 
application of mustard plasters and dry cups over the kidneys. 

During the acute stage of the illness the condition of the stomach is such that 
the administration of food is almost impossible, but milk diluted one-half with 
Vichy water or with water containing bicarbonate of sodium may be given. 

During convalescence the greatest possible care must be exercised that the 
patient does not take food in too large quantities. No solid food should be per- 
mitted before the end of a week, and, if the patient has been very will, not for two 
weeks. In the meantime the diet should consist of partially peptonized milk, 
milk-toast, broths, and eggs. 

As in all exhausting diseases, the physician must insist upon the patient remain- 
ing in bed until the heart muscle has entirely recovered from the profound depres- 
sion of the disease. Bitter tonics, such as iron, quinine, and strychnine, may be 
given. 

PLAGUE (BUBONIC PLAGUE). 

Definition. — Plague is an acute, specific, infectious, and contagious disease 
caused by the Bacillus pestis. It occurs in widespread epidemics, is character- 
ized by fever, inflammation of various glandular groups, and profound depression. 
The course of the disease is exceedingly rapid and the mortality extremely high. 

History and Distribution. — In ancient times plague occured in pandemics, spread- 
ing over the whole known world. Most of the old world epidemics about the 
beginning of the Christian era have been described as plague on wholly insufficient 
evidence. Hirsch dates the first recognizable epidemic in the second century, B.C. 
Following this, historical descriptions do not satisfactorily identify the disease 
until the pandemic which persisted for nearly sixty years, during which time it 
ravaged the whole of Europe (a.d. 542). Following this epidemic, known in his- 
tory as the plague of Justinian, the disease appeared from time to time, but only 
twice to so great a degree. The first of these two extensions was during the four- 
teenth century, during which it is estimated that 25,000,000 persons died in all 
Europe and England, and Wales lost 2,500,000 or half its population; the second 
pandemic, known as the Great Plague of London, began in 1664 and lasted until 
1679. During the first year of this epidemic one-sixth of the total population of 
London perished. The advance of sanitary science since that time has gradually 
forced plague out of Europe and limited the area of its extension. During the last 
three decades it has lingered in Southeastern Europe. 

We are now in the presence of what must be considered a world-wide extension 
of the disease, limited only by effective preventive measures. The present epi- 
demic began in Hong Kong in 1894. In 1896 it reached the Presidency of Bombay, 
and since that time it has spread through nine British provinces and fifty-one 
native States, the cases increasing in spite of all restrictive efforts. It is estimated 
that to the middle of the year 1903 two million persons perished in the Deccan. 
In the city of Bombay over one hundred thousand persons died, and in the 
Presidency of Bombay alone during January, 1903, the deaths averaged eighty 
thousand weekly. Later, the disease appeared in Japan, Madagascar, and South 
Africa. It has obtained a temporary foothold in Glasgow, Lisbon, and Oporto. 
In 1900 it reached Sydney, Australia. On the American continent it appeared 
in Brazil and the Argentine Republic. In 1889 it established a foothold in San 
Francisco, in which city rigorous measures have limited it to a very great degree. 



PLAGUE 195 

During the year 1902 the disease appeared in Peru, Mexico, and Alaska. In 1904, 
1,141,300 persons died of plague in British India notwithstanding active efforts 
on the part of the government to arrest the disease, and the deaths from this 
disease in India in the five years and four months, ending April 30, 1907, reached 
over 4,500,000 or almost the total population of Greater New York and Philadel- 
phia combined. 

Etiology. — Plague is caused by Bacillus pestis, a specific micro-organism dis- 
covered by Kitasato and Yersin in 1894, during the epidemic in Hong Kong. 
This organism is a short, oval, non-motile, coccobacillus resembling the bacillus 
of chicken cholera. It occurs singly, joined in pairs, and occasionally in long 
chains. It is found in large numbers in the pus of plague buboes and in smaller 
numbers in the viscera and blood. It has been cultivated from all the accessible 
tissues of the body during life, and from all the excretions except the sweat. It 
has also been recovered from the floors and soil in the houses of patients sick with 
plague. 

The bacillus stains with all the ordinary staining reagents and is decolorized 
by Gram's method. It takes up the stain much more strongly at its poles. Some- 
times a capsule is observed, but there is no spore formation. It grows best at the 
body temperature and on all the ordinary media. In fluid culture media, overlaid 
with a film of bland cocoanut oil, the bacillus grows in the form of long stalactites 
hanging from this oily layer, that are considered characteristic of this organism. 
Its viability is rather low. If kept moist and cool, it may keep alive and virulent 
for months, but if dried at the room or body temperature it dies in from three to 
four days. Exposure to direct sunlight destroys it in a few hours. The bacillus 
is pathogenic for nearly all domestic animals. Indeed, most of them are subject 
to plague and aid in its dissemination. Sheep, calves, pigs, ducks, and fowls 
readily contract the disease, and the bacilli may be recovered from their viscera 
and excretions. The disease also occurs in bats, and the common rat is peculiarly 
susceptible to it. The great mortality among rats, preceding and often signalizing 
an epidemic of plague, is an observation that was well known to the ancients. 

The Chinese long ago recognized the association between the death of the rats 
in a house and the development of plague a few days later. Finally, the fleas 
that infest rats and the flies in infected houses also serve to carry the contagion. 

The method of conveyance to man has been established with a fair degree of 
certainty. Inoculation experiments in man and animals have shown that when 
virulent bacilli are introduced into the tissues plague develops. Thus at Cairo in 
1835 plague blood was used to inoculate two criminals, but though they developed 
the disease both recovered. The list, too, of physicians and laboratory workers, 
who have contracted the disease from accidental inoculation and dissection wounds, 
is a large one. Among them may be mentioned Whyte, who, in 1802, infected 
himself and perished, and Aoyama and his assistants who contracted plague from 
dissection wounds. 

In 1898 three deaths occurred in Vienna as a result of laboratory inoculations, 
one in 1899 in Lisbon, and one in 1902 in Berlin, while 13 cases resulting from 
accidental inoculations in postmortem examinations have been collected in India. 

In rare cases man is infected by the inhalation of the germ. That infection 
takes place through air and food has not been substantiated. The disease enters 
through the skin, by direct infection through slight wounds or abrasions, or through 
the bite of suctorial insects. It has been shown that rats suffer more intensely, 
perhaps, than any other animal from plague. The rats are infested with fleas, 
which are also infected, and the disease is transmitted from rat to rat and finally 
from rat to man by the bite of these insects. Wherry, of the U. S. Public Health 
and Marine Hospital Service, has also shown that plague affects ground squirrels 
and that the disease may be transferred by the fleas which infest them. As fleas 



196 DISEASES DUE TO A SPECIFIC INFECTION 

may be transferred from place to place in litters, baggage, or clothing, they may 
readily spread the disease. The supposition that rat fleas attack man when there 
is a great mortality among their chief hosts is well borne out by the occurrence of 
human plague following closely upon epidemics among rats. 

Fox believes the actual transmission of the bacilli by the flea is by means of 
its infected feces. These are deposited on the skin at the time of biting and are 
carried into the wound by the mandible of the insect or by later scratching of 
the site by the host. 

The possibility of infection taking place directly into wounds and abrasions from 
infected soil must be admitted. Calvert reports an interesting case where the 
disease was acquired in sexual intercourse, and one case where the bite of an in- 
fected rat caused a fatal infection. Direct transmission from patient to patient, 
while always possible, occurs very rarely. This is borne out by the observations 
in Bombay, Hong Kong, and other places, that cases are extremely rare among the 
physicians, nurses, quarantine guards, and disinfection laborers, who are con- 
stantly in intimate contact with plague cases. 

The disease principally attacks the poorer classes of the native population, 
those who live in the slums under poor hygienic surroundings. Lack of personal 
cleanliness and deficient light and ventilation in living rooms are predisposing causes. 

Frequency. — Plague affects all ages and both sexes equally. Neither geographical 
location, character of soil, nor elevation have any influence on its spread. It pre- 
vails at all seasons of the year, although, generally speaking it is least active in 
the seasons of greatest heat or cold. 

Epidemics begin slowly. The common history is that in the beginning a few 
isolated cases develop, the epidemic slumbering along in this way for a year or 
more before rapid extension takes place. It declines in the same way. Not only 
do the number of cases grow less, but their virulence notably diminishes. It creeps 
slowly from town to town, following the routes of travel. Its extension from one 
country to another over sea is due to the presence of infected rats on the ships ply- 
ing between them. Thus the epidemic in Peru was shown to have spread from the 
rats on a ship carrying grain from India. 

Prophylaxis. — Personal prophylaxis should be directed in the first place to avoid- 
ing too close contact with plague cases, although direct infection is very rare. 
Wounds, abrasions, and skin eruptions on the limbs should be carefully guarded, 
particularly against a germ-carrying finger-nail and fleas, and it is well to put 
kerosene upon the feet and legs to drive away fleas. Tight leggings or gaiters 
should be worn to prevent the bite of fleas. Attendants should wear a mask to 
prevent pneumonic plague. These measures combined with personal cleanliness, 
a good water supply, and abundant ventilation are efficient. 

The general measures to be taken for the prevention of plague are, inoculation, 
evacuation of infected houses, and the extermination of fleas, rats and mice by 
trapping and poisoning. 

The danger from contact is not very great. Exposed persons should be disin- 
fected, given a prophylactic inoculation, have their clothing destroyed, and then 
be released. The quarters in which a plague patient has lain should be thoroughly 
scraped, disinfected, and repainted or whitewashed. Better still, when practical, 
they should be burned. The evacuations and bedding of the sick should be cre- 
mated. 

In spite of the most stringent prophvlactic measures, plague is very difficult 
to control. As a matter of fact, where it has once attained even a slight foot- 
hold it has not been successfully eradicated by any of these measures. Witness 
the cases in San Francisco, where after several years of effort the disease still 
persisted. It sees likely that the most we can expect with our present means is to 
hold the disease in check. 



PLAGUE 197 

Pkotective Inoculation. — Haffkine introduced a prophylactic inoculation 
against plague. His method has been modified by Lustig and recently by Bes- 
redky. Briefly, these methods consist in injection of plague cultures killed by 
heat. Extensive experience has shown that these inoculations confer an immu- 
nity against plague, beginning in twenty-four hours and lasting from three to four 
months, and, according to Simpson, three or four years. Simpson has shown by 
statistics based upon nearly one and a half million persons inoculated that the 
mortality ranges from to 57 per cent. Whereas among about four million not 
inoculated the mortality varied from 2 to 100 per cent. Recent studies seem to 
show that, given during the period of incubation, they have the power to abort 
the disease in many cases. This system of protective inoculation was being tried 
on an extensive scale in the Punjab, when a very deplorable accident cut the 
experiment short. After more than 100,000 persons had been inoculated without 
untoward results, nineteen men received their injection from the same package, 
developed tetanus on the fifth day, and all died. This unfortunate affair practic- 
ally stopped prophylactic work in India, by greatly increasing the aversion the 
natives had always shown to it. 

Pathological Anatomy. — The visceral lesions of plague are constant and uni- 
form. Punctate hemorrhages appear not only on the skin, but throughout the 
whole gastro-intestinal tract. They are found on the peritoneum, pleura, and 
pericardium, as well as in the capsules of the spleen, kidney, and liver. The cerebro- 
spinal system is congested and there is an increase of its fluid. The liver and 
kidneys are hyperemic and the spleen very much enlarged. In pneumonic cases 
the bronchi are injected and swollen and there are small areas of consolidation 
scattered throughout the lung. This pleural cavities frequently contain moderate 
quantities of seropus. 

The glandular system shows constant involvement. In the bubonic form the 
glands appear on section as large, diffused masses, with extensive hemorrhages 
into their substance. This appearance is not confined to one group of glands, 
but extends along the lymphatic trunk and invades the glands in the immediate 
proximity to the main buboes. 

Microscopically, intense hyperemia with hyperplasia is found not only in the 
glandular but also in the periglandular structure. Before the glands break down 
the bacillus pestis is found alone; after suppuration is established other organisms 
are found with it. 

In the septicemic and pneumonic cases, or in those cases dying before marked 
bubo formation has taken place, the gross changes in the lymphatic system are 
not so apparent, but there is always enlargement of one or more groups of glands 
or slight tumefaction and congestion of the entire lymphatic system. The patho- 
logical process is identical in all the types, only that in the bubonic form the inten- 
sity of the affection is expended on one gland or group of glands, while in the other 
form the adenitis and lymphangitis are diffuse. 

Symptoms. — Clinically, plague may be divided into four varieties: 

1. Bubonic plague, pestis bubonica, malignant adenitis. 

2. Septicemic plague, pestis siderans. 

3. Pneumonic plague. 

4. Larval plague, pestis minor, pestis ambulans. 

Bubonic Plague. — This is by far the commonest type, averaging 80 per cent, 
of all cases. The incubation period varies from two to eight days, averaging four 
days. 

The attack begins with fever, lassitude, severe headache, and pain in the limbs. 
Rigors may or may not be present, but vomiting is usual in this stage. There 
is drowsiness, vertigo, and extreme anxiety. After lasting from twelve to twenty-four 
hours, fever begins and the temperature rises rather quickly to 103° to 107°. There 



198 DISEASES DUE TO A SPECIFIC INFECTION 

is now hurried pulse and respiration. The face is heavy, swollen, and flushed; 
the tongue is coated with a heavy black fur; the teeth are covered with sordes. 
Vomiting is often persistent and diarrhea may develop. The patient is most 
profoundly depressed, the depression being out of all proportion to the duration 
of the disease, and a low muttering delirium is present. Death may occur in 
this stage, accompanied by convulsions and collapse or by uremic coma with total 
suppression of urine. 

In from twenty-four to seventy hours — that is, from the third to the fifth day 
of the disease — the characteristic glandular swellings develop. The glands involved 
are in the groin in 60 per cent, of the cases, the axilla in 35 per cent., and the neck 
and angle of the jaw in 5 per cent. The buboes are usually single and are much 
more common on the right side than on the left. Occasionally they are bilateral, 
rarely multiple. In size they vary from a pigeon's egg to the size of a fist. They 
are frequently painful and always exquisitely tender. 

Coincident with the development of the buboes, small areas of gangrene of the 
skin, carbuncles, or generalized pustular skin lesions may develop. 

The buboes increase in size for three or four days and then become stationary. 
In a small proportion of cases gradual resolution takes place. In the larger 
proportion softening and suppuration occur and the bubo is opened or ruptured 
and discharges a foul-smelling pus. At this stage free suppuration is usually 
a good omen. If the pus continues scanty and sanious the disease remains 
virulent. 

In free suppuration the bacilli disappear from the pus in a very few days and 
convalescence is rapidly established. In the cases that terminate favorably a 
marked amelioration is observed with the development of the glandular swelling, 
and usually about the seventh day the temperature falls and the profound depres- 
sion disappears. 

Septicemic Plague. — In this form the symptoms are much more severe and 
the stage of bubo formation is lacking. That is, there is no one gland or group 
of glands conspicuously involved, but the whole glandular system is engorged and 
swollen. The essential difference seems to lie in that the infection is more severe 
both quantitatively and qualitatively. There is a marked bacteriemia. Clinically, 
these cases differ from the former in the more profound depression, more moderate 
fever (100° to 102°), and the greater tendency to hemorrhages. 

Pneumonic Plague. — This form begins suddenly with rigors and all the symp- 
toms of acute pulmonary inflammation. Respiration is rapid and labored and there 
is a painful harrassing cough. So far the symptoms resemble an ordinary lobar 
pneumonia. The sputum, instead of being scanty, tenacious, and of the usual 
prune-juice color, is copious, watery, and spotted and streaked with bright blood. 
Physical examination shows areas of consolidation scattered throughout the lungs. 
An entire lobe is rarely involved. This form of the disease is the most fatal of 
all, patients rarely surviving after the third day. In these cases, too, although it 
is not clinically apparent, postmortem examinations show general involvement 
of the glandular system. Pneumonic plague is more common in children than in 
adults, and at the beginning of epidemics than at the end. 

Hemorrhages occur in all the various clinical types of plague, more commonly 
perhaps in the septicemic. They appear in the skin as petechia? and ecchymoses. 
There may be epistaxis, hematuria, and hemorrhage from the stomach or bowel. 
Hemoptysis is a very sinister symptom. 

The urine is diminished and commonly contains large quantities of albumin 
with more or less kidney structure. Albuminuria is never absent in severe or fatal 
cases. 

The blood changes are not characteristic. There is a marked leukocytosis, vary- 
ing from 20,000 to 50,000, with moderate reduction of the hemoglobin. 



PLAGUE 199 

Relapses occur in a small percentage of cases and are always grave. Convales- 
cence may be very much prolonged by indolent ulcers and burrowing sinuses at 
the seat of the buboes. 

Larval Plague, Pestis Minor. — Cases of this type occur in all epidemics 
and are very common toward their close. In larval plague the typical buboes 
develop with few prodromata. The constitutional reaction may be very mild, 
the fever is slight, and the patient is but little annoyed by the disease. Some 
epidemics are characterized by large proportions of such cases. 

Diagnosis. — In the presence of plague in epidemic form, the rapid onset of the 
disease, the profound depression, the glandular swelling can hardly suggest any- 
thing else than this disease. The identification of the Bacillus pestis in the blood, 
in fluid from the buboes, or in the sputum assures the diagnosis. Inoculations 
and culture experiments are important in the early stages of an epidemic with 
large numbers of atypical cases of plague. The best routine method of diagnosis 
is the microscopic examination of a drop or two of the fluid obtained from the 
buboes by means of a hypodermic syringe. The few drops of bloody lymph col- 
lected in this manner contain large numbers of bacilli. The diagnosis of the pneu- 
monic form can be made only by demonstrating the micro-organism in the sputum. 

Prognosis. — Varying in different epidemics, the average mortality runs from 70 
per cent, to 95 per cent. The variations depend on the stage of the epidemic, 
the proportion of pestis minor cases, and the race and hygienic conditions of the 
patients. In the Hong Kong epidemic the average mortality was 93 per cent, 
among the Chinese, 88 per cent, among the Indians, 60 per cent, among the Jap- 
anese, and 18 per cent, among the Europeans. This gradation, as Manson has 
remarked, is "in general correspondence with the social and hygienic conditions 
of these different nationalities." 

The influence of the type of the disease on mortality is shown in the following 
figures from an analysis of 13,145 cases. In the bubonic cases the mortality was 
77.25 per cent., in the pneumonic cases 96.69 per cent., and in the septicemic 
cases 89.62 per cent. 

The number of the buboes and their location has no bearing on the mortality. 
Visceral hemorrhages are always unfavorable symptoms, while free suppuration 
of the buboes must be considered as a very favorable omen. 

Pregnancy complicating plague is also very unfavorable. Abortion invariably 
occurs and death is almost certain. 

Treatment. — Treatment of plague is wholly symptomatic. For the fever, 
headache, and delirium nothing is so effective as cold sponging. Cantlie recom- 
mends initial purging with calomel in large doses, followed by salines. This 
remedy frequently checks vomiting and permits nourishment to be taken. 

For the pain and restlessness there is no remedy so effective as morphine, given 
hypodermically, in small doses. In the profound depression and collapse, diffusible 
stimulants are indicated; ammonia to the nose, mustard to the skin, and ether or 
camphor subcutaneously. Alcohol should be given freely, particularly in a septi- 
cemic form. 

Suppuration of the buboes should be hastened by poultices and hot fomen- 
tations. When fluctuation occurs they should be opened freely and dressed 
antiseptically. 

Thomson reports excellent results in the epidemic in Hong Kong from the 
internal use of carbolic acid in large doses. He gave 144 grains daily in doses of 
12 grains every two hours in a mixture of syrup of orange and chloroform-water. 
One patient took over 2500 grains of pure carbolic acid before his blood was free 
from plague bacilli. Beyond a few cases of carboluria no toxic symptoms devel- 
oped. He considers this the most hopeful method at our disposal. 

Yeserin, Calmette, and Borrell have developed an antitoxic serum by the 



200 DISEASES DUE TO A SPECIFIC INFECTION 

injection of ascending doses of cultures killed by heat into susceptible animals. 
Experimentally, plague in animals has been arrested by this means. Clinically 
the results with the antitoxic sera have been most contradictory. While they have 
not entirely fulfilled the hope that they first seemed to hold out, later experience 
in this direction is more encouraging. The antitoxin needs further study, and 
particularly needs standardization. 

CLIMATIC BUBO. 

Definition. — Climatic bubo, tropical bubo, tropical adenitis (non- venereal), is a 
subacute inflammation of the lymphatic glands of the groin, attended by a fever 
remitting in type and persisting from three to four weeks. The disease is widely 
distributed in tropical climates. It occurs on the coast of Africa and Asia, and 
is common enpugh in the Philippines, Japan, Malaya, the West Indies, and the 
Mediterranean. 

The disease commonly affects individuals living together under the same 
hygienic conditions, as sailors and soldiers, and occurs in small epidemic out- 
breaks. There is some evidence to show that its origin is due to the entrance of 
bacterial infection, either through minute wounds in the legs and genitals or the 
bites of insects. It has been described as due to tropical heat and to paludism, 
as a sequel to dysentery, and even as a form of bubonic plague (pestis minor). 
Bacterial evidence disposes of the last theory, but in the presence of epidemic 
plague these cases demand careful study. 

Symptoms. — They begin with moderate swelling, redness, and tenderness of the 
inguinal or crural glands of one or both sides. At the outset there is usually a 
chill, fever of a remitting type, headache, and backache. The buboes slowly increase 
until they attain the average size of a hen's egg, after which the fever gradually 
diminishes. After persisting from one to two months or longer they gradually 
disappear. In the large majority of cases the inflammation is limited to the gland 
structure proper. The periglandular tissues and skin are not involved and there 
is very little pain or tenderness. In from 3 per cent, to 5 per cent, of all cases the 
inflammation spreads to the periglandular tissues. The skin becomes adherent 
over the glands and they finally suppurate. In these cases the constitutional 
symptoms are intensified and the pain and tenderness are very great. The 
abscesses tend to burrow freely. After a period of free suppuration deep, sharp- 
edged, indolent, painful ulcers remain. The average duration of the suppurating 
cases is from two to three months. 

Treatment. — The febrile condition is not severe enough to demand special treat- 
ment. Iodine and ichthyol may be applied to the skin over the gland, and, after 
acute symptoms subside, mercurial ointment and elastic pressure should be used. 
When suppuration takes place the gland must be laid open. Rife advises calomel 
as a dusting-powder to control the severe pain in the chronic ulcers. 

DYSENTERY. 

Definition. — Dysentery is a condition characterized by diarrhea, abdominal 
pain, and the presence, as a rule, of considerable quatities of mucus in the stools. 
When the condition becomes chronic it is often interrupted by periods in which 
constipation supplants the diarrhea. Dysentery is to be separated from the 
diarrhea due to indigestion and to catarrh of the small bowel by the facts that 
tenesmus is usually marked, the lesions are chiefly in the large bowel, and the 
stools may be, in the early part of the attack, rather scanty and consist of mucus 
and blood. 



DYSENTERY 201 

It is, moreover, to be distinctly understood that dysentery is not a single disease, 
but that this term is applied to the conditions and symptoms which develop as the 
result of several distinct causes, although at present there is much confusion as 
to the causes of the various forms. Strictly speaking, amebic dysentery should be 
classed among the diseases due to animal parasites, but it is best, from the clinical 
stand-point, to discuss it here. 

At the present time at least ^.ve well-defined types of dysentery are recog- 
nized, namely, that which is known as bacillary dysentery, which is due to infection 
with the specific bacillus of Shiga, or a bacillus nearly related to it. Second, ent- 
amebic dysentery, intestinal amebiasis (Musgrove and Clegg), which is due to the 
entamebic dy sentence. This form is found in all parts of the world, but is much 
more frequent in the tropics, whence most of the cases seen in this country 
come. Strong, of the United States army, reports 561 cases of entamebic dysen- 
tery out of 1328 cases of dysentery in his service. A third form is that due to the 
Balantidium coli and is also tropical in origin. Fourth, catarrhal dysentery, which 
is apparently not due to a definite infection, but to acute congestion of the 
mucous membrane of the colon, and finally, fifth, diphtheritic dysentery, which is 
not due to the Klebs-Loeffler bacillus, but is characterized by a yellowish exudate 
on the mucous folds of the bowel with areas of ulceration and necrosis. A form 
of catarrhal dysentery sometimes also develops as the result of renal disease. 

Bacillary Dysentery.— Epidemics of bacillary dysentery have occurred since 
the earliest times, and Herodotus mentions one which attacked the army of Xerxes 
in the year 480 B.C. During the first part of the Christian era the disease raged in 
France, Germany, and England. It has existed in Europe in pandemic form on at 
least two occasions, namely, in the years 1538 and 1779. 

In the year 1729 an epidemic, in which 5000 persons died, occurred in Holland, 
Friesland, Guilders, and Liege. More than 2000 of Napoleon's soldiers died from 
it during the expedition to Egypt, and 4000 cases occurred in the English army 
during the Crimean war. About one-fourth (288,000) of all cases of sickness among 
the soldiers of the War of the Rebellion were said to be cases of dysentery. In the 
year 1890 an epidemic broke out in the province of Tuhuoka, Japan. This province 
had a population of 1,231,387, of which 25,272 were attacked. Of these 25,272 
cases 4742 proved fatal. Smaller but equally fatal epidemics of the disease have 
repeatedly occurred on crowded ships and in periods of famine. Further than 
this it has long been recognized that this epidemic form of dysentery was distinctly 
infectious, and it can even be spread from one continent to another by infected 
ships, as in the great outbreak in the United States from 1846 to 1856, when it was 
probably conveyed by emigrants from Ireland, where the disease was rampant. 

Marshy lands seem to have a pronounced predisposing influence. Water which 
has been contaminated by those who are ill with the disease is an important factor 
in its spread. Milk and solid food may also carry the infection. 

Dysentery in its various forms is, in a large proportion of cases, the result of 
bad sanitation both as to surroundings and diet. It is much less frequent at present 
than in times past, and rarely ravages modern institutions or armies as it did fifty 
years ago. 

Epidemic dysentery being exceedingly prevalent in Japan in 1897, Shiga, a 
Japanese investigator, became interested in its bacteriological study, and isolated 
from the stools of 36 patients suffering from this disease a slightly motile bacillus 
having rounded ends and decolorizing by Gram's method. When brought into 
contact with the blood serum of patients suffering with dysentery this bacillus 
usually agglutinates (as does the typhoid bacillus in the Widal test), although in 
a few mild cases the reaction fails to take place. Flexner, Strong, Kruse, Vedder, 
and Duval, Vallard, Musgrave, Craig and Dopter, Spronck, Rosenthal, and other 
investigators have isolated in such cases organisms which they consider closely 



202 DISEASES DUE TO A SPECIFIC INFECTION 

related to or identical with the one observed by Shiga, and which they believe to 
be the cause of acute, epidemic, sporadic, and institutional dysentery. 

Duval and Bassett in 1902 obtained a similar organism from the stools of 
children suffering from dysentery or the summer diarrhea of infants. Still 
more recently (1903) Wolf stein, Park, Dunham, and Carey have not only con- 
firmed these findings, but have shown that at least two bacilli are present in 
cases of cholera infantum and dysentery. One of these corresponds to Shiga's 
bacillus, but they believe that in all probability several closely allied pathogenic 
bacilli will be found responsible in different epidemics. The bacilli are found in 
numbers proportionate to the severity of the illness, but often are not demonstrable 
in the stools until the latter are typical of the disease, and usually only after the 
lapse of five to seven days of illness. Chantemesse and Widal assert that a bacillus 
which they found in the stools of five dysentery patients, and which they also 
recovered from the mesenteric glands and intestinal wall of a patient who died 
of dysentery, is identical with the Shiga bacillus, and as their observations were 
made in 1888, ten years before Shiga published the results of his work, they claim 
priority of discovery. In France and Italy it is generally conceded that they 
were the first to find a specific organism in cases of dysentery. 

Amebic Dysentery. — Our recognition of the presence of amebce in cases of 
dysentery dates from 1859, when Lambl first discovered an ameba in the stools 
of this type of diarrhea. Later the parasite was studied by Losch (1875) and 
Kartulis, but it was not until Osier (in 1890), Councilman, and Lafleur (1891) 
reported upon its presence in several cases of dysentery, and in the past decade, 
that it received the attention that it deserves. Leukart has placed the Ameba 
dy sentence in the class of rhizopoda of the Protozoa. Schaudinn called it Entameba 
histolytica or Entameba dysenterice, the former term being now quite commonly 
used. Recent investigations indicate that the Entameba tetragena of Viereck is 
identical with the histolytica. 

The Entameba histolytica is a spheroidal cell, four to eight times the size of the 
red blood cell. It consists of two parts, an internal part called the endosarc, or 
endoplasm, and an external part called the ectosarc, or ectoplasm. These two 
parts cannot always be clearly recognized when the organism is at rest, but they 
are easily identified when motion is present. The endosarc makes up the greater 
part of the body and its granules may be fine or coarse. In this portion several 
vacuoles are not rarely found and a distinct nucleus is discernible when the organ- 
ism is stained. As in ordinary amebse the histolytica often contains foreign bodies 
such as red blood cells, and even bacteria. The pseudopod, or arm, which is pro- 
truded from the ameba when it is engaged in ameboid movement, is of the hyaline 
ectosarc. (See Plate IV.) 

The parasite is found in the stools of acute and chronic dysentery, in the 
floors of the intestinal ulcers, and in the secondary abscesses which it is prone to 
produce. 

Walker and Sellards have shown by their extensive feeding experiments with 
men in the Philippines that the ameba? cultivable on Musgrave and Clegg's medium 
are incapable of living parasitically in the intestinal tract of man, that they are 
non-pathogenic, and that they play no role in the etiology of endemic tropical 
dysentery. They also conclude that the Entameba histolytica is the essential 
etiologic factor in this dysentery and that an accurate laboratory diagnosis of the 
disease is possible. With the distinction between the harmless Entameba coli 
and the pathogenic Entameba histolytica established, there is no longer a reason 
for indiscriminately treating all persons having entameba? in their stools. 

Amebic dysentery may occur at any age from infancy to senility, but it is most 
common between twenty and thirty years of age. It is much more common in 
men than in women. 



PLATE IV 




NdUp?' 









: 'k 





* ,* 



^ ■* . 



•-, ■/. 



. ~^ 



".'■ 







» ■ ■ 







M ; - H 



:' 



• 

















> 








Amoebae from Cases of Dysentery and Enteritis. (Roemer.) 



DYSENTERY 203 

Balantidium Dysentery. — Walker concludes from recent studies that every 
person harboring Balantidium coli is sooner or later liable to develop balantidial 
dysentery. He finds that in the Philippines the chief source of infection is the 
domesticated pig. 

The Balantidium. coli is a protozoon found inconstantly in the feces of those it 
infects, and is often present without causing symptoms. 

Prevention. — Dysentery in all its forms is to be prevented by the use of boiled 
water and cooked foods, by the establishment of proper drainage, and by the 
avoidance of cold and wet. Persons who are subject to catarrh of the colon and 
rectum should wear a flannel binder. When the disease develops, the stools of the 
patient should be thoroughly destroyed and the greatest care exercised that the 
food and drink of the healthy are not contaminated by his discharges. 

As Musgrave has shown that intestinal amebiasis may occur without diarrhea 
it is evident that "ameba carriers" may be active factors in spreading the disease 
and in the presence of an epidemic this factor should be attended to among other 
measures. 

The conclusions of Walker and Sellards, based as they are on numerous feeding 
experiments with 50 volunteer men, are most valuable. 

1. The data on which they base their prophylaxis are: 

(a) Entameba histolytica, the essential etiologic agent in the disease, is an obliga- 
tory parasite and cannot propagate outside the body of its host. 

(b) The motile forms of this entameba, which are passed in the bloody mucous 
stools in acute dysentery, quickly die and disintegrate and are probably incapable 
of withstanding passage through the human stomach. 

(c) Owing to the prevalence of chronic and latent infections and the frequent 
failure of treatment to kill all of the entamebse in the intestine, "carriers" who are 
constantly passing in their stools large numbers of the resistant, encysted stage 
of Entameba histolytica are common in endemic regions. 

2. These facts make it probable that "carriers" of Entameba histolytica consti- 
tute the chief, if not the sole, agents in the dissemination of the disease. Pro- 
phylactic measures should be directed toward them and should include: 

(a) The identification of "carriers" by the examination of the stools of con- 
valescents, servants, and other suspects whose employment make them particularly 
dangerous to the public health. 

(b) The sanitary disposal of feces. 

(c) The treatment of all "carriers." 

3. The most efficient personal prophylaxis is frequent stool examinations, as 
an index for treatment, of all persons residing in endemic regions. 

Shiga, in Japan, has used a polyvalent serum, made by the use of the Shiga- 
Kruse and Flexner organisms, combined with a mixture of dead bacilli as a means 
of preventing the occurrence of the disease. He treated 1000 persons and although 
he failed to materially diminish the incidence of the malady, the mortality in 
those attacked was reduced from the average 20 or 30 per cent, to almost nothing. 
(See Treatment.) 

Frequency. — Until very recently it was generally supposed that amebic dysen- 
tery was the type of the disease most commonly met with in the United States, 
but now that Shiga's bacillus has been found in many cases of sporadic and epi- 
demic diarrhea in this country it must be regarded as the less frequent form of the 
two. Indeed, it would seem probable that many of the cases hitherto regarded 
as catarrhal are due to this bacillus. (See also Cholera Infantum.) 

Pathology and Morbid Anatomy. — In bacillary dysentery, when death has oc- 
curred in the first week, the autopsy reveals the mucous membrane of the colon 
to be intensely corrugated and swollen, so that its natural rugosities are greatly 
emphasized, while over them is spread an easily detached layer of superficial epi- 



204 DISEASES DUE TO A SPECIFIC INFECTION 

thelium, which has undergone necrotic changes. Numerous spots of ecchymosis, or 
hemorrhage, into the mucous membrane are often present, but ulcers are not found, 
although the necrotic process just named may be so severe that a superficial gan- 
grene may be present. When the inflammation is very intense the whole thickness 
of the bowel wall may be indurated, and even the visceral peritoneum may be 
infected. In some instances an associated inflammation of the small bowel is 
present, somewhat similar changes being present in its coats. 

Shiga described the morbid process of acute bacillary dysentery as a catarrhal 
inflammation proceeding to hemorrhagic, diphtheritic, or ulcerative inflammation. 
Kruse also observed diphtheritic membranes in eight cases which came to autopsy, 
and Flexner recognizes the tendency to their formation, although he did not find 
any in the cases which he examined postmortem in the Philippines. 

Craig has reviewed the morbid anatomy of chronic cases of infectious or bacillary 
dysentery, recognizing follicular, diphtheritic, and gangrenous stages. In the first 
the coats of the colon usually are thickened, and the follicles, particularly of the 
cecum, ulcerated. The mucosa is of a gray-slate color, and shows patches of acute 
congestion; the gut is narrowed, but there are areas of dilatation. The ulcers 
appear at the summit of the follicles as minute, ragged erosions. Later the necrotic 
areas extend, and their margins appear stamped out, but undermined. The ulcers 
measure J to J cm., but may attain diameters of 1.5 cm. and extend to the sub- 
mucosa or muscular layer. Cicatrized and open ulcers may be found together. 
In the diphtheritic stage, which may be implanted on the follicular, the colon is 
grayish or greenish-blue, marked by red or dusky-brown areas and greatly thick- 
ened. The mucosa becomes necrotic, exfoliates in masses or irregular patches 
composed of granular detritus, leukocytes, and innumerable bacteria. Ulceration 
practically always accompanies the formation of the membrane. The gangrenous 
stage seems but an intensification of the diphtheritic. The serosa is more affected, 
and matted adhesions are the rule. The necrotic colon is easily torn, greenish- 
black, and marked by inky-black areas. The ileocecal region is sacculated, and 
the sigmoid flexure and rectum dark olive-green in color. Tumefied, purulent 
elevations show through the serous coat. Internally the mucosa shows an inde- 
scribable admixture of necrotic or gangrenous lesion, with purulent suffusion of 
all the coats of the colon. In each of the foregoing forms parts of the mucosa 
escape, and these manifest more or less catarrhal inflammation. The protean 
manifestations of bacillary dysentery, both acute and chronic, are so influenced 
by the pathogenicity of the infecting organism, the activity of mixed or asso- 
ciated infection, susceptibility of the patient, duration of the process and other 
factors that an exact description is impossible. 

The noteworthy difference between the lesions produced in children and adults 
by the Bacillus dysenteries is that in the former the solitary and agminated lym- 
phatic tissues are much more commonly and more severely affected than in adults. 

In the acute type of bacillary dysentery the entire intestine, large and small, is 
affected by a fibrinous inflammation with only superficial ulceration. In the 
chronic type, which has lasted from a month to a year, the lesions are limited to the 
colon and occur chiefly in its lower part. These lesions consist in extensive ser- 
piginous depressed ulcers and are found in a greatly thickened bowel wall. 

The lesions of entamebic dysentery are quite different from those of bacillary 
dysentery. In the first place the ulceration is confined almost entirely to the large 
intestine, although' the lower part of the small intestine may be slightly affected. 
The submucous tissues become infiltrated and swollen in patches, which project 
above the level of the normal mucous membrane. These infiltrated areas undergo 
necrosis and slough away, leaving ulcers which may be superficial or deep, and 
which may extend as far as the peritoneal coat of the intestine, but perforation is 
rare. They are often very large and extend laterally as well as downward. The 



DYSENTERY 205 

edge of the ulcer may be undermined and the floor honeycombed. Not rarely 
the extension laterally takes place under the mucosa or dissects the muscle coat 
so that there is only a small opening to a large area of necrotic tissue. Occasionally 
the submucosa is necrotic without evident superficial lesions. The amebce are found 
in the ulcers in the neighboring lymph spaces and sometimes in the bloodvessels 
of the part, but there is an extraordinary lack of pus when the severity of the 
necrotic process is considered. 

When recovery takes place fibrous tissue covered by epithelium closes the 
spaces made by the ulcers, and as these scars contract strictures may develop. 
The colon becomes thickened and it may be adherent to the adjacent structures, 
and uneven contractions form pockets in which the parasites may linger after 
apparent clinical recovery. The appendix may be involved. 

The changes in the liver in amebic dysentery consist of two alterations. The 
first are multiple areas of local necrosis, and secondly abscess, either single or 
multiple. The single abscesses are usually large and in the convexity of the right 
lobe or else in the concavity of the liver where it lies nearest the large bowel. 
Boston has collected statistics of 2340 cases of amebic dysentery. Of these, 486, 
or 20 per cent., suffered from hepatic abscess. (See Hepatic Abscess.) The 
percentage varies from 60 per cent. (Kartulis) to 21 per cent. (Councilman and 
Lafleur.) Roux has collected 639 cases of amebic abscess of the liver. Of these, 
435, or 70.8 per cent., were in the right lobe; 85, or 13.3 per cent., were in the 
left lobe, and 2, or 0.3 per cent., were in the lobus Spigelii. The multiple 
abscesses are usually small and widely scattered and often near the surface. It 
is noteworthy that these so-called abscesses do not contain true pus unless 
secondary infection with pus organisms has occurred. They are composed of a 
grumous material made up of a thick, coarse, irregular reticulum, in the meshes 
of which lie the semi-fluid contents. As the area increases in size the fluid 
becomes reddish, brownish, greenish-yellow, or chocolate color, and is mixed with 
pieces or shreds of broken-down hepatic tissue. Amebae may be found in the 
contents of these cavities. 

Abscess of the liver due to the Entameba dysenteric nearly always develops in 
the first few weeks of the disease. Occasionally one of the larger abscesses ruptures 
into the right lung. (See Complications.) 

A valuable contribution to the subject of the associated lesions of dysentery 
has been made by Craig, of the United States Army Medical Staff. Analyzing 
120 cases of dysentery, of which 60 were of the bacillary and 60 of the amebic type, 
he found that in nearly every instance the autopsy revealed an increase in the 
cerebrospinal fluid and edema of the brain. In the amebic cases an intense con- 
gestion of the cerebral vessels was also present, and in 50 per cent, minute capillary 
hemorrhages were present. In the bacillary cases, on the other hand, the brain 
seemed unduly anemic. In the respiratory system bronchopneumonia is the most 
common lesion in the bacillary disease. Craig believes that fully 60 per cent, of 
the cases of dysentery seen in the San Francisco Military Hospital have coincident 
nephritis, and of the 120 cases already cited no less than 101 had this condition, 
usually of the parenchymatous type. More cases of nephritis occur in the entamebic 
than in the bacillary type. 

In the acute catarrhal form there is a free production of mucus which coats the 
surface of the lower bowel, chiefly in the sigmoid flexure and rectum. This mucus 
is filled with exfoliated epithelium, some of which has undergone fatty degenera- 
tion. Not infrequently blood cells are present in the mucus. When the inflam- 
matory process is severe, marked congestion and infiltration of the mucous 
membrane and submucosa may be present, and even a purulent and superficial 
ulceration may occur. 

The diphtheritic type is characterized by congestion of the mucous membrane 



206 DISEASES DUE TO A SPECIFIC INFECTION 

and the development upon its surface of a false membrane. The connective tissue 
under it, and between the glands, is infiltrated and filled with fibrin and pus. In 
cases in which the process is very active, the inflammation may reach not only the 
muscular coats, but even the peritoneal coat. The area covered by the false mem- 
brane varies greatly in different cases. In some only the rectal mucous membrane 
is affected, in others a continuous exudate covers the entire colon, and in still others 
it appears in scattered patches. If the process is severe healing takes place by 
sloughing of the necrotic tissues, which may reach to the deeper layers of the 
bowel, leaving ulcers which gradually undergo cicatrization, or the ulcers remain 
granulating surfaces for months and heal only under direct treatment. 

Symptoms. — The symptoms of all the various forms of dysentery are closely 
similar. The onset is usually sudden, or it may develop in the course of a grad- 
ually increasing diarrhea, which at first is thought to be an ordinary attack of 
looseness of the bowels. The patient suffers from wretchedness, which is thought 
to be the result of the intestinal disorder, and often has, in the earliest stages, a 
considerable degree of griping pain. The initial diarrhea soon sweeps the bowels 
clean of their normal contents, and as soon as this is accomplished the stools be- 
come scanty and consist largely of mucus which, not rarely, contains blood. The 
griping pain increases in violence, and there is marked tenesmus which often causes 
the patient to break out in a profuse sweat. The rectal irritation causes a con- 
stant desire to go to stool, which is not satisfied by the small evacuation that 
occurs. At first the constant irritation of the anUs may cause spasms of the sphinc- 
ters, but later when the disease is severe the sphincter ani may become relaxed, 
and even rectal prolapse may ensue. The centres in the spinal cord controlling the 
bladder become reflexly irritated and difficult urination may add to the suffering 
of the patient. 

It is manifest that such symptoms must speedily cause grave systemic disturb- 
ance by reason of the loss of nutritive material, the constant pain, the loss of sleep 
and straining, and so the pulse soon becomes rapid and feeble, and the patient 
rapidly emaciates not only because of the reasons just cited, but also because the 
local lesion in the bowels soon results in general systemic infection, either with 
the specific cause of the attack or with other micro-organisms which gain access 
to the general system through the diseased intestinal wall. 

The tongue is very foul and the secretions of the mouth scanty. 

If the disease persists the scanty mucous stools may be supplanted by more 
profuse serous discharges, which are often reddish in hue, and seem to contain 
small particles of flesh (probably bloody mucus and mucous membrane). This 
fluid is highly albuminous. The debility and emaciation of the patient speedily 
becomes profound, as the loss of fluid and albumin continues. Whether the 
stools are mucous or serous, they are fetid and have an odor which is quite 
characteristic. 

When examined by the sigmoidoscope the appearance of the bowel is fairly 
typical in that small, superficial ulcers covered by grayish mucus which is easily 
wiped off, leaving a granular surface, are numerous. This mucus will often reveal 
the ameba when the feces are negative. 

In that form of dysentery called bacillary the fever at first may rise as high 
as 103°, but in the entamebic form the temperature is usually not greatly disturbed 
unless secondary abscess develops. It rarely rises above 102°, and may be sub- 
normal after the stage of onset. 

When the infection with Shiga's bacillus is very virulent, death from toxemia 
and exhaustion may occur as early as the fourth day, but, on the other hand, the 
case may last for much longer periods before the fatal result ensues. There is 
sometimes met a subacute form, which lasts, in a modified type, for weeks or even 
months. 



DYSENTERY 207 

Cases of entamebic dysentery may be divided into three types: (a) A mild form 
in which the general health remains good, although the number of stools may vary 
from two to six in a day. (6) A moderately severe form in which the general health 
is greatly impaired and there is much loss of flesh, with an evening rise of tempera- 
ture and frequent stools, (c) A very severe type is met with in which the prostra- 
tion and loss of weight are extreme, the stools are bloody and very frequent, and 
the extremities cold. In all these cases the patient may without any apparent 
cause pass to better or worse with extraordinary speed, (d) A chronic form of 
entamebic dysentery also exists which lasts for months and has temporary periods 
of constipation. These periods of constipation, if abscess does not develop, give 
the patient an opportunity to be nourished, and so he may be able to retain 
strength and flesh. 

Entamebic dysentery may cause death in a few days or last for weeks, and may 
cause death finally by the secondary abscess in the liver. Free hemorrhages from 
the bowel may also occur in this form, and perforation from deep ulcers is recorded. 

In the acute catarrhal form of dysentery there may be fever at onset and scyba- 
lous masses will often be found mixed with the mucus which is expelled. After 
an illness of from four to seven days the quantity of blood in the stools is decreased, 
and they become less frequent. 

Marked abdominal tenderness over the course of the large bowel is usually 
present in all cases. 

In the acute diphtheritic form the patient is usually extremely ill from the very 
first. The systemic depression is marked and profound adynamia is quickly devel- 
oped. The belly is distended and painful upon pressure. Bloody mucus is not 
uncommonly absent from the stools. Just as in the other forms so in this, a sub- 
acute or chronic type is met with in which the abdominal signs are mild and the 
number of stools a day is as low as four or five. 

Complications and Sequelae. — Perforation of the bowel has already been named 
as a possible sequel of the amebic form of the disease. In other instances a local- 
ized peritonitis develops, and as the result of infection of the tissues about the colon 
a perityphlitis or periproctitis comes on. Rupture of an hepatic abscess is a very 
frequent occurrence. The pus finds its way through the diaphragm into the right 
lung or right pleural space. Rarely it has burst into the duodenum and even into 
the vena cava, or backward and downward along the psoas muscle, or into the 
kidney. Even the pericardium and the bladder may be perforated. Strong has 
called attention to the occurrence of profuse intestinal hemorrhage. 

In many epidemics of dysentery there is associated mild or severe malarial 
infection which renders the case difficult of treatment in that two infections have 
to be controlled simultaneously. Septic arthritis, pericarditis, and endocarditis 
sometimes occur as terminal infections. (See Pathology and Morbid Anatomy.) 

Diagnosis. — The diagnosis that the patient has acute inflammation of the large 
bowel, and is therefore suffering from dysentery in one of its forms, is easily made 
if the symptoms just described are present. It is not, of course, so easy to deter- 
mine which of the several forms of dysentery is present. The bacillary form 
is separated from the amebic variety by the presence of marked fever, which is 
usually absent in the latter disease; by the discovery of the specific bacillus in the 
stools, which discovery, however, requires special training in searching for it; 
and by the agglutination test of the bacillus with the patient's blood serum, which, 
as in the case of the Widal test of the blood in typhoid fever, gives us much valuable 
information. This reaction is uncertain in the first week, often positive after the 
sixth day, but in some cases it does not occur for two weeks. For this reason it does 
not possess great diagnostic importance in the early stages of the disease. To 
be of value it must take place in a dilution of 1 : 200. The percentage of positive 
reactions according to Rosenberger is 80.2. 



208 DISEASES DUE TO A SPECIFIC INFECTION 

The amebic variety can be recognized during life only by finding the ameba 
in the stools. This requires some practice and skill. The small pieces of blood- 
stained mucus are the parts in which the organism is to be sought for, first with 
a low-power and then with a high-power lens. (See Plate IV.) The light coming 
through the instrument should be stopped down by an appropriate diaphragm. 
Several negative examinations do not exclude entamebic dysentery, and particularly 
in chronic cases is it necessary to make repeated examinations. In such cases 
acute exacerbations may afford stools relatively rich in amebse even when inter- 
current examinations have been negative several times. The stools should be as 
fresh as possible, unmixed with urine, and, if not warm, the slide examined should 
be warmed gently or placed on a warm stage so as to induce movements of the 
amebse. If an organism which possesses active ameboid movement is discovered 
and if it contains several red blood cells the diagnosis is practically assured. 

The failure to discover the amebse or the signs of the presence of the bacillus of 
Shiga should cause a search for the Balantidium coli. This is essential to successful 
treatment. (See Treatment.) 

When examining the stools it is essential to bear in mind that a multitude of 
intestinal bacteria are also present and that various parasites other than the specific 
ameba may be present. Thus, the Trichomonas intestinalis and the Cercomonas 
intestinalis are often found. Thayer has recorded a case in which the Strongyloides 
intestinalis was present as an additional parasite. 

The diphtheritic form is to be suspected if from the first the patient seems pro- 
foundly adynamic. Typhoid fever is to be separated from dysentery by the fever, 
the rose rash, and the Widal test. 

Prognosis. — The prognosis in dysentery depends to some extent upon the variety 
of infection which is present, and upon the hygienic surroundings and vitality of 
the patient, for even the mildest types may be fatal if the patient receives bad 
food and is exposed to excessive heat or cold or wet. When the bacillus of Shiga 
is the cause the prognosis in acute cases must always be most guarded, both as to 
the recovery and the duration of the illness. The mortality varies greatly in 
different epidemics in different parts of the world. Thus in Japan, Shiga found 
it varied from 22 to 55 per cent. In this country the mortality has been as low 
as 3 per cent. The general state of emaciation and depression must always be 
considered. If the stools contain gangrenous sloughs, the outlook is of course 
very grave; and if hiccough, great nervous depression, and low delirium develop 
the outlook is probably fatal. 

In the entamebic type the development of abscess in the liver of course adds 
very greatly to the gravity of the case; but even when amebic abscess is present 
and ruptures into the lung, it is possible for recovery to take place, if proper surgical 
measures of relief are undertaken. 

Even the most urgent cases may, when apparently near to death, recover, but 
convalescence is protracted. 

According to Duncan prognosis can be based, to some extent at least, on the 
character of the stools. He believes a good result can be foreshadowed in those 
cases in which are passed mucus with minute fecal lumps, stained or not with blood, 
and in which the blood and mucus disappear, after which the ordinary fecal char- 
acters will soon manifest themselves. 

The prognosis is of evil omen, according to Sir Joseph Fayrer: (a) in the cases 
in which pulpy stools without blood or mucus are passed; (b) where fluid fecal 
matter is from time to time passed throughout the illness, the prognosis is unfavor- 
able, inasmuch as these characters of the stools show the disease to be extensive, 
and affecting chiefly the upper part of the large as well as in some cases part of 
the small intestine; (c) the prognosis is of the worst possible character where the 
stools consist of blackish-red or blackish fluid with a horribly putrescent odor, and 



DYSENTERY 209 

of bits of gangrenous tissue. Duncan has never seen a patient passing this 
character of stool recover. 

Treatment.- — In all forms of dysentery the following rules as to treatment 
apply: So far as diet is concerned it is self-evident that the food should 
consist of those substances which are readily digested and absorbed from the 
stomach and the duodenum, in order that as small a residue as possible may pass 
on downward into the large bowel. Milk, which is so universally resorted to in 
the treatment of all forms of diarrhea, is not always as useful a form of nutriment 
as it is thought to be; for not uncommonly it will be found that when milk is taken 
it remains undigested, or forms curds which are indigestible because of the feeble 
secretion of digestive juice. These curds pass through the bowels and afford 
pabulum for micro-organisms which, in turn, are injurious to the mucous membrane. 
If it is given, it should certainly be diluted freely with lime-water, barley-water, 
or Vichy-water, or else it should be peptonized in order that its digestion may be 
readily performed; and it is of vital importance in this connection that it should 
be given in small quantities, frequently, rather than in large quantities. Solid 
food is, of course, contra-indicated, but semi-solid foods like milk-toast, the digestion 
of which is aided by pancreatin or taka-diastase, and a very soft-boiled egg, will 
often prove a better diet than one which is more liquid, but less nourishing, since 
the physician, in the presence of dysentery, is faced by two opposing factors; on 
the one hand a feeble digestion, and on the other hand the necessity of supporting 
vitality to the highest possible point by the administration of proper foodstuffs. 

Musgrave and Sisson state that the routine treatment in the Philippine General 
Hospital which has given the most satisfactory results in bacillary dysentery 
consists in the following: 

First, absolute rest to save the strength of the patient and to prevent the involve- 
ment of the larger segment of the intestine. 

Secondly, the early administration of some mild laxative, preferably sodium 
sulphate or magnesium sulphate, preceded by fractional doses of calomel in order 
to diminish the presence of infecting material in the gastro-intestinal tract, as 
well as to get rid of some irritating material that might be present there. The 
administration of simaruba officinalis combined with some opiate is highly recom- 
mended, for it has given the writers the most satisfactory results in comparison 
with the use of other drugs. As an adjuvant to this treatment, the judicious use 
of normal salt solution as an enema, or given in the form of the drop method per 
rectum in the amount of 1 liter once a day, is sometimes very beneficial. 

When the acute stage of the disease has subsided, enemata of hydrogen peroxide 
in a weak solution (about 25 cubic centimeters in 500 cubic centimeters of water) 
once a day are a great help towards prompt recovery. 

The use of astringents and the so-called gastro-intestinal antiseptics the writers 
have given up as unsatisfactory. Although there is a small percentage of patients 
who recover under this treatment, one should remember that there are cases that 
get well even without any medical treatment, and these writers consider it problem- 
atical whether or not the usual astringents and gastro-intestinal antiseptics are 
really beneficial in the treatment of this disease. The fact must be kept in mind 
that most of the astringents and so-called intestinal antiseptics, such as bismuth, 
tannic acid preparations, salol, beta-napthol, benzo-napthol, benzoic acid, and 
others, have an irritating action upon the stomach and intestines, especially if 
they are given in large amounts and over a considerable period of time. 

The use of the ice-bag over the abdomen is a great help in diminishing the abdom- 
inal pain, and hot turpentine stupes frequently are useful for the same purpose. 

The essential part of the treatment, however, is dietetic. During the first 
twenty-four hours of the acute stage of the disease food must be withdrawn. Pieces 
of cracked ice may be given to allay thirst. At the end of twenty-four hours, the 
14 



210 



DISEASES DUE TO A SPECIFIC INFECTION 



patient is allowed albumin-water or rice- or barley-water and later skimmed or 
peptonized milk. When improvement has begun, milk, broth, beef juice, and 
orange juice may be given. The mouth must be frequently cleansed with an 
antiseptic mouth wash to prevent the frequent complications of parotitis and 
gastritis. 

The serum treatment, first recommended by Shiga in 1898, has both advantages 
and disadvantages. If the identification of the bacillus which is the cause of 
the infection can be carried out with readiness, as well as with accuracy, this 
scientific treatment ought to yield a greater percentage of cures than usually is 
obtained. For practical purposes, however, especially in those cases that have 
to be treated in places where the means of identifying the infecting micro-organisms 
are not available, it is a failure in most instances. The sera of patients suffering 
from one form of bacillary dysentery will not agglutinate other varieties of Bacillus 
dysenterise. 

Fig. 45 



May 1909 




















































1110 


DAY OF DIS. 


4 

M E 


5 

M E 


6 7 

■■' l M E 


8 9 

IE IE 


10 

M E 


11 

M E 


12 

H E 


13 

M E 


11 
M E 


15 

M E 


10 

M E 


17 

M E 


18 

M E 


19 

M E 


20 

M E 


£1 
M E 


22 

M E 


23 

M E 


24 

M E 


25 

U E 


SO 

M E 


27 

M E 


2S 

M E 


29 

M E 


30 


31 

M E 


1 
'J E 


112 














































































































111 


30,000 












































































































110 


28,000 


O 


a 








































































































109 


20,000 


03 










/ 


/ 


\ 
\ 


























































































108 


21,000 




S 








\s 






\ 


























































































107 


22,000 


> 

_) 
3 


1 


7 














\ 
























































































100 


20,000 


















V 






















































































105 


13,000 




1 


















\ 


\ 




l 
/ 


' » 


'a 


■v. 


«^ 








































































104 


10,000 


I 






















\ 


/ 












N 


^ 

V 




































































103 


11,000 


1 








11 


_A 
































s 


1— 








V 






















































102 


12,000 












f\ 






































































'"v 






■«. 




















101 


10,000 










l 


\ 












































































1 


* 
















100 


8,000 










' 1 


' \ 
































































































99 


G.OO0 










































































































98 


4,000 










|j 








































































































V 


























































































N 




97 


2,000 












































































































90 


1,000 










1 



































































































Effect of ipecacuanha on the leukocyte curve and temperature in amebic hepatitis. (Greig.) 

Broken line, leukocytes. 



It is possible that Flexner's polyvant serum might be used for any acute bacillary 
dysentery. However, streptococci, staphylococci, colon bacillus, and others 
concerned in the production of colitis under certain circumstances, will make the 
use of even a polyvalent serum unsatisfactory in many instances. 

The treatment of amebic dysentery may be divided into three methods, and each 
one of these plans finds ardent advocates among those of the profession who 
have had sufficient experience to make us feel that their opinions are of value. 
Before discussing these, however, it may be stated that in the early stage of the 
disease the bellyache may be relieved by a hypodermic of J grain of morphine 
and followed by castor oil and laudanum to sweep out the bowel. 

The ipecac plan is to be considered the first of these. Leonard Rogers has shown 
that emetine hydrochloride given hypodermically in the dose of J grain daily 
exercises a specific healing effect and results in speedy cure in many cases. In 
severe cases the emetine should be given intravenously. This type of treatment 
has for obvious reasons supplanted the use of ipecac itself but if emetine is not 
at hand ipecac should be given as Woodhull advises as follows: 

"The stomach must be empty and the patient recumbent. About twenty 
minutes before giving the ipecac it is well to paint the epigastrium, not the whole 



DYSENTERY 211 

abdomen, with tincture of iodine, or to apply a mild sinapism sufficiently to induce 
gentle counter-irritation. This precaution, however, may sometimes be omitted, 
or may be deferred until the medicine has been taken. Ten or 15 minims of lauda- 
num may be given, always on an empty stomach, to be followed in ten or twelve 
minutes by from 15 to 30 or more grains of ipecac in pill form, or as a paste, with 
a very small quantity of water. No food or fluid should be taken for at least 
four hours, and recumbent rest should be strictly maintained. If the ipecac is 
administered in pill or capsule the laudanum may be mixed with it instead of given 
previously. One scruple of ipecac and 1 grain of opium can be made into four 
pills, or the laudanum can be put in the pills. When pills are used they should 
be freshly made. Or 20 grains of ipecac can be suspended in 2 fluidrachms of 
water with a few drops of an aromatic to disguise the taste. It is never advis- 
able, on account of the popular idea associated with it, to disclose the name of 
the medicine, and the patient should be warned to resist any inclination to vomit. 
The size of the dose should be in proportion to the gravity of the case. Just as 
in severe colic very large doses of opium are tolerated, and in pernicious fever 
enormous quantities of quinine are indicated, so in dysentery surprisingly large 
doses of ipecac are well borne, although the magnitude of the dose should bear 
some relation to the severity of the disease. With a little experience, that relation 
will soon be determined. Sixty grains is not a maximum dose for an adult, but 
with the ordinary acute dysentery from 15 to 25 grains at a time should suffice. 
If the first or any subsequent dose is rejected, which rarely happens if these rules 
are carefully followed, it is to be repeated after a short interval. The retching 
or vomiting of exhaustion or the restlessness of delirium is no bar, but rather an 
inducement to this treatment; and small children or delicate women can take it 
with impunity in proportionate amounts. 

"The common course in acute dysentery is, first, the relief of pain, next the 
subsidence of fever, and then the cessation of the bloody discharges. The usual 
sign that recovery is at hand is a painless, copious, semi-fluid evacuation, much 
the color of the ipecacuanha powder, not black as has been stated. The medicine 
then may be reduced or entirely suspended. In acute cases these results will 
follow very quickly. In chronic dysentery complete recovery may be delayed or, 
indeed, may fail of absolute attainment, but great amelioration may be confidently 
anticipated. That the powder should be pure and comparatively fresh is always 
essential. " 

Walker calls attention to the fact that the ipecac treatment, while very efficient 
in relieving attacks and causing the entamebse to disappear temporarily from the 
stools, does not always kill all of them in the intestine. Treatment should there- 
fore be controlled by stool examinations in order to prevent the relapses so common 
in dysentery. 

The second method of treatment is the purgative plan, which has come forward 
largely within the last few years, probably because of increasing experience on 
the part of American and English surgeons in the Philippines and in South Africa. 
Clinical evidence is rapidly accumulating which proves beyond all doubt that in 
a certain proportion of cases of acute dysentery the employment of sulphate of 
magnesium combined with aromatic sulphuric acid is a most advantageous method. 
The bowels are first thoroughly moved with Epsom salts or with Rochelle salts, 
and then aromatic sulphuric acid is given freely, so that it will exercise its well- 
known astringent or constipation influence. 

The third plan of treatment consists in the administration of intestinal antiseptics, 
of which perhaps bismuth salicylate, benzonapthol, and salol have been most 
commonly employed. Theoretically, it is easy to conceive that these substances 
may be advantageous, but practical experience has shown that they fail to exercise 
the degree of antiseptic influence with which they are credited, and they are not 



212 DISEASES DUE TO A SPECIFIC INFECTION 

of sufficient importance to justify their employment to the exclusion of the ipecac 
or saline methods which have just been described. The employment of calomel 
and corrosive sublimate with good results in these cases rests upon the fact that 
they increase the activity of the liver, both in destroying toxic material and in 
secreting bile. 

Without doubt local treatment by high intestinal irrigations is of value. Copious 
clysters which will reach far up into the descending and transverse colon are 
necessary. In a number of instances the writer found that injections of phenol- 
sulphonate of zinc, in the proportion of 20 grains to the pint, have produced 
very satisfactory results, the zinc acting both as an astringent and antiseptic. 
Other practitioners have employed copious injections of weak solutions of nitrate 
of silver of the strength of 1 drachm to 4 pints. Rogers has obtained the best 
results in bacillary dysentery by injecting albargin or silver gelatose in the strength 
of 1 to 500 of water, using half to 1 pint as an injection each day. The tenesmus 
which is frequently associated with the dysenteric condition, or on the introduction 
of ths soft rectal tube, can sometimes be avoided by the use of a 10 grain iodoform 
suppository used half an hour before the injection is to be given. This suppository, 
by its local anesthetic effect, is of service, and I have thought that the absorption 
of the iodine from it was also advantageous. 

The method of giving the intestinal lavage is of considerable importance. It 
should not be given with a Davidson or other pumping syringe, but always by 
means of a fountain syringe or surgical irrigator. The hydrostatic pressure em- 
ployed should never be greater than two or three feet, and it is much better that the 
injection should be gently given, so that it takes fifteen or twenty minutes to find 
its way up into the intestine, than that it should be delivered forcibly enough to 
produce angry contractions of the bowel, which will cause great agony and so 
much irritation that the treatment makes the patient worse. 

Where great irritability of the bowel exists it is probably better to employ two 
rubber catheters side by side, one being for the intake and the other for the outflow, 
since in this way great distention of the bowel is avoided. In instances in which 
cold-water injections seem inadvisable very hot water may be employed, but it is 
distinctly disadvantageous to employ tepid water, which has a relaxing and enervat- 
ing effect, and does not possess the healthy stimulant effects of marked cold or 
high heat. Often it is best to employ normal saline solution, since by this means 
maceration of the intestinal mucous membrane is avoided. 

The use of vaccine of Shiga's bacillus has given very variable results in the 
hands of different clinicians. It seems uncertain and not very safe. 

Another form of specific treatment is that which is directed to combating amebic 
dysentery by means of injecting quinine bisulphate, in the strength of 1 : 5000, suf- 
ficiently high in the rectum for it to exercise its fatal effect upon the ameba coli. 
Thymol 1:2500 may also be used in this way (Thomas). Harris has highly 
recommended hydrogen peroxide given by injections as a parasiticide. 

The complicating hepatitis or hepatic abscess can be prevented in a large propor- 
tion of cases if Leonard Rogers' advice be followed, namely, the use of ipecac 
or emetine hydrochloride as soon as the ameba is demonstrated or as fever and 
hepatic tenderness develop. (See earlier part of Treatment.) When abscess has 
developed Rogers has shown that the proper treatment is puncture, aspiration 
and repeated injection, without drainage, of quinine solution. Opening such an 
abscess by the ordinary means converts a sterile amebic abscess into an infected 
pus cavity. Usually three grains of the quinine at one injection are sufficient, 
dissolved in water 1:500. One to three aspirations and injections are all that are 
needed. 

Stimulants well diluted with water or with nutritive broths should be given if 
needed, and strychnine and quinine employed in convalescence as tonics. 



EPIDEMIC GANGRENOUS PROCTITIS 213 

For the control of diarrhea when excessive, enemata of deodorized tincture of 
opium and starch-water are very useful. 

During convalescence it is needful to avoid any article of food which can disturb 
intestinal digestion. 

Walker has shown that ipecac and emetine are practically useless in the dysentery 
due to the Balantidium coli. Neither do arsenical compounds, or quinine, or the 
aniline dyes, usually destructive to the protozoa, do much good, but the salts of 
silver and mercury are very active and it would seem that organic compounds 
of silver like argyrol will give the best results if used by colonic irrigations. 



EPIDEMIC GANGRENOUS PROCTITIS. 

Definition. — Epidemic gangrenous proctitis is an acute contagious disease appear- 
ing as a rapidly spreading ulceration of the anus and rectum, with prolapse and 
gangrene of the ulcerated rectum and, in a large proportion of cases, death in 
coma or convulsions. 

This disease, originally believed to be limited to narrow areas in Central and 
South America, is now known to occur much more widely throughout the tropical 
zones. It is generally distributed in tropical South America and in Central America. 
It has been observed in the Philippines, the Celebes, and New Guinea. 

There is some question whether this affection should be regarded as a distinct 
disease entity or not. 

Etiology. — Nothing is known of the direct cause of this curious condition. Ackers, 
of Curacao, states that it is the common belief of the natives in Venezuela that the 
disease is caused by eating unripe maize, of which the children are particularly 
fond. This seems hardly probable. The disease has been observed in countries 
in which maize is practically an unknown food product. Kieffer has reported 
one case in which the Bacillus pyocyaneus was undoubtedly the active organism. 
A high degree of humidity seems an essential condition to the development of the 
disease. Ackers observed this disease in fowls and the smaller domestic animals, 
occasionally in calves. In Venezuela and New Guinea the disease is confined 
to children, particularly those of the poorer classes, and in the rest of the tropical 
world it also holds true that children are more frequently attacked than adults. 

Pathology. — The rectum and anus in early stages are affected by deep ulcers 
overlaid with a diphtheroid pseudomembrane. Two forms can usually be distin- 
guished: the low form with limitation of the lesions to the rectum between the 
sphincters, and the high form in which the disease extends well up to the sigmoid. 

Symptoms. — The disease begins with local symptoms referred to the anus and 
rectum. There is burning and intolerable itching followed by severe dysenteric 
symptoms. After twelve to twenty-four hours there is more or less constant and 
severe tenesmus. 

The evacuations, at first feculent, become mucoid and finally consist entirely 
of mucus and blood. The distress grows urgent, effort and pain become continu- 
ous, and there is a constant flow or bubbling out of slimy mucus stained with blood, 
or almost pure frothy blood. The evacuations are very fetid. As the disease 
progresses there is profound collapse. Nervous symptoms appear and the patients 
become either delirious or comatose. In children there may be convulsions. 
Emaciation is rapid and death usually occurs in convulsions or coma. If the 
patient survives this stage the rectum is extruded and undergoes rapid necrosis 
and sloughing. 

In the early stages the diagnosis between epidemic gangrenous proctitis and d}' sen- 
teric lesions in the descending colon can only be made by examination of the rectum. 
In advanced cases the condition is self-evident. The mortality is very high, but 



214 DISEASES DUE TO A SPECIFIC INFECTION 

even comatose patients need not be despaired of. Recovery occasionally occurs 
after prolapse and sloughing of the rectum. 

Treatment. — The Venezuelan treats this disease by introducing lemon-juice 
or diluted aguardiente into the rectum. When extrusion of the rectum occurs 
he keeps it dry by dusting with wood-ashes. Indications are for active antisepsis 
of the rectum with diluted creolin or hydrogen peroxide. Opium will be necessary 
for the control of pain, and is best applied directly to the diseased area. If pro- 
lapse occurs no effort should be made at first to replace it. The rectum should be 
dusted with an antiseptic powder or freshly made charcoal. If gangrene occurs 
the rectum must be extirpated. 

HELL DIARRHEA. 

Definition. — An acute morning diarrhea with white stools and attended by 
marked flatulency. It is a disease of the acclimatized and not of the new-comer 
in the tropics. 

Etiology. — The etiological factors in the production of hill diarrhea are, first, 
prolonged residence in hot countries with the establishment of acclimatization, 
and an unaccustomed altitude, five to six thousand feet, with a high degree of 
humidity. The dweller in the low, hot plains who goes to the hills is very prone 
to fall a victim to this disease. It is consequently observed when business or 
relaxation takes the colonists into mountainous portions of the tropics. It is 
common in the hill sanatoria of tropical countries, particularly in India, where 
it was named hill diarrhea, Simla diarrhea, etc. Hill diarrhea bears a very close 
resemblance to sprue. The cardinal symptoms differ only in degree, but the 
tendency of hill diarrhea is so constantly to recovery, and that of sprue so con- 
stantly downward, that they must be considered separately. 

Pathology. — Very little is known of the pathology of this peculiar condition. 
It seems to be clear that there is a temporary suspension of function of the liver 
and pancreas. This is probably the expression of exhaustion resulting from the 
extra strain on already overworked digestive organs seeking to adapt themselves 
to a further change of climatic conditions. Scheube thinks this condition depends 
on an atonic state of the colon which he believes to be a common sequel to long 
residence in hot countries, and that the diarrhea is due to chilling of the abdomen 
in the unaccustomed cold and dampness of the early morning hours of the mountain- 
ous region of the tropics. 

The tendency in the vast majority of cases is to prompt readjustment and 
restoration within one or two weeks. A small proportion of cases persist and may 
end in typical sprue. Crombie reports cases in which cure has taken place only 
when the patients returned to the plains. In these cases every visit to the hills 
was followed by this diarrhea. 

Symptoms. — Shortly after arrival in the mountains the patient is troubled with 
dyspeptic symptoms and a morning diarrhea. On the succeeding days the diarrhea 
becomes more troublesome until it reaches eight to ten movements daily. It 
comes on in the early morning, at or near dawn, with a sudden call to stool. It 
continues during the forenoon and ceases abruptly about mid-day. There is very 
little pain and that only as a vague, indeterminate discomfort over the colon, 
and no tormina or tenesmus. The movements are large and frothy, they are devoid 
of coloring matter, and look like stirred mortar or whitewash. They have an 
unpleasant, mawkish odor. Dyspeptic symptoms are pronounced. There is 
distress after eating, particularly in the morning, and there may be marked tympanitic 
distention of the abdomen. 

Treatment. — Treatment is directed to the restoration of intestinal digestion and 
the maintenance of a relative degree of rest to the gastro-intestinal tract by putting 



MALTA FEVER 215 

the patient on liquid or milk diet. Small doses of calomel to stimulate the hepatic 
function are of value. Similarly pilocarpine has been tried with the idea of 
increasing the flow of the pancreatic secretion. Judicious use of the digestive 
ferments should be made. These patients should be advised to keep to their beds 
during the morning hours. In persistent cases it may become necessary to send 
the patients down to, or near, the sea level. 



MALTA FEVER. 

Definition. — Malta fever, or, as it is sometimes called, "undulant fever," is a 
disease which is comparatively common in the island of Malta. The malady 
occurs not only in Malta, but along the shores of the Mediterranean Sea, and so 
is sometimes, called "Mediterranean Fever." When it occurs at Gibraltar it is 
called "Gibraltar Fever" or "Rock Fever," and when in Italy, "Neapolitan Fever." 
It is endemic in Texas all through the goat-raising districts and is probably often 
thought to be typhoid fever. The malady is due to an infection by the Micro- 
coccus melitensis. Its chief clinical characteristic is wave-like or undulant curves 
of febrile movement. There are also recurring exacerbations of fever with profuse 
sweats, pains in the limbs, swelling of the joints, and enlargement of the spleen. 

History and Geographical Distribution. — Although the first accurate account 
of this disease was published in 1861 by J. A. Marston, who described it under 
the name of Mediterranean, remittent, or gastric remittent fever, it probably 
has been endemic in the islands and along the shores of the Mediterranean Sea 
for centuries. Hippocrates described cases of continued remittent fever which 
in their entire symptom-complex correspond with certain manifestations of undulant 
fever, and references to a protracted form of fever prevailing in Mediterranean 
countries were made by writers of the eighteenth century and by Sir William 
Burnett and Dr. Hennon early in the nineteenth century. While the disease 
is most common at Malta, Gibraltar, in the Balearic Islands, in Cyprus, in Crete, 
and along the southern coast of Italy, evidence is constantly being produced to 
show that it has a wide distribution throughout tropical and subtropical regions. 
Cases of undoubted authenticity have been reported from China, India, Porto Rico, 
and the Philippine Islands, and a fever occurring in Venezuela closely resembles 
it clinically, although no cases in which the specific organism has been obtained 
in that country are on record. Investigations have revealed its presence in the 
United States. 

To Great Britain the disease is of great importance because it incapacitates 
so many of the troops sent to garrison the Island of Malta. Thus from 1898 to 
1904 no less than 2229 cases occurred and resulted in 75,000 days' sickness per 
annum, for each case lasts about 120 days. 

Etiology. — The pathogenic organism of Malta fever is the Micrococcus melitensis, 
which was discovered in 1887 by David Bruce, who isolated it in pure culture from 
the spleens of nine patients who died, and found it in two instances in blood drawn 
from the spleen during life. This microbe is a minute, round or oval coccus, 
staining readily with the aniline dyes, but not by Gram's method. It grows very 
slowly in bouillon, agar-agar, and gelatin, and agglutinates when placed in blood 
serum drawn from individuals affected with the disease. A joint commission, 
appointed by the British Government, has proved it possesses great vitality, for 
the organism was found alive after sixty-nine days in dried, sterilized manured 
soil, after eighty days on dried fabrics, after seventy-two days in damp soil, and 
after thirty-seven days in sterilized water. When injected into monkeys it produces 
a malady similar to Malta fever, and its specific action in the human subject has 
been demonstrated by several cases of accidental inoculation. Monkeys have 



216 DISEASES DUE TO A SPECIFIC INFECTION 

been infected at the will of an experimenter, when forced to breathe an atmosphere 
laden with dust containing the specific organism. 

A commission was appointed by the British Admiralty to investigate this dis- 
ease the report of which published by the Royal Society in April, 1907, showed 
that the specific micrococcus escapes by the urine and the milk, but that the breath, 
saliva, sweat and probably the feces do not contain it. As goats are very prone to 
the disease the milk of this animal is a frequent cause of its spread. Since the use 
of goats' milk has been stopped in the British Army and Navy the disease has been 
almost eradicated. The Commission also showed that the infection may be con- 
veyed by flies and suggested that infected women may transfer the disease in coitus. 

Malta fever is a disease of summer, being most prevalent in June and July. 
Persons of all ages are subject to it, although the period of its greatest incidence 
is said by Maltese physicians to be between the sixth and the thirtieth years. 
Sex appears to be without influence in its causation. One attack appears to confer 
immunity, at least for a number of years. 

Pathology. — The gross morbid changes observed after death vary somewhat 
according to the stage of the disease in which death occurs. In those cases which 
die during the first four weeks of the attack, the spleen is invariably congested 
and enlarged and often is so soft that it resembles a large mass of clotted blood. 
The meninges, the liver, the stomach and intestines, and the kidneys are also 
frequently congested, and the lungs are always congested at their bases, while in 
some cases lobular consolidation takes place. The heart occasionally shows granu- 
lar or fatty degeneration and in a few instances pericardial effusion occurs. In 
cases which die late in the disease there is evidence of a prolonged toxic action 
upon the tissues. The liver and spleen are larger than normal and of firm consist- 
ency, due to the formation of fibrous tissue, and the heart is usually pale, its walls 
are thin and its cavities dilated. The spleen is the only organ which shows charac- 
teristic microscopic changes, namely, an increase in lymphoid tissue and the presence 
of large numbers of the specific micro-organism. Sections of the liver and kidneys 
show granular or fatty degeneration. As to blood changes there is a reduction 
in the number of red cells, alterations in their size and shape, and a deficiency of 
hemoglobin. The white cells are often relatively increased, the basophiles being in 
excess. 

The incubation period is from three to twenty days, most commonly fifteen. 

Symptoms. — The onset of the typical or undulant form of the disease is gradual, 
and is attended by lassitude, anorexia, nausea, headache, insomnia, and slight evening 
elevation of temperature. As the morbific process advances the digestive and nervous 
symptoms become intensified,, and the temperature rises slowly day by day, 
remitting somewhat each morning, until it reaches a level varying from 103° to 105°. 
Here it is maintained for a varying period of time, and then falls slowly with pro- 
fuse sweating. The other symptoms abate simultaneously. Soon, however, the 
temperature rises again and a condition similar to the one just described supervenes, 
constituting a relapse, of which several occur. The most noteworthy symptom of 
Malta fever is therefore the persistent recurrence of febrile movements which are 
wave-like in character, and which last from seven to twenty-one days. They are 
followed by a period of apyrexia or of very moderate fever, which lasts for a few 
days, when the febrile movement returns as before. In this manner the disease 
may persist for months, not being self-limited, as is the course of typhoid fever. 
The active fever,' the profuse sweats, and the pain continuing for so long a period 
produce great exhaustion and emaciation. Sometimes cardiac or pulmonary 
complications arise which determine a fatal issue of the malady. 

In the majority of cases of this type, however, convalescence ensues, but it 
is slow and often attended by neuralgic and rheumatoid symptoms, and occasionally 
by orchitis. 



MALTA FEVER 



217 



Variations from the typical form of the disease are not 
at all uncommon. Some cases are characterized by rapid 
onset and the early development of severe constitutional 
symptoms, which usually end in death, while other cases 
run an extremely mild course with little constitutional 
disturbance other than general malaise and slow but 
progressive anemia and emaciation. In this form the 
temperature is often intermittent, rising several degrees 
each afternoon and falling to normal or nearly normal 
the next morning. 

Diagnosis. — Accurate diagnosis of Malta fever depends 
upon the agglutinative serum test between the blood and 
the micrococcus, which should be made whenever possible. 
This reaction is almost always obtainable by the sixth 
day after the development of pyrexia and often as early 
as the fourth. F. J. A. Dalton, of the British navy, finds 
that trustworthy results are obtained by the use of a 
dilution of 1 : 50, with a time limit of half an hour. 

Clinically, the diagnosis presents many difficulties, for 
the different manifestations of the disease make it par- 
ticularly liable to be confounded with a variety of affec- 
tions, such as typhoid fever, tuberculosis, chronic rheu- 
matism, malaria, and malarial cachexia. Suspicion as to 
the nature of typical cases should be aroused by the 
presence of an undulating temperature curve and the 
characteristic frequent relapses. Additional aids to the 
differential diagnosis may be named as follows : 

From malarial fever we can separate Malta fever by 
several factors which make differentiation possible. In 
the first place the absence of the plasmodium of malaria in 
the blood, and the presence of the Micrococcus melitensis 
in the spleen on puncture is of course a definite means of 
separation. Again, the fever does not yield to quinine 
as does that of malaria, and the pyrexia is too persistent 
for the intermittent type of that disease, although at 
times the waves of fever may be abrupt enough to re- 
semble it. Again, the marked arthritic symptoms and 
the neuralgic pains are not met with in malarial infection. 

The possibility of tuberculosis must be also considered. 
Careful physical examination of the thorax and abdomen 
will usually reveal signs of tuberculosis if it be present, 
and if need be the tuberculin test can be applied. Typhoid 
fever presents a temperature range after the first few 
days which does not resemble that of Malta fever, and 
the absence of rose spots in Malta fever is also an impor- 
tant differential point. The presence of the Widal test 
will also aid in the differentiation. 

Duration and Prognosis. — The average duration is from 
seventy to ninety days, although some cases last as long 
as six months. Prognosis as regards life is favorable, the 
mortality being about 2 per cent. From the evidence thus 
far accumulated it seems that the serum test may afford 
prognostic as well as diagnostic information, for it has 
been observed that those cases in which the agglutinating 



Fig. 46 



i'Z ** 






~V- 



<n e? c< 



(•JJHVJ) 3HrUVaidW3L 



Temperature chart of the 
undulatory form of Malta 
fever. (Hughes.) 



218 



DISEASES DUE TO A SPECIFIC INFECTION 



power of the blood serum is high during the early stages of the fever run a favorable 
course, while those in which the agglutinins remain low during the entire course 
of the fever are subject to many relapses and a protracted convalescence. A 
continuous rise with improving clinical symptoms indicates approaching convales- 
cence (Bassett-Smith). 

Complications. — The principal complications are hyperpyrexia, cardiac failure, 
and pulmonary congestion. Pleural and pericardial effusions sometimes occur, 
and persistent vomiting has been observed by Hughes, who regards it as a very 
dangerous complication. 

Fig. 47 



1 

_ 104 ° = 

jjj 103° : 

iio2°; 


lit 




44 1 1 1 -t— 
-- f ]' 


.--- 




■ ■ 


Ez-d-zz±±:z: 


Sg^^iFE 




ujl^-J-- 


1- if t - 


3:~~eW~ 


""i 


1 I~T~'i"r~i = 1 ==!= f 


: -——_-^l = '- 




"TTfE 


W O - 

j= 101 i 


fp~^S~ 




111/ If 


- 3E - \ 7 i 


- 




.. Sffi^ 




f - 44 




— '* : X / \ / \ IH"V ~fH 


~f IFiM f H 7 i RTl il~ f ~-l — 


=441 ; ^ ^ - ^\-/-\- 


=?s^TF^\{=' 


< 1UU _ 


tm^ 


_1 IJ.J_1_L1__T.J 1 l_M.I_l.l_»_l.j.l 1 I.I..L|_L J.l.J .1 .__ 


— -if — ■ — x — PJ ■ -/- -l-f- Vy~^ — \j- _ 




^i--^ 


l = |~l-FfM F-- if- |f frir"^ if - f HH | ifrH i ~tt 


"f\~f \ / :"• f ]J y 1 -5 — 1P- 




==U=t=t± 


m — tf-r-H — h : 111 U~"j[~ ttII Ir 11 ~\\"\l If If if ' 


rXI \i 1 ' 


'""i~;"ll~i~ 


H 98°- 




- BsEjE * ! Hi- j vl -JUH+KTif rrr 


1 -i-'iT-Hrhj- 


i 1 1 l ; -|- 


i-n-l-H 
— ^p 




==F^H- 




nfl-U4=={=p+ 




= = # 



Temperature chart in the intermittent form of Malta fever. (Hughes.) 

Treatment. — Malta fever has to be treated solely on the expectant method, for 
there are no specific remedies. The diet should be nutritious and supporting. 
Dalton, of the English navy, deprecates the practice of keeping Malta fever patients 
on liquid food. All his patients who do not have an evening temperature higher 
than 103° are put on solid food, such as eggs, bread, and rice, and in addition 
receive two or three pints of milk a day. If this diet is well borne, it is supplemented 
in the course of a few days by fish or meat. In severe cases with high temperature, 
foul tongue, and diarrhea, nothing but liquid diet is given. Dalton also believes 
that patients whose temperature keeps below 102° are benefited by being allowed 
to sit up part of the time, it being necessary, of course, to have them avoid exertion 
and not remain up too long. The bowels should be carefully regulated. Cold 
spongings with friction should be used to reduce fever and the kidneys be kept 
active by mild diuretics. When the patient is strong enough to travel, he is greatly 
benefited by change of climate. During the early stages of convalescence he 
should receive inunctions of oils and cocoa-butter, get plenty of fresh air and sun- 
shine, and receive aids to digestion, with iron to overcome his anemia, which is 
alwavs marked. 



PHLEBOTOMOUS FEVER. 

Phlebotomous Fever, sometimes called "Pym's Fever" or "three day fever" 
is met with in countries bordering on the Mediterranean, in the Sudan and in the 
Far East. It has been particularly frequent in the English troops in Malta, and 
in Dalmatia and Herzigovina in warmer months of the year. One attack confers 
immunity, although the disease rarely lasts over 3 or 4 days. The infection is 
produced by the bite of a sand fly, the Phlebotomous papatasii which feeds on blood. 
This fly becomes - infective seven to ten days after biting an individual suffering 
from the malady. The period of incubation is four to seven days. The virus 
passes through a Pasteur-Chamberland filter. Mosquito nets do not protect 
as their mesh will not obstruct so small a fly. The symptoms consist in headache, 
malaise, backache, flushing of the face, a foul tongue, infected conjunctiva and 
marked constipation. Recovery practically always occurs, the temperature 



ANTHRAX 219 

reaching normal by the third day, although in severe attacks the patient may feel 
weak and miserable for several days after the fever ceases. 
Treatment. — The treatment is purely symptomatic. 

ANTHRAX. 

Definition. — Anthrax is an infectious disease due to the presence of the Bacillus 
anthracis. It is much more common in Europe and in South America than in the 
United States and England, and affects animals far more frequently than man. 
While it is possible for one man to convey it to another by contact, the infection 
in the great majority of instances takes place directly from one of the lower animals. 
Among animals it is met with most frequently among herbivora, next among omni- 
vora, and least frequently among carnivora. Anthrax is sometimes called malignant 
pustule, splenic fever, charbon, and carbuncle. The first synonym is unfortunate, 
for in many cases no pustule is found ; the second synonym is incorrect, as in man 
the spleen is not particularly affected, and the last is equally erroneous, as it is 
an entirely different state from ordinary carbuncle due to the staphylococcus. 

History. — Anthrax as it occurs in man has been recognized for over 2000 years, 
and as long ago as the time of the Romans it was treated by the cautery. During 
the seventeenth and eighteenth centuries it was very prevalent. Barthelemy 
proved in 1823 that animals could be inoculated with it. In 1850 Heusinger 
published an accurate exhaustive account of the disease. The bacillus was observed 
in the blood by Pollender in 1849 and its relation to the disease was more fully 
worked out by Davaine in 1863. Since then this discovery has been confirmed 
by many observers, the chief of whom are Pasteur and Koch. 

Etiology. — As already stated, anthrax is due to the entrance into the body of 
the anthrax bacillus. It usually occurs as a result of handling some part of an 
animal which has suffered from this malady. Of Legge's 211 cases 72 were in 
workers in wool and 65 were handlers of hides. The infection takes place through 
some break in the skin, as a rule, and in the great majority of cases the site of 
inoculation is the hand or forearm, but it may appear on the face and chest. In 
Legge's series infection occurred in the neck in 84 cases, in the face and head in 77, 
forearm 16, and in but 1 case was the finger thought to be the point of infection. 
Sometimes more than one point of infection is present; but it occasionally happens 
that no external lesion is to be found, although general systemic infection is mani- 
fest. In such instances the bacillus gains access to the body by being inhaled 
in dust, or by being swallowed in milk or other food. Rarely infection of an external 
wound takes place by the transference of the bacillus by flies from an infected 
animal to the break in the skin of man or animal. 

Prevention. — The disease can be prevented in man by forbidding workmen to 
handle raw hides or infected animals if they have any superficial wounds, by the 
use of respirators designed to prevent the inhalation of dust laden with the bacillus 
of the disease, and by the disinfection of wool, hair, rags, and other articles of 
commerce which may convey the infection. 

All animals suffering from anthrax should be killed and then destroyed by burning. 
Mere burial is insufficient, for it is claimed that earth-worms are capable of carrying 
the bacilli to the surface and so causing the reinfection of healthy animals. When 
incineration is impossible burial in quicklime may be resorted to. It is needless 
to add that the utmost care must be exercised by physicians and nurses in dressing 
cases of this disease when it occurs in man. 

Frequency. — In the United States anthrax is not a very common disease, even 
among sheep and cattle, and is rarely met with in man. Inquiry among employers 
of men who handle raw hides in Philadelphia develops the fact that it is very seldom 
met with, and when it occurs is nearly always the result of handling imported hides. 



220 DISEASES DUE TO A SPECIFIC INFECTION 

Pathology and Morbid Anatomy. — The changes in the skin produced by primary 
external anthrax will be described later under the head of Symptoms. When 
systemic infection occurs as the result of either external or internal primary inocula- 
tions, very marked lesions of the viscera become apparent. The bronchial glands 
are generally swollen, and their increase in size may be quite remarkable. The 
pericardium may be dotted by petechial spots, and its cavity may contain a consid- 
erable quantity of gelatinous material. The muscles, including the heart, are 
dark colored, soft, and flabby. The blood is fluid and dark in hue — sometimes 
almost black. Clots may be found in the pericardial space. Clear, straw-colored 
fluid may be present in the pleural cavity, and if the lungs are affected they are 
found engorged with dark-colored blood, the right lung being more affected than 
the left as a rule ; the posterior portion is most congested and edematous, particularly 
at the bases. Sometimes pulmonary infarctions are present. 

In the abdominal cavity numerous extravasations of the blood may be found in 
the mesentery. Petechial hemorrhages may be present in the stomach and intes- 
tines. The spleen is usually enlarged and contains a large amount of grumous 
blood. Microscopic examination of the tissues of the body, when general infection 
is present, discloses the bacillus usually in large numbers. They are particularly 
numerous in the small bloodvessels and lymph glands which are near the site of 
the primary lesion. 

Symptoms. — Anthrax occurs in two forms, the external and internal. The 
external manifests itself by the development at the point of infection, about three 
to six days after contact with the source of the disease, of a small, itching papule, 
which is soon surrounded by an inflamed area. Usually this lesion is so insignificant 
that no attention is paid to it save the scratching or rubbing of it. There may be a 
history of an abrasion, scratch, or pimple through which infection has occurred. 
The papule speedily becomes red and angry-looking, and at its summit a vesicle 
develops which is filled with bloody serum. Around this centre of infection, on 
the reddened and edematous zone or base, additional papules and vesicles appear 
and the inflammatory process spreads rapidly in all directions. The vesicles may 
become dry and crusty, and as they do so the tissues underneath undergo softening, 
the central part becoming black and necrotic. Curiously enough, this rapid 
process rarely causes much pain, but the neighboring lymphatic vessels become 
reddened and the nodes enlarged. By the end of forty-eight hours after the papule 
first appears the anthrax bacilli may be found in the blood, and in such a case the 
symptoms of systemic disturbance rapidly become very marked. 

The local lesion rapidly spreads up the arm if the hand be the part first attacked, 
and the part becomes intensely swollen and livid, the skin being dotted by blebs, 
but it is a noteworthy fact that the rapid spread of the surrounding inflammation 
is due largely to secondary infection by other organisms. In cases of pure anthrax 
infection the central papule is often surrounded by an area of induration, but no 
red areola even after the slough has formed. There is general wretchedness and 
rapidly increasing debility, followed by rigors, high fever, sweats, and diarrhea, 
but after the early stages the fever falls and the temperature may be normal. 
Delirium rapidly ensues, and dyspnea and cyanosis, with profound evidences of 
septic infection, close the scene in death. In some cases, however, the mind 
remains perfectly clear. 

When recovery takes place the local area is walled off by protective efforts on 
the part of the body, so that severe constitutional symptoms do not appear. The 
diseased tissues at the focus of infection undergo necrosis, are thrown off, and 
healing is finally accomplished. 

A second form of external anthrax infection is that which, because of its course, 
is called malignant anthrax edema. This usually develops on the face or head and 
differs from the type just described in that no papule or similar local lesion is 



ANTHRAX 221 

present, but in its stead an intense edema of the tissues is produced. So active 
may be the local process that the parts may speedily slough or become gangrenous. 
Death usually comes rapidly to such cases. 

The internal form of anthrax manifests itself in the lungs or alimentary tract. 
In the first instance the anthrax bacilli enter the respiratory passages by inhalation 
in the dust arising from the handling of dried hides or wool. Hence it is called 
"wool-sorters' disease." The symptoms in these cases vary to an extraordinary 
degree in their severity. In some instances the patient feels wretched and miser- 
able, and soon has a chill which is followed by fever and very marked thoracic distress. 
There may be pain in the side and labored, difficult breathing. Cough may or 
may not be present. The face becomes livid, marked cyanosis develops, and the 
patient dies in a few hours or days in asthenia and collapse. Pneumonia is rare, 
but areas of impaired resonance on percussion and bronchial breathing may be 
found as the result of enlargement of, and pressure by, the bronchial and mediastinal 
glands. In other cases the symptoms are so mild and indefinite as to possess no 
diagnostic value. A workman may feel only weak and feeble, his hands may be 
cold, and his breathing oppressed, yet he may die within twenty-four hours in 
collapse. Bell records several cases in which death came within twenty-four 
hours of what seemed to be perfect health. 

When the intestinal tract is infected, there are present diarrhea, vomiting, great 
weakness, and failure of the circulation, followed by collapse and death in from two 
to five days. 

Diagnosis. — In the external form of the disease the occupation of the patient 
and the presence of an itching papule should at once arouse the suspicion of anthrax 
infection, which will be strengthened by the rapid formation of the vesicle already 
described. The diagnosis can be confirmed by a microscope examination of the 
fluid for the bacillus, or by inoculating a mouse with one drop of the fluid from a 
vesicle. This will cause the death of the mouse in about forty-eight hours, and 
in its organs the bacillus will be found in immense numbers, and from these cultures 
may be made. 

This condition is separated from carbuncle by the lack of pus and by the absence 
of its sloughing core. From erysipelas of the phlegmonous type, or from diffuse 
cellulitis, it is separated in the later stages by the absence of pain and fever. From 
malignant edema it is distinguished by the absence of crepitation due to gas in 
the tissues. Agglutination tests based on the same principle as the Widal test 
in typhoid fever have not been generally adopted. 

Prognosis. — The prognosis of the external form depends upon the degree of 
general systemic infection, and therefore the size of the local lesion has not any 
great importance in determining the outlook. It not rarely happens that a small 
papule may be followed by the death of the patient in a few days, whereas a larger 
lesion may be recovered from. Thus, Bell states that a patient with so severe a 
lesion on the face as to have large bullae and a free discharge of straw-colored 
fluid, with swelling of the entire head and the submaxillary glands, may recover. 
In other words, everything depends upon the degree of systemic infection. A 
rapid-running pulse is always an evil omen. 

Death may come as early as the first day of illness, but the majority of deaths 
occur on the fourth to seventh day. So far as mortality is concerned statistics 
vary very greatly, probably because of variations in the virulence of the infection. 
Thus, Woolmer states that out of 50 cases he lost only 2, and Muskett treated 50 
cases with one death; whereas in England, even when the workmen have been 
taught to present themselves for treatment at once, the mortality has been 21 
per cent., and in some collections of statistics it has reached 50 per cent. In 
Eppinger's epidemic among rag-pickers 78 out of 88 cases were fatal. 

In the internal form the prognosis is bad and death often comes, as already 



222 DISEASES DUE TO A SPECIFIC INFECTION 

stated, as early as twenty-four hours after the primary symptoms. Cases in 
which recovery has taken place are, however, on record. 

Treatment. — The treatment of the external form consists in the destruction by 
actual cautery of the primary focus of the disease at the earliest possible moment. 
If this is not done it should be excised. Not only should the infected tissues be 
removed, but the surrounding tissues for at least an inch as well. As soon as this 
is done the part is to be swabbed with pure carbolic acid and then dressed, so that 
drainage into the dressings may occur. The patient's vitality should be main- 
tained by good food and stimulants, and anthrax antitoxin should be given. 

Within the last few years an anti-anthrax serum has been employed with success. 
Legge states the following facts as to its use: (1) In very large doses it is innocuous; 
(2) it can be well borne even when introduced into the veins; (3) no case taken in 
an early stage, or of moderate severity, is fatal if treated with serum; (4) with the 
serum some cases are saved when the condition is most critical and prognosis 
almost hopeless; (5) when injected into the veins the serum quickly arrests the 
extension of the edematous process so as to reduce notably the danger from suffo- 
cation which exists in many of the cases where the pustule is situated on the face or 
neck; (6) the serum, if used early enough, reduces to a minimum the destruction 
of tissue; (7) in some situations of the pustule, as the eyelid, serum must be used 
in preference to any other treatment; (8) persons attacked, when treated with 
the serum, appear to become convalescent in the course of a few hours; to these 
I may add (9) that in internal anthrax if it is administered intravenously it is 
the only treatment which can hold out any hope. 

In almost all cases injection of the serum is followed by a rise in temperature 
often to over 105°, and with this there is an improvement in the general condition 
of the patient. The prognosis where there is this rise Sclavo regards as favorable. 
In the same way the necrotic process itself is to be regarded as a sign that the 
organism is making effort to resist the anthrax infection. 

HYDROPHOBIA. 

Definition.— Hydrophobia is an acute infectious disease of animals communi- 
cable to man, the specific cause of which has not as yet been isolated, but which is 
without doubt a micro-organism. It is characterized by great restlessness and delir- 
ium, by an apparent dread of water in some instances, and by delirium and para- 
lysis in its later stages. It is often called "rabies" or "lyssa." 

History. — Hydrophobia was well described as long ago as nearly 500 B.C. by 
Democritus, but not until about 200 years B.C. was it described in man. Since 
then it has been discussed by many ancient and modern writers, of whom Gruner, 
in 1813, found that the saliva was the vehicle of infection. 

Trousseau wrote its best description in modern times in 1850. In 1882 Pasteur 
first clearly discussed the cause of the disease and devised a plan of rational 
treatment. 

Distribution. — No less an authority than Virchow believed that hydrophobia 
was not to be met with in Greenland, Denmark, Africa, and parts of Asia and 
South America, and with others claimed that it is peculiar to temperate zones, 
but in 1860 an epidemic occurred in Greenland among animals when the tempera- 
ture was 25° below zero. Boulanger is probably correct in stating that no part 
of the world is free from it. The idea that it is more prevalent in summer than in 
winter is erroneous. Suzor has reported twice as many cases in animals in March, 
April, and May as in the summer months. Two-fifths of all cases in human beings 
are under fifteen years of age. The disease affects dogs, skunks, foxes, and wolves 
more commonly than other animals, but all animals are apparently susceptible to 
it. Cows may develop it from dog-bites or from bites of other infected cows, and 



HYDROPHOBIA 223 

in 1888 I saw a number of deer from the royal herd in Richmond Park, near 
London, which suffered from this disease and which were studied at the Brown 
Institution. 

Etiology. — As already stated, the cause of this disease has not been determined 
with certainty, although recently Negri claims to have established that it is due 
to a protozoal organism. These are known as Negri bodies. They are round or 
oval in shape, 10 to 25 microns in diameter, and are almost always intracellular. 
They are found especially in the pyramidal cells of Amnion's horn but also occur 
in the cerebellum and the large cells of the cerebrum. Watson pictures sexual and 
asexual phases of these bodies and places them, as protozoal parasites, in the sub- 
order of cryptocysts of the sporozoa. Some observers believe these bodies are 
reaction products of cells and contain the real cause of the disease either in the 
shape of the chromatin portion or as structures yet undemonstrated. Filtration 
studies lend some weight to the view that the virus may be ultramicroscopic. 
It is known that its cause has a special affinity for the nervous system, and is 
found in the saliva, but not in the urine or the blood. The disease can be passed 
from animal to animal, from an animal to man, and from man to an animal, and 
it can be passed on from one to another without rapidly losing its virulence. The 
transfer is always made through some solution of continuity, usually a bite, but it 
has occurred through a pimple. The milk of animals suffering from rabies is 
capable when inoculated into the tissues of healthy ones of inducing the disease 
but not when taken as a food. 

In the dog it has been proved that the saliva may be virulent as long as three 
days before any symptoms of the disease appear. 

The incubation period varies greatly, from a week to several months. In man 
it is from fifteen to sixty days, but cases are on record in which it has developed 
after a year has elapsed, probably because the virus has been temporarily encap- 
sulated. A bite received as long as two days before the development of symptoms 
in an animal is rarely, if ever, infectious. The period of incubation is much shorter 
when the bite is on the face than when it is on the hand. 

Prevention. — The only efficient measures of prevention are the universal muz- 
zling of dogs, particularly when a mad dog is known to have been in the neighbor- 
hood, and the killing of all animals found suffering from the disease. In London 
the muzzling of dogs decreased the disease from 176 cases in dogs in 1889 to 3 in 
1892, but on relaxation in enforcing the law the number of cases in dogs and man 
rose again to about the original number. "If all rabid dogs could be prevented 
from biting other animals, rabies would in the course of a year be a mere historical 
curiosity of medicine, an illegitimate field of research for the investigator in pure 
pathology." (Stimson.) (For preventive inoculation see Treatment.) 

Frequency. — Hydrophobia is riot a common malady in animals, and is rare, 
comparatively speaking, in man. Sporadic cases are met with in animals in every 
large city during the year. (See Bulletin 449 of the U. S. Department of Agricul- 
ture, 1911, by Mohler.) Woodhead states that only about 16 per cent, of those 
bitten by rabid animals become victims of the disease. 

Pathology and Morbid Anatomy. — It has been generally stated that there is 
nothing pathognomonic in the morbid anatomy of rabies, but this is only true 
of macroscopical appearances. Examined microscopically the medulla and spinal 
cord show small hemorrhages and large numbers of small round cells in the peri- 
vascular lymph spaces and around the motor ganglia cells, and progressive degen- 
erative changes in the spinal nerve cells appear, consisting in chromatolysis and 
overgrowth of the nucleolus. These changes are, however, by no means pathogno- 
monic, as they may be found in other diseases. 

Van Gehuchten and Nelis have, however, discovered changes in the peripheral, 
cerebral, and sympathetic ganglia, in the intervertebral ganglia, and in the plexi- 



224 DISEASES DUE TO A SPECIFIC INFECTION 

form ganglia of the pneumogastric nerve, which they consider to be diagnostic of 
rabies. These changes consist in the destruction of the nerve cells by newly formed 
cells from the capsule. The rabic tubercle of Babes is an accumulation of embryonal 
cells around the nerve cells. The cells of the bulbar nuclei undergo degeneration 
and manifest various stages of chromatolysis. As a diagnostic sign both of these 
have been largely discarded in favor of the Negri body. 

Symptoms in Animals. — The symptoms of rabies in animals vary greatly. In 
the dog we find that he is at first stupid and heavy and often cross and restless. 
When he stands up he may sway slightly and stagger when he runs. At this time 
he is easily frightened and his reflexes are acutely increased. He usually refuses 
food and drink, but will often gulp down all sorts of substances not food, such as 
rags, manure, and pieces of wood. Even at this time he may be obedient, and 
may not bite his master, although he will snap at a stranger. The bark is muffled 
and peculiar, and may be a series of yelps or howls, the lower jaw never completely 
closing as in health. Thirst may be manifest, but though the animal may lap the 
water, spasm of the throat prevents swallowing. The idea that a mad dog has a 
peculiar dread of water is erroneous. Any repulsion he may have to it is due to the 
spasm of the gullet. 

He next becomes delirious and maniacal, galloping or swiftly trotting, with a 
slouching demeanor, as if shrinking from some enemy. The jaws are usually open, 
and the saliva may flow freely from the mouth. Some amblyopia may develop 
so that he is prone to run into objects which should be easily avoided. This may, 
however, be due to stupidity or muscular inco-ordination. Sometimes he seems to 
see imaginary objects and snaps at them. Rapid emaciation is a noteworthy 
symptom. Finally, the animal becomes more feeble and paralyzed. The paralysis 
is gradual in onset. The hind legs are at first moved with difficulty and finally the 
animal sinks on his haunches, there being a simultaneous loss of power in the fore- 
legs, upon which, however, he can occasionally raise himself. During this period 
convulsions may ensue. Death occurs on the fifth or sixth day as a rule, but life 
may be prolonged until the eighth day, but never longer than the tenth day. 

In some cases, probably in those which are very severe, the paralysis may develop 
almost at once. 

Animals sometimes manifest symptoms of what is known as "dumb rabies," 
which is to be distinguished from the maniacal form. In this condition the lower 
jaw is dropped and the animal is unable to close the mouth. The tongue hangs 
out and the saliva dribbles. As the jaw is paralyzed the dog is unable to bite, 
and does not attempt to do so. This form usually causes death in about two to 
four days. It is important that these manifestations of dumb rabies be remembered. 
Dr. Gill, a veterinary surgeon of New York, asserts that this is a very common 
form of the disease, which frequently misleads persons into thinking that the dog 
has a bone in its throat. They are still further deceived by the fact that the animal 
has no hydrophobia and not infrequently actually plunges his head into water, 
or will even swim a river. He adds as additional advice: "Beware of a dog when 
it becomes dull and hides away, appears restless, is always on the move and prowl- 
ing, whose countenance is sombre and sullen, and which walks with his head down 
like a bear. Beware of one which barks at nothing when all is still. Beware of 
the dog that barks incessantly and tears up things. Look out for the dog which 
has become too fond of you and is continually licking your hand and face; and 
beware, above all, of the dog which has difficulty in swallowing, which appears to 
have a bone in its throat, and of one which has wandered away from home and 
returns covered with dirt, exhausted and miserable." 

These symptoms in the dog have been described in detail because a correct diag- 
nosis of the malady in the dog is of vital importance in determining whether a 
patient is to be a victim of rabies and if he should be given Pasteur's treatment. 



HYDROPHOBIA 225 

Cats with rabies usually hide under pieces of furniture and spring suddenly 
into the face of a passerby, scratching and clawing any exposed part. 

Symptoms in Man. — It is usually shorter in young children than in adults. At 
the end of the period of incubation the part infected begins to itch and tingle 
and then to burn. The skin in its neighborhood may develop vesicles, and the old 
wound may open. 

The primary systemic symptoms in man are apprehension, restlessness, and 
finally marked anxiety. This is followed by thirst, but when the water is brought 
near the patient he seems to have great fear of it — hydrophobia. This fear is 
chiefly due to the pharyngeal spasm, which is produced at the sight of water, which, 
if the patient tries to swallow, becomes exaggerated. This spasm is the most 
pathognomonic symptom of rabies in man. 

This stage lasts about five days and is followed by the stage of excitement, with 
labored respirations and spasm of the laryngeal and pharyngeal muscles. The 
reflexes are greatly exaggerated and delirium or mania may come on. Occasion- 
ally the jaws may be snapped together, although snapping is said to be characteristic 
of false rabies. Very commonly the curious symptom of spitting develops, the 
patient ejecting small quantities of spittle upon surrounding objects. 

If the patient survives the convulsive stage paralytic symptoms, exhaustion, 
and death follow. 

Diagnosis. — It is only in the early stage of the disease in either the animal or 
man that any difficulty can exist as to its diagnosis. As the saliva of a dog for 
several days before it seems very ill is virulent, all sick dogs, ill of unknown causes, 
should be regarded with suspicion or caution. In man the history of having been 
bitten will usually be obtainable. An animal which bites and is suspected of rabies 
should not be killed at once but carefully imprisoned and watched to determine the 
true nature of the disease. 

Occasionally a hysterical person, after reading or hearing a description of rabies, 
develops symptoms which resemble it. The fact that the patient is of this type, 
and that threats, or inhalations of amyl nitrite, speedily cure the ailment will 
permit a differentiation. This state is called pseudohydrophobia or lyssaphobia. 
It is important to remember that symptoms of pseudohydrophobia or hysteria 
simulating the true disease often develop as early as twenty-four or forty-eight 
hours after exposure; whereas true hydrophobia rarely develops in less than four- 
teen days. Again, the hysterical patient often presents the symptoms of the second 
convulsive stage, without having shown any primary symptoms. He is apt to 
show a disposition to bite, which is very rare in true human hydrophobia, and if 
he barks, growls, or snaps it is an imitation and not the true disease. Finally, 
should the patient survive for a period of active symptoms longer than ten days 
the case is probably hysteria. 

True hydrophobia is to be differentiated from tetanus by the presence of marked 
lock-jaw in the latter disease, and by the fact that in tetanus there is no dribbling 
of saliva and no expression of terror. The convulsions in true hydrophobia are 
rarely as tonic as in tetanus. The paralytic form of rabies may resemble Landry's 
paralysis. 

Prognosis. — No case of recovery has ever been reported in which there was 
undeniable evidence that the diagnosis was correct. 

Treatment. — The treatment of hydrophobia is entirely in the line of preventive 
medicine, for, once the disease is developed, curative measures are not possible. 
As soon as the bite is received the wound, if a punctured one, should be washed 
and then sucked and the spittle expectorated. If the part injured be an extremity 
a tourniquet should be used until this is done. The punctured wound should be 
converted into an incised wound, and the opening should not be closed, but given 
free drainage and kept open, well protected from other infection, for several weeks. 
15 



226 DISEASES DUE TO A SPECIFIC INFECTION 

Where possible, without great mutilation, the part should be excised as is now 
recommended for the prevention of tetanus. The value of caustics depends on 
the one employed. Fuming nitric acid is one of the best and may be wisely used 
even if several days have elapsed since the bite. Formaldehyde solution is also 
useful. If the wound is incised, well washed with normal saline or with bichloride 
of mercury, real tissue destroyers may be set aside. 

The specific and rational method of treatment is that proposed and instituted 
by Pasteur by means of attenuated virus. This investigator found that if the virus 
of hydrophobia is propagated, through the inoculation of a series of rabbits, it 
increases in virulence, and the spinal cords of the rabbits of the last series of inocu- 
lations contain the poison in a very active state. If these spinal cords are preserved 
under certain conditions this degree of virulence progressively diminishes. If an 
emulsion be made from the attenuated cords and a dog inoculated with it in small 
amount the animal survives, and if successively inoculated with virus of increasing 
virulence gradually becomes immune as larger doses are given, until he is able to 
stand inoculation with the most virulent matter obtained from the cords of rab- 
bits. This same process is now employed for the treatment of a man who has been 
bitten, the endeavor being made to produce an artificial immunity before the stage 
of incubation following the bite is completed. 

Out of 17,395 cases treated at the Pasteur Institute in Paris in this manner 
between 1886 and 1895 there were 139 deaths from rabies. If the average mor- 
tality after inoculation is in the neighborhood of 20 per cent., as already stated, 
it is evident that instead of there being 139 deaths there would have been approxi- 
mately 3476 deaths, which shows the great value of the plan. As the treatment 
is absolutely harmless if properly employed, the value of Pasteur's method can- 
not be doubted. It is, of course, useless after the malady is well developed. 

Two methods of producing immunity to hydrophobia are now employed. One 
is known as the "simple" and the other as the "intensive." In both methods 
spinal cords of infected animals are employed in gradually increasing strength 
until finally what is known as a three-day cord — that is, one which has been kept 
three days — is administered subcutaneously. In the "simple" method nineteen 
injections are given in fourteen days. 

In those cases which have severe lacerated wounds of the face, in which not only 
infection has taken place, but the tissues have been devitalized by traumatism, the 
"intensive" method is used. This consists in the administration of twenty-eight 
injections in twenty-one days. During the first three days as many injections are 
given in the "intensive" method as are given in five days by the simple method. 

Cumming describes a method of treatment devised in the Pasteur Institute 
of the the University of Michigan. A vaccine is prepared by dialyzing a sus- 
pension of rabic brain against running distilled water. Two c.c. of this is given 
daily for fifteen to twenty-five days, depending on the type and severity of the 
lesion. A local reaction on the seventh or eighth day and lasting for twenty-four 
hours is not uncommon. This vaccine protects animals against 8 M. L. D. (mini- 
mum lethal dose) while the Pasteur material protects against only 2. It has 
been given to more than 800 persons, 62 per cent, of whom had been bitten by 
animals proven to have been rabid, without the development of a case of rabies. 
This so-called vaccine appears on the market in packages containing seven doses 
in syringes ready for use. Twenty-one doses are needed in every case, given over 
the space of twenty-one days. The injection is given as is antidiphtheritic 
serum. 

This antirabic vaccine should always be used in preference to the attenuated 
virus originally devised by Pasteur. 

After the disease is established care must be taken that the patient does not 
wound his attendants. His sufferings should be relieved by morphine or chloral 



TETANUS 227 

in sufficient doses to spare him from much misery. Nutrient enemata may be 
used to help support nutrition if food cannot be swallowed. 

Efforts have been made from time to time to provide an antirabic serum, but so 
far without success. 

TETANUS. 

Definition. — Tetanus is an acute infectious disease due to the entrance and 
development in the body of a specific organism, the bacillus of tetanus. It is 
characterized by the development of rigidity of the muscles so that the limbs are 
fixed and the jaw locked. 

History. — Tetanus has been known for many centuries as a disease that occa- 
sionally follows small wounds, but it was not until 1884 that Carle and Rattone 
discovered that when an animal showed symptoms of tetanus it was possible to 
produce similar symptoms in healthy animals by injecting virus obtained from 
the first. In 1885 Nicolaier obtained from the pus of infected animals, bacteria 
which, when inoculated into healthy animals, caused tetanus, but he was unable 
to isolate the organism absolutely, although he described it as a small, slender 
bacillus. In 1886 Rosenbach confirmed Nicolaier's discovery, but he also did not 
get a pure culture of the bacillus of the disease. In 1889 Kitasato, Tizzoni, and 
Cattani succeeded in its complete isolation. Faber also proved that he could 
obtain from a culture of this bacillus a toxin which, when injected into animals, 
caused symptoms identical with those met with in human beings suffering from 
this malady. 

Distribution. — Tetanus is met with everywhere in tropical and temperate zones. 
Its bacillus is particularly prevalent in garden soil and about stables and dungheaps. 
In the United States it is most prevalent in Louisiana, New York, Pennsylvania, 
Texas, and Ohio in the order named. Wells has shown that the curve of deaths 
in this disease starts in May, reaches its highest point in July, and then declines 
to October. 

Etiology and Frequency. — The specific organism, the Bacillus tetani, is 4^ to 
5jjl in length and about 0.4^ wide; during sporulation one end enlarges giving the 
organism a drumstick appearance. This bacillus is an anaerobic, slightly motile, 
flagellated rod, possessing unusually resistant spores and the faculty of producing a 
highly poisonous toxin. It is frequently demonstrated in discharges from wounds in 
cases of tetanus, and has been found on the object producing the wound and in 
freshly made wounds. 

The chief causative factor in tetanus is the presence of a wound through which 
the specific germ may enter the body. This wound may be so insignificant as to 
be overlooked. In other cases the infection takes place through a break in the 
mucous membrane of the mouth. I have seen it follow an operation for piles, 
the bacilli being in the stools from infected food. Accidents of this type prob- 
ably account for the cases of so-called idiopathic tetanus. Small, punctured 
wounds are much more apt to result in the development of the disease than 
large ones with free drainage, for the accumulated necrotic tissues of punctured 
wounds afford approximately ideal conditions for the development of the anaerobic 
bacillus. Within the last few years several outbreaks of tetanus have followed the 
use of contaminated vaccine. 

Tetanus is not a very common disease, but nearly every large hospital service 
has presented to it occasionally an isolated instance. It has been epidemic in 
many hospitals and camps; it has also been epidemic among newborn infants, 
infection taking place through the umbilicus and causing a frightful mortality, par- 
ticularly in the West Indies, where at times more than 60 per cent, of all children 
born died within eight days after birth from its ravages. In this country it is seen 
in hostlers, gardeners, agricultural laborers, men employed about stables, and in 



228 DISEASES DUE TO A SPECIFIC INFECTION 

children who run about with bare feet. By far the most common Incidence of the 
disease occurs in children who suffer from wounds produced by toy pistols and 
fire-crackers. As many as 466 cases of this disease were due to these causes in 
the celebration of the Fourth of July in 1903 in the United States; but it is interest- 
ing to note that owing to the warning issued by medical men against the use of 
these explosives the number of deaths due to this cause has been reduced to 
almost nil. 

Incubation. — The incubation period is one to twenty days, but the maximum 
number of cases occur after seven days. 

Prevention. — Tetanus is to be prevented by the excision or conversion of all 
punctured wounds into incised wounds, washed out with 3 per cent, tincture of 
iodine followed by hydrogen peroxide, packed with gauze laden with a dusting 
powder made of powdered antitoxin serum and provided with free drainage; by 
the use of tetanus antitoxin as soon as the wound is received, and, if the disease 
develops in a hospital or camp, by the careful isolation of those who are ill with it. 

The measures taken to destroy the bacillus and its spores outside the body, 
as in dressings and clothing, must be very radical, because the spores are extra- 
ordinarily resistant to those measures usually employed to destroy pathogenic 
germs. Thus, the spores can survive two hours' exposure to corrosive sublimate 
1 : 1000, and even survive exposure to boiling water if the exposure is brief. So, 
too, fifteen hours' treatment with 1 : 20 of carbolic acid is necessary to destroy 
their vitality. Drying does not kill the bacillus. Miguel has produced the disease 
from infected soil kept for eighteen years. 

Pathology and Morbid Anatomy. — A most important fact to be remembered in 
regard to tetanus is that the specific organism primarily does not spread through 
the body, but develops at the site of infection, and from this focus the toxin which 
produces the symptoms of the malady is disseminated. It has been proved by 
Meyer and Ransom that the poison passes to the central nervous system through 
the axis-cylinders of the motor nerve trunks and lymph channels. Another fact 
of importance is that the toxin combines with the cells of the nervous system with 
remarkable celerity, and having done so forms so firm a combination that it can- 
not be dislodged, and in consequence the subsequent use of antitoxin often fails. 

The tetanic convulsions are not due to any influence of the poison on the nerves 
or muscles, but upon the spinal cord and brain. 

In cases of death from tetanus there are no characteristic changes in the tissues 
of the nervous system. 

Symptoms. — The symptoms of tetanus are so characteristic that they can hardly 
be mistaken for any other disease save hysteria and strychnine poisoning. The 
dominant symptom is the state of rigidity of the voluntary muscles, which, when the 
disease is well developed, are practically constantly contracted, although at inter- 
vals they relax and contract spasmodically, causing the well-developed convulsions 
of the disease. It is a curious fact that the earliest symptoms often emanate from 
the muscles nearest the focus of infection, but very commonly they originate in the 
muscles of the jaw and neck, producing the symptom called "lock-jaw," that is, 
a state in which, by reason of the spasm in the masseter muscles, the lower maxilla 
is firmly pressed against the upper jaw. 

The contraction of the facial muscles in the spasm gives the face a peculiar 
expression of painful mirth, or risus sardonicus, and it is a noteworthy fact that 
this expression may be the first warning of an oncoming attack of the disease, for 
as the patient attempts to show his tongue to the physician who is inquiring as 
to his general health, the physician is startled to see the facial muscles produce 
this strange expression. 

The muscles of the back and abdominal wall are rigid to the touch, and pain 
and oppression due to spasm of the diaphragm may be present when the disease is 



TETANUS 229 

» 

well developed. The muscles 'of the hand ^are the least affected of all the volun- 
tary muscles, as a rule. 

If the more powerful muscles contract forcibly the patient's body is arched, 
resting on his heels and the occiput; this is called opisthotonos. If the muscles 
of the anterior part of the body are the more powerfully contracted he may be 
arched forward— emprosthotonos. 

Pain in the affected muscle is not severe as a rule, but is rather the aching due 
to prolonged strain and weariness. Sometimes, however, it is severe. There may 
be alarming spasm of the glottis or fixation of the respiratory muscles endangering 
life, and, indeed, in severe cases, this is the cause of death, particularly when, by 
reason of exhaustion, the patient is unable to withstand asphyxia for any length of 
time. 

The mind usually remains clear till the time of death. The temperature is 
moderate if the convulsions are moderate, and high if they are severe, ranging 
from 100° to 106°. The pulse varies in speed, becoming rapid during a seizure. 
Finally it becomes feeble from exhaustion. 

Diagnosis. — Tetanus rarely is as sudden in onset as is strychnine poisoning, 
and it very rarely causes death so rapidly. It affects the muscles of the face primar- 
ily, which strychnine very rarely does. There is usually a history of punctured 
wound in one case or of the ingestion of poison in the other. In strychnine poison- 
ing the convulsions are followed by periods of complete relaxation, whereas in 
tatanus constant spasm is present with exacerbations. 

In hysteria the ecstatic facies of the patient, the presence of clonic movements, 
the fact that the patient is a woman of a neurotic type, and that laughing and cry- 
ing are often present, aid greatly in the diagnosis. Further, areas of anesthesia 
are often present in hysteria and inhalations of nitrite of amyl may cause relaxa- 
tion, followed by sobs and tears as the spasm is relieved by the drug. 

Tetany rarely presents such severe contractions, but it may do so. The spasms 
are often localized, and if they occur in children signs of rickets or gastric dilatation 
may be present. Tetany practically never causes death, and it affects chiefly the 
hands and feet, which tetanus does not. 

Prognosis. — The prognosis in tetanus depends very greatly upon the severity 
of the paroxysms and upon the virulence of the infection. In virulent infections 
death comes as early as the second day and usually by the sixth. Hippocrates 
said, "The patient dies in four days, or if he passes these days he lives. " It is 
essential that two forms of the disease be recalled in studying this question. There 
is an acute form with a very high mortality of 80 per cent., and a chronic form 
in which recovery takes place in a large percentage, about 50 per cent. So, too, 
the shorter the period of incubation the worse the prognosis. Hill has shown that 
not until the tenth day does the patient have an equal chance for life or death. 
After the eleventh the prognosis constantly improves. The mortality is very 
high in children in all cases. An opinion as to recovery must be given with caution, 
for death often comes when recovery seems assured and recovery takes place when 
the condition seems hopeless. 

Treatment. — Before everything else in the treatment of tetanus must be con- 
sidered the use of tetanus antitoxin in the form of antitetanic serum or antitetanic 
globulin, the latter preparation making a less bulky dose, even after it has been 
dissolved in water or normal salt solution. Its value, however, is chiefly limited 
to those cases in which it can be administered as soon as the inoculating wound 
occurs, or within a short time after this. Its failure to be of value when employed 
after the symptoms are well developed is not due to any lack of power on the 
part of the tetanus antitoxin, but to the fact that the tetanus toxin so rapidly 
and firmly combines with the nervous protoplasm of the brain and spinal cord 
that it is impossible for it to be disassociated from this protoplasm, and therefore 



230 DISEASES DUE TO A SPECIFIC INFECTION 

the antitoxin cannot combine with it and prevent it from damaging the central 
nervous system. 

When children are wounded by means of toy pistols tetanus antitoxin should be 
injected at once, since the proportion of cases in which tetanus develops from this 
injury is very large, and by the prompt administration of the remedy the disease 
may be prevented from producing its characteristic symptoms. Thus in 1903, out 
of 56 cases of so-called Fourth-of-July tetanus treated without antitoxin 16 died, 
whereas in 1904, out of 36 cases treated with antitoxin none died. In 1216 cases of 
tatanus treated by antitoxin, Packard and Wilson found that the mortality was 
42.2 per cent., and Moschowitz in 461 cases treated in this way found a mortality 
of 40.3 per cent. As the death rate of acute tetanus is about 80 per cent, and of 
chronic tetanus about 50 per cent., it is evident that antitoxin saves many lives. 
Even after tetanic symptoms have developed tetanus antitoxin should still be 
used, and should be given intravenously in the dose of 20,000 units daily or by 
spinal puncture in the dose of 6,000 daily. 

A suggestion has been made that in severe cases the patient be trephined and 
the antitoxin injected by the hypodermic needle between the membranes of the 
brain or into a cerebral ventricle. It does not seem that this measure offers suffi- 
cient promise of usefulness to justify so serious a method of treatment, as intra- 
spinal injection is equally useful. The needle should be introduced according to 
the directions given in the article on Cerebrospinal Meningitis, and proof that 
it has entered the membranes of the cord assured by the discovery that a few 
drops of cerebrospinal fluid drip from its external orifice. The syringe containing 
the tetanus antitoxin is then attached to the needle and the injection is made. 
According to Luckett it is best to withdraw a considerable quantity of cerebro- 
spinal fluid before injecting the antitoxin. Antitoxin should also be injected into 
the nerve trunk supplying the part of the body through which the infection is 
threatened, because the infection spreads along the nerve. 

The wound, by means of which tetanus infection has possibly taken place, 
should, if small, be excised, or if it is large it must be thoroughly cleansed first 
with normal salt solution. No antiseptic is to be employed as it is useless and 
interferes with the vitality of the tissues with which it comes in contact. The 
vitality of these tissues is of greater value in protecting the individual against in- 
fection than are the ordinary antiseptic drugs. If the wound is a punctured wound, 
it should be converted into an incised wound in order that the tetanus bacillus 
may be thoroughly washed out of it and that free drainage may be provided. 
This is exceedingly important. Nothing aids in the production of tetanus so 
certainly as the closure of such a wound in its early stages. Adhesive strips or 
collodion are death-dealing; keep the wound open. Wounds should be allowed to 
heal by granulation, as this is the surest way to prevent the development of the 
disease. 

The patient must be fed with nutritious and easily digested foods in order that 
his nutrition may be maintained. In the rapid type of tetanus death usually comes 
so soon that great emaciation does not occur. But in the more chronic form the 
question of nutrition must be constantly kept in mind. 

If the jaws are so locked that food cannot be introduced into the mouth, one 
or more teeth should be removed in order that a stomach-tube may be passed, 
or a rubber tube may be passed by way of the nostril, as in feeding insane patients 
who refuse to take nourishment. Humphrey has gone so far as to recommend 
in these cases that a gastrotomy be performed, the tube introduced, and the 
patient nourished through the operative wound. This seems, however, an unneces- 
sarily heroic method when the tube can be used. 

The severity of the tetanic seizures can be to some extent modified by the ad- 
ministration of full doses of chloral and the bromides, which act as sedatives to 



GLANDERS 231 

the motor and sensory portions of the spinal cord. These remedies are, however, 
in no way curative, but simply symptomatic in that they diminish to some extent 
the force of the convulsions without in any way influencing the deleterious influ- 
ence of the poison upon the system. 

Meltzer has shown that the injection of 1 c.c. to each 25 pounds of body weight 
of magnesium sulphate solution in the strength of 25 per cent, materially reduces 
the convulsions, but it is not a cure. It possesses the danger of respiratory failure 
and may be difficult of performance because of spasms. Chloretone seems to 
be of undoubted value; 30 to 60 grains may be used by rectal injection as a means 
of controlling convulsions, producing sleep and preventing exhaustion. 

Care should be taken that the activity of the kidneys is maintained by the 
administration of mild diuretics and by providing the patient with plenty of water. 
The state of the bladder should also be watched, as retention of urine is not un- 
common. To prevent this, repeated catheterization should be resorted to. 

Under the name of "Kopf -tetanus," or head tetanus, a modified form of the 
disease sometimes occurs. It is said to be particularly apt to take place after 
injuries to the face. In these instances the spasm is chiefly confined to the muscles 
of the neck and face, but often extends to the abdominal muscles, and there is 
frequently spasm or paralysis of the glottis, which not rarely becomes a most 
serious symptom. In some instances the disease gradually spreads until it becomes 
like an ordinary case of tetanus. It is to be treated by the employment of anti- 
toxin and other antitetanic measures. 

GLANDERS. 

Definition. — Glanders is a disease which is usually met with in the horse, but 
it* may also affect man. It is due to the presence of the Bacillus mallei. When 
it appears as nodular masses in the nostrils of the horse it is called "glanders." 
but when these nodules are in the skin it is called "farcy." Analogous types 
occur in man. 

Etiology. — The Bacillus mallei is usually conveyed to man while caring for a 
horse suffering from glanders, and enters his body through some break in the skin. 
It may also find its way into the system by way of the nasal mucous membrane. 
Rarely one person is infected by another by contact or through a wound. The 
bacillus is a slender organism, somewhat thicker in proportion to its length than 
the bacillus tuberculosis, with rounded ends. It is easily stained with aniline dyes, 
but is equally readily decolorized by feeble acids or alcohol. It can be readily 
cultivated outside the body. 

Pathology and Morbid Anatomy. — The Bacillus mallei produces a circumscribed 
infiltration of the tissues with accumulations of leukocytes and connective-tissue 
cells, which resemble macroscopically small miliary tubercles, but, as Baum- 
garten has shown, these nodules histologically occupy a position midway between 
tubercles and miliary abscesses. The surrounding tissues are infiltrated with 
blood or show many, or few, petechial extravasations. After a short time they 
undergo necrotic changes, and as they break down abscesses are formed, which 
by necrosis of the overlying tissues are changed into ulcers, which may be super- 
ficial or deep. Like tuberculosis, the infection tends to spread along the lymphatics 
and eventually the bacilli may reach the blood and be distributed in the viscera, 
causing nodules in various organs. Such nodules occur in the testicles, lungs, 
spleen, liver, and kidneys, and sometimes the bones are affected causing an osteo- 
myelitis. 

When the nodules break down secondary infections perpetuate the suppuration, 
the specific bacilli become much diminished, and it may be impossible to discover 



232 



DISEASES DUE TO A SPECIFIC INFECTION 



them by staining, because at this period they lose their property of being readily 
stained. 

Symptoms. — Acute glanders develops, in about four days after inoculation, 
with general ivretchedness, some fever, and the appearance at the site of infection 
of a circumscribed red swelling. This is followed in a few days by breaking down 
of the granulomatous mass, in ulceration of the nasal mucous membrane, and the 
discharge of mucopus from the anterior nares. Secondary infection of the lymph 
glands in the neck may occur, and if the process is severe the nose may become 
necrotic. Cough and dysphagia may be present. Upon the face and about the 
joints there develops an array of papules which as they become pustules may very 
closely resemble the eruption of smallpox. A septic pneumonia often comes on. 

Fig. 48 




■: .:: 



yy, ^^%^lfe 11; * &>W$i$$$& 1 

4 :?y: v- ' ; :-. ;: - : • ■;•■■■■• y^->&:\^ - s *. **■ '■■'■- 

^S - y : s^r' 1 •• ■** : ^" : b>^»^B^S^i""'-r'X-C: J^m^^ 

•.■■>-:■■-•?<:■■ ;.:■•. : 

*■ 



11 







■\' ; V"'VV''>:;^r^v:^:.'" 



•i ■ ■■ - . ■ ,-.. ■ ■■ .. : ■■■■; 

'■■.■■ ■■■■■■;' 



Character of the cutaneous eruption in human glanders. The variation in size and general lack of 
umbilication are noteworthy points in differentiating it from that of smallpox. On account of shrinkage 
the skin and pustules appear more wrinkled than they did before removal from the body. (Photograph, 
natural size, by Roman Mercado, assistant photographer of the Bureau of Animal Industry, U. S.) 

Death comes to such cases almost invariably by the end of a week or ten days. 

In rare instances the process becomes subacute or chronic, and the nasal dis- 
charge, unless accompanied by the severe symptoms described, may make a diag- 
nosis difficult, if not impossible, by the ordinary methods of observation. 

When the inoculation is by the skin, producing farcy, the same acute localized 
swelling takes place and the neighboring lymphatics become inflamed and swollen. 
Not only does this occur as it does in most acute local infections which are severe, 
but small nodules are found scattered along the neighboring lymphatics forming 
the so-called "farcy buds." These undergo necrosis, and sloughs form. A septic 
arthritis may develop. The nasal passages escape, as a rule, in farcy. Death 
takes place in the majority of these cases in from ten to twelve days. 

Chronic farcy lasts, like chronic glanders, for a longer period of time than the 
acute disease, sometimes for years. It presents the picture of multiple abscesses 
and sloughs, associated with more or less general septicemia, death taking place 
from this cause. Very rarely recovery occurs. 

Diagnosis. — Glanders — that is, infection of the nasal mucous membrane by the 
Bacillus mallei — can scarcely be mistaken for any other disease. Farcy must be 
separated from multiple abscesses and carbuncles. This is done by the history 
of exposure, the distribution of the "farcy buds," and, finally, by the injection 
of mallein, which produces a reaction as does tuberculin in the tuberculous. 



ACTINOMYCOSIS 233 

Treatment. — The swellings should be promptly opened and free drainage provided. 
If possible the local focus should be well removed by excision or by the cautery. 
A nutritious diet should be given and stimulants used if needed. Mallein has been 
used as a curative agent, but nearly all acute cases die, do what we will. 



ACTINOMYCOSIS. 

Definition. — This is a chronic infectious disorder produced by the Streptothrix 
actinomyces, sometimes called the "ray fungus." It is far more common in cattle 
than in man, and in cattle it usually affects the lower jaw, producing a tumor or 
growth which gives the disease the popular name "lumpy jaw." In other cases 
the tongue is involved, producing the so-called "wooden tongue." 

Etiology. — The actinomycotic infection may be conveyed from cattle to man by 
the hands of the individual, or by straws used for picking the teeth, whereby 
infection of the jaw occurs. Direct transmission from man to man, or beast to 
beast, or beast to man does not appear to be of very frequent occurrence ; apparently 
both are infected independently by some common route or source, the exact char- 
acter of which often cannot be determined. Grain which has been soiled by the 
slobber of an infected animal may infect other cattle. Cereals are thought by 
some to be the most frequent carriers of the disease to man and beast. 

The organism appears, in the discharges from the areas of infection, as a minute, 
rounded mass so tiny as to be microscopic in some instances, but in others as aggre- 
gated masses, called granules, which are as large as a pin's head. These masses 
are yellowish-white, resembling particles of sulphur or iodoform, grayish or drab 
in hue, and even with slight magnification often appear in groups or clumps of 
radiating filaments, which have caused the organism to be called the "ray fungus." 
Each terminal filament in some stage of its evolution develops a bulbous end. 

Pathology and Morbid Anatomy. — In the lower animals the disease produces a 
slow, suppurative, and proliferative process, which results in the development 
of large fungous growths, which may in part become calcareous. From these 
growths, which are usually situated primarily in the jaw, secondary extensions 
occur, so that the fungus is found in the tissues of the tongue and pharynx, and 
even in the lungs, the intestines, and in the nearly related glands and skin. When 
the disease affects man it does not so commonly involve the jaw, but results in the 
development of abscesses which often change into ulcers or form fistula? . These 
may lead to the deeper tissues although the disease is usually superficial. 

Histologically the new tissue may closely resemble sarcoma, for which it is often 
mistaken, but its richness in pus cells and resemblance to granulation tissue, com- 
bined with the presence of the fungus, should prevent this error. 

The lower jaw is more frequently attacked than the upper; cutaneous or sub- 
cutaneous forms occur and invasion of the alimentary and respiratory organs, 
both primarily and as a secondary process, is not uncommon. A chronic bronchitis 
actinomycotica and cerebral actinomycosis are among the rarer manifestations of 
the disease. 

Symptoms. — The symptoms of actinomycosis in man depend to a great extent 
upon the part of the body which is affected. When the infection takes place 
through a carious tooth or by ulcer of the gum the jaw is invaded, and the tissues 
covering it become swollen. To such an extent may this swelling increase that 
the neck and face may be involved. In these tissues suppuration ensues and pus 
is discharged from chronic and somewhat puckered sinuses, which heal in one 
place only to break out elsewhere. Rarely the disease may spread to the fauces 
and to the tongue. 

By the swallowing of the fungus it may infect the intestines and even the liver, 



234 DISEASES DUE TO A SPECIFIC INFECTION 

and in all these organs it often causes the formation of abscesses. It has been 
found in the stools in these cases. 

Actinomycosis affects the lungs even more frequently than the alimentary tract, 
and produces symptoms of subacute bronchitis or bronchiectasis or even those 
of pulmonary abscess. The patient suffers from cough and from fever, and expecto- 
rates purulent material in which the micro-organism is often found. The pulmo- 
nary lesions are not very acute in their course, but rather chronic, life usually being 
prolonged in these cases for a year or even longer than this. Rare cases of brain 
abscess have been recorded as the result of the organism reaching this organ. 
Howard has been able to find only four primary cases beside his own, and thirteen 
secondary cases. Such cases must not be confused with those equally rare instances 
of streptothrix infection which Musser has reported. 

Diagnosis. — The disease, when the jaw is affected, must be separated from ordi- 
nary necrosis and from sarcoma. In the first the swelling is not so widespread 
and the sinuses not so numerous. In the second condition there is no suppuration, 
the growth is usually more rapid, and the surface is not so fluctuating. An examina- 
tion of the pus in those cases in which it escapes will decide the diagnosis by revealing 
the ray fungus. It is to be remembered that secondary pyogenic infection and 
extensive necrosis may render the detection of the specific fungus difficult if not 
impossible, and undoubted cases are on record in which for relatively long periods 
the characteristic organism was absent. Search for the germ is most likely to be 
rewarded during recrudescence in old lesions and in newly formed nodules or 
extensions, when they are freshly opened. 

Treatment. — This is largely surgical when the growth is so placed as to permit 
of its being attacked by this means. The mass and the surrounding tissues should 
be excised and all dead bone and infected tissue removed, after which drainage 
should be maintained and the sinuses irrigated with weak solutions of iodine or of 
iodoform in oil. When the pleura is involved iodoform injections are particularly 
useful. Iodide of potassium is also an effective drug when given internally in 
doses of from 20 to 60 grains a day, it being thought that in its liberation of iodine 
it acts as a specific against the ray fungus. 

Periods of marked improvement and even apparent cure should not cause relaxa- 
tion in treatment, nor do they justify a too hopeful prognosis, as a recrudescence 
of lesions long obsolescent is of frequent occurrence. 

MYCETOMA (MADURA FOOT, FUNGUS FOOT OF INDIA). 

This is a mycotic disease, usually invading one or both feet and rarely appearing 
in other parts of the body. It is most commonly observed in India. Sporadic 
cases occur in other parts of Asia, in Europe, and in South America. A number 
of cases have been reported in the United States. Two varieties of the disease 
are recognized; the melanoid, or mycetoma with black granules, and the ochroid, 
with white or yellow granules. They are due to distinct varieties of streptothrix 
(Streptothrix madurce and Streptothrix mycetomce). The disease is closely related 
to actinomycosis; indeed, some of the cases reported in the United States as myce- 
toma are undoubted cases of actinomycotic feet. 

The disease commonly attacks one foot; beginning as a firm, hard nodule on the 
sole, which gradually softens and discharges an oily, fetid pus containing the black 
or yellow granules. The sinus thus formed persists. Other nodules appear and 
go through the same course. The foot gradually enlarges and the sole is greatly 
thickened. The disease attacks the deeper tissues until eventually all structures, 
including the bones, are converted into a greasy, yellowish mass. The appearance 
of the fungus foot, with the thickened sole, the toes strongly extended upward, and 
the plantar and dorsal surfaces covered with the button-like orifices of the sinuses, 



FRAMBESIA 235 

is characteristic. Occasionally, the disease shows some tendency to the formation 
of secondary deposits, spreading along the lymphatic vessels. The diagnosis 
between mycetoma and actinomycosis rests on the microscopic character of the 
organisms. 

Treatment. — The treatment consists of conservative resection in early cases and 
amputation in older cases. 

FRAMBESIA (FRAMBESIA TROPICA, YAWS). 

Definition. — Frambesia, or yaws, is a chronic contagious and infectious disease, 
characterized by the appearance of a diffuse granulomatous eruption on the skin. 

History. — The history of yaws begins with the historians of the Spanish conquest 
of America. It is a disease very closely confined to tropical countries and very 
widely distributed in Africa, in the coast countries of tropical Asia, and in many 
of the Pacific Islands. It also occurs in Central and tropical South America and 
the Antilles. The disease was exceedingly common in Cuba and the southern 
United States during the first half of the nineteenth century, having been brought 
there during the slave-trading days. At one time it caused such a degree of dis- 
ability among the negroes that the planters were forced to adopt stringent rules 
for its limitation. Most of the large plantations maintained isolation barracks, 
or "yaw houses/' for these cases. The disease still lingers in Cuba and the rest 
of the Antilles. It has all but disappeared from the United States. 

Etiology. — Many bacterial forms have been isolated from yaw lesions, although 
as yet the specific cause has not been determined, but Castillain of Colombo has 
isolated a spirochete or treponema which he thinks is the specific cause and called 
it the Treponema pertenius. The disease can be, and frequently is, conveyed by 
direct inoculation, intentional or accidental. Such inoculation may take place 
in wounds, abrasions, and other injuries of the skin. In some yaw countries, 
notably in Fiji, it is a common practice for mothers to inoculate their children, 
under the same idea which prevails among our lower classes, who frequently expose 
their children to pertussis and eruptive diseases, on the theory that the illness 
must be gone through with some time, and the earlier the better. Heredity 
has no bearing on the etiology of yaws. Neither does a pregnant or nursing woman 
with yaws necessarily infect her child. Outside of direct inoculation the disease 
is conveyed by food, particularly by cooking utensils. In persons particularly 
susceptible, infection may take place by sleeping in a yaw house. All ages are 
attacked, but the majority of cases are seen in children. The black, yellow, and 
white races are susceptible in the order named. As a rule, one attack confers 
complete immunity. Frambesia is also seen in domestic fowls. 

Symptoms. — The incubation period of yaws is very variable. Generally speaking, 
in inoculation cases, it varies between fifteen and twenty days. In cases ordinarily 
acquired, the incubation is longer, ranging from fourteen to sixty days. In a 
small proportion of cases prodromal symptoms, languor, malaise, headache, and 
rheumatic pains are observed. This condition is followed by what is known as 
the primary eruption or the primary sore, concerning which there is some dispute 
among tropical practitioners. In experimental inoculation cases the primary 
sore is constant and occurs at the point of inoculation. It begins as a small papule, 
which, in the course of a week, is converted into a shalloto ulcer. In another week 
the ulcer heals, leaving a slight, thickened scar. In ordinary infection by yaws it 
is sometimes present and sometimes absent. 

The generalized eruption, the so-called secondary eruption, begins with the 
primary sore in exceptional cases, but, as a rule, is delayed for several weeks. 
Occasionally, in the period between the eruption of the primary and secondary 
lesions, a dry, scaly affection of the skin is seen. 



236 , DISEASES DUE TO A SPECIFIC INFECTION 

The secondary eruption begins as small papules, which itch intensely. They 
are scattered all over the body, but are most commonly seen, in order, on the face, 
neck, limbs, genitals, and trunk. The hairy scalp is not commonly invaded; 
the axilla very rarely. The lesions are particularly numerous at the mucocutaneous 
borders, the mouth, nose, anus, and vulva. The eruption is roughly symmetrical. 
The papules, at first the size of a pinhead and slightly prominent under the skin, 
gradually increase in size till they are as large as a pea or a hazel-nut. Small, 
yellow spots of pustulation appear on the summit of the lesions ; the skin cracks ; a 
sticky, yellow, seropurulent fluid exudes, which hardens and forms rupia-like 
crusts or caps over the summit of the growths. The cap is tough and adherent. 
When it is pulled off it reveals a shiny, red papilloma underneath. This warty 
growth, the true yaw, resembles a berry in appearance, hence the name yaw, i. e., a 
strawberry; frambesia from framboise, a raspberry. Indeed, most of the local 
native names for the disease are words which mean berry in their dialect. 

The growths resemble syphilitic condylomata in their appearance. They spring 
from the papillary layer of the skin, and the warty-like lobulations represent the 
greatly hypertrophied papillae. The uncovered yaw freely exudes the sticky, 
yellow pus, already mentioned, and in a little while the cap is reproduced. As a 
rule, the lesions are painless, excepting where they occur under thick, dense skin, 
as in the palms and the soles, where tension may cause great pain. Itching is, 
however, very persistent and annoying. After persisting weeks and months, 
sometimes passing through recrudescences and successive crops, the lesions grad- 
ually grow smaller, the papillomata disappear, and a dry eschar is left, which falls 
off, leaving a patch of thickened skin, bleached in the negro and pigmented in the 
light-skinned races. 

In old, long-standing, and neglected cases, severe bone and joint pains develop, 
and occasionally extensive periostitis and caries occur. These are the so-called 
tertiary lesions of frambesia. They are not constant; indeed, they never appear 
in properly treated cases. 

Diagnosis. — There are only two diseases with which typical yaws can be confused, 
syphilis and verruga. Hutchinson believes yaws and syphilis, if not the same 
disease, are descendants of the same parent stock; that originally they were identical 
and have become differentiated by thriving for long periods on different soils. 
Yaws undoubtedly suggests syphilis very strongly, but there can be no question 
of the duality of the diseases. Syphilis and yaws have frequently been observed 
in the same individual; syphilitics have been successfully inoculated with yaws, 
and vice versa. Finally, the histological differences are marked. No giant cells 
are seen in yaws and no thickened bloodvessels. 

Scheube believes yaws and verruga to be identical, but Glogner has recently 
drawn a clear distinction between the histology of the two diseases, and has clearly 
shown that they are not identical. 

Prognosis. — The prognosis is uniformly good. 

In patients reduced by disease and in infants the prognosis of yaws is not so 
favorable. 

Treatment. — Iodide of potash is the remedy for frambesia as is also salvarsan. 
Mercury not only does not do these patients good, but actually seems to do them 
harm. Stomatitis occurs with the greatest facility and is very severe. When the 
general condition is low, arsenic, iron, and the bitter tonics are indicated. Most 
tropical practitioners advise local treatment of the lesions. This includes antiseptic 
and stimulating applications and removal of old lesions with the curette. The 
prophylaxis of yaws consists in cleanliness and isolation of the infected. Great 
care must be taken of abrasions and cuts, and infected dwellings should be avoided. 



TUBERCULOSIS 237 

TUBERCULOSIS. 

Definition. — Tuberculosis is an infectious disease caused by the presence in the 
body of the Bacillus tuberculosis. It is characterized by a local inflammatory 
process followed by the development of areas of necrosis. While the lesions pro- 
duced by the disease are varied, the typical manifestation is the formation of small 
nodules which appear as gray, or white, or sometimes yellowish bodies called 
tubercles. It is because of these tubercles that the name "tuberculosis" is applied 
to the malady. 

Etiology. — The chief etiological factors in this disease are the specific bacillus 
and the presence of a favorable state in the tissues of the individual for the growth 
of the germ. As the disease is constantly present all over the world, except in a 
few scattered areas, the specific germ is always at hand, and as a large number 
of causes produce a condition of the tissues which is favorable to their development 
the disease is only too prevalent. 

The bacillus of tuberculosis appears as a straight, slightly curved or bent rod 
with rounded ends, devoid of motility, and reproducing itself by fission ; the often- 
expressed belief that it is a spore-bearing organism is not unequivocally established. 
It stains with the ordinary aniline dyes and by Gram's method. (See Pathology.) 

The Bacillus tuberculosis enters the body by several pathways, of which the 
most common one is undoubtedly the respiratory passages (Fig. 49). It also gains 
access by way of the alimentary canal with the food, particularly in children, 
and occasionally by accidental inoculation. Recent studies have shown that 
the tonsils and lymphoid tissues of the pharynx are portals through which the 
tubercle bacillus frequently enters. The position of the tonsils exposes them to 
both air-borne and food-borne infection, and their crypts and lymphatic communica- 
tions afford favorable opportunities for the entrance and dissemination of the 
micro-organism. Very rarely true hereditary transmission takes place by the 
passage of the bacillus through the placenta or possibly by the infection of the 
ovum by this organism. Such instances are, however, so rare that they are medical 
curiosities. 

When the infection takes place by inhalation it usually occurs by the bacilli 
being dissipated through the air in the form of dust, or by their expulsion in small 
masses of sputum which, falling on pillows, bedding, or clothing, are easily taken 
into the respiratory passages when the sputum dries. Flugge has shown that when 
a patient coughs with his mouth open the ejected air may contain droplets holding 
the bacillus, thereby rendering the immediate neighborhood of the sufferer especially 
dangerous. There can be no doubt of these facts, for they are proved by the very 
great frequency of the disease in the lungs, particularly when opportunity exists 
for infection by dust, and by the fact that susceptible animals can be infected by 
this disease if forced to breathe dust which has been contaminated by dried tuber- 
culous sputum. 

Kingsford found in analysis of 339 cases that 216, or 63.7 per cent., occurred 
by inhalation, 65, or 19.1 per cent., by ingestion, and 17 per cent, were of doubtful 
origin. 

Von Pirquet gives the relative frequency of paths of infection in infancy as 
represented in Fig. 49. 

Tuberculous infection by way of the alimentary tract occurs very commonly 
as the result of drinking milk from tuberculous cows, or milk that has been con- 
taminated by the sputum from tuberculous human beings. The infection of milk 
by coughing or sneezing by persons suffering from this disease occurs quite fre- 
quently. The milk of a tuberculous cow will convey the infection even if local 
tuberculous lesions are not present in the udder, and the bacillus may be found 
in butter made from such milk. The fact that tuberculosis is so frequently found 



238 



DISEASES DUE TO A SPECIFIC INFECTION 



in the mesenteric glands of young children is significant in this connection. Infec- 
tion by the meat of a tuberculous animal can only occur if the meat actually con- 
tains the bacilli and is eaten uncooked. This form of infection is probably very 
rare except when sausages made from what are known as bologna cows 1 are eaten 
in a raw or half -cooked state. 

Medical publications have teemed during the last few years with rather heated 
debates as to the communicability of bovine tuberculosis to man. In the minds 
of some bacteriologists, in Germany in particular, this question is still sub judice, 
but the majority of those best qualified to judge now agree that no doubt can exist 
of its transference, particularly from the udders of tuberculous cows to the mesen- 
teric glands of children who drink the milk from these animals. 



Fig. 49 




GENOUS 



INFECTIONS AND DEATHS 



INFECTIONS AND DEATHS 



a 

n 



BRONCHOGENOUS 

INFECTIONS 

95 PER CENT 



DEATHS BY 

BRONCHOGENOUS 

INFECTIONS 



Incidence and mortality from tuberculosis in infants. Diagram showing approximate proportions 
of different channels of infection among the infants of Vienna. (Von Pirquet, modified from Edin- 
burgh Medical Journal.) 

Raw, Theobald Smith, and others have maintained that man is subject to two 
forms of tuberculosis, one derived from members of his own zoological group and 
another due to infection by the bovine bacillus. The wide distribution of tubercu- 
losis in the animal kingdom, the morphological, cultural, and pathogenic differ- 
ences in the bacillus found under different conditions, and the generally admitted 
possibility of ranging these organisms in a scale, or at least in closely allied groups, 
explain, at least in part, the different phenomena as seen in man. 

The mere presence, however, of the tubercle bacillus is not the only requisite 
for the development of tuberculosis, for as already stated the tissues must be in a 
favorable state for its growth. This favorable state is produced by any cause which 
impairs vital resistance and prevents the body from destroying invading micro- 
organisms soon after they enter it. Of these causes, aside from diseases which 
impair the general health, we find the most potent are bad air, particularly that 
due to poor ventilation when large numbers of persons are crowded together; lack 
of exercise, so that all parts of the lungs are not thoroughly expanded; and, lastly, 



1 A bologna cow is an animal so feeble and wasted that it cannot be used for milking, breeding, or for 
the providing of ordinary butcher's meat. It is killed and used to make sausage. 



TUBERCULOSIS 239 

those conditions of air and soil which are associated with excessive humidity, 
particularly if there be much dust in the atmosphere, as in large cities. 

In addition to these causes, which increase the susceptibility of all persons, we 
also find that certain individuals inherit conditions which undoubtedly predispose 
them to this disease. They belong to two classes: those who by inheritance 
possess faulty thoracic development, or bad chest configuration, so that the apices 
of the lungs never expand properly, and those who seem to inherit a condition of 
the tissues which is unable to cope with the infection when it takes place. Both 
these causes are often present in one case. Such persons are usually lightly built 
and have small bones and delicate features, with a thin skin and superficial veins 
about the temples. It is a mistake, however, to think that this configuration is 
always present, for another type exists in which the bony structures are large and 
the muscles powerful, the so-called "lanky" type, in which tuberculosis is very 
apt to run a rapid course. Every clinician of experience has been astonished to 
find active tuberculosis of the lungs in heavy and powerfully built men, and has 
seen more than one generation of the same family, though strongly built, succumb 
to this malady, although promising in early life to escape all danger from it, In 
these instances the vital resistance to infection is poor, although the physique may 
seem excellent. 

The influence of age upon the development of the disease is distinct, but it is 
not sufficiently powerful to confer immunity upon any period of life. In the first 
ten years of life tuberculosis is quite common, affecting the lymphatic system 
most frequently, the bones being also commonly involved, and more rarely the 
membranes covering the brain. After puberty the pulmonary tissues are the parts 
which are affected in the majority of cases, and this predisposition of the lungs to 
the disease persists throughout the rest of life, although after the thirty-fifth year 
the frequency of pulmonary tuberculosis rapidly decreases, so that in persons over 
fifty years of age it is really very uncommon as a new ailment, unless they have 
been specially exposed to infection by the malady. The only cases I have seen of 
primary pulmonary tuberculosis which began in persons of over fifty years of age 
were miners and grinders. 

The sexes are about equally affected by tuberculosis. 

Of the races, negroes and North American Indians are very susceptible, and 
half-breed negroes and half-breed Indians are peculiarly prone to the malady. 
I have had opportunities of studying the frequency of tuberculosis among both of 
these classes and have been impressed by this well-recognized fact. Perhaps this 
susceptibility is due to the fact that the white father is usually a degenerate, or 
one whose vitality is impaired by alcohol and abuse. 

Of the occupations which favor the development of tuberculosis may be named 
knife-grinding, mining, weaving, and other pursuits which cause large quantities 
of dust to enter the lungs. (See Pneumonoconiosis.) 

All the infectious diseases which diminish the vitality of the patient predispose 
him to infection by this bacillus. Thus, pneumonia, particularly that of the catar- 
rhal type, not rarely causes pulmonary tuberculosis to develop, and influenza 
renders the patient especially prone to its development. In many cases the catar- 
rhal process provides the centre in which a new, or an old and slumbering, infec- 
tion can become active. Among the acute infections, measles and whooping-cough 
are active predisposing factors, causing catarrhal pneumonia or exhaustion and 
diminished vitality. Diabetes mellitus very commonly ends in a rapidly developing 
tuberculosis. 

A very important point is the relation of injury to the development of tubercu- 
lous lesions. There can be no doubt that trauma to the chest wall may be followed 
by an outbreak of pleural or pulmonary tuberculosis, that injuries to the joints, 
even if seemingly trivial, may cause tuberculous arthritis, and blows on the abdo- 



240 DISEASES DUE TO A SPECIFIC INFECTION 

men may incite tuberculous peritonitis or tuberculosis of the retroperitoneal or 
mesenteric glands. (See also article on Pneumonia for traumatic lesions of the 
thorax followed by pulmonary disease.) 

Prevention. — In the prevention of tuberculosis the most important factor is the 
destruction of the bacillus as soon as it leaves the body of the patient. This is 
by no means as easy to accomplish as would appear at first sight, since it is often 
expelled in enormous numbers by sneezing and coughing. The moustache or beard 
of the consumptive is a veritable nest of infection, and his bed-clothing may be 
equally virulent unless he holds something in front of his face when he coughs. 

All sputum should be received into rags, which should be burned in a hot fire 
before they become dry, or into a paper spit-cup which can be burned. If a china 
cup is used, it should always contain bichloride of mercury solution. 

The health departments of nearly all large cities are active in stamping out 
tuberculosis, or consumption. Under ordinances, physicians are required to report 
every case of this disease that comes under their care. In the poorer districts this 
is followed by inspection, and, if necessary, disinfection of the quarters occupied 
by the sick man, and this again has been supplemented by the distribution of cir- 
culars in which directions are given whereby the patient can take precautions against 
the infection of his family, and the family can protect themselves. 

The second great preventive of tuberculosis is sunlight, for sunlight destroys 
the bacillus. If this were not the case our streets would infect more thousands 
than they do. Sunlight not only destroys the bacillus, but increases the vital 
resistance of the patient and of the uninfected as well. The absence of sunlight 
and the presence of bad air are the most potent auxiliaries to the disease. This is 
shown by the prevalence of the malady in tenement houses, in prisons, and in 
asylums which are badly arranged or managed. These facts have not only been 
proved on a gigantic scale by unintentional tests with human beings, but experi- 
mentally as well, particularly by Trudeau, who inoculated two sets of rabbits 
with the bacillus tuberculosis. He kept one set in a dark cellar and these animals 
suffered an unusually high mortality. The other set he turned out-of-doors, and 
these animals survived or were affected only by a modified form of the disease. 

In those who have an hereditary predisposition to the disease or who have a 
faulty thoracic development, out-door life is in many cases an absolute necessity 
to prevent the disease. 

As bovine tuberculosis can be conveyed to man, careful inspection and testing 
of cows supplying milk should be frequently made and especially when the milk 
is to be used as an infant food. 

Frequency. — The prevalence of tuberculosis in its various forms is very great. 
About one death in every seven is due to this cause, and when we add to this fact 
the additional statement that a very large proportion of those who die of other 
diseases show more or less well-developed tuberculous lesions, it becomes evident 
that tuberculosis contributes to the death of a still larger proportion of persons. 

Thus Schlenker in 100 autopsies made on adults and children dying of various 
diseases found that 65 per cent, had tuberculosis. Biggs found it in 60 per cent, 
of his postmortems, and out of 4000 consecutive autopsies in Breslau about 1300 
showed tuberculosis. These statistics, which give some conception of the ordinary 
prevalence of the disease, are outclassed in an extreme degree by the reports of 
Naegeli in Zurich, who found in the Pathological Institute of that canton that 500 
consecutive autopsies revealed tuberculosis in some form in 97 per cent. This 
percentage held true of adults as well as of children. Naegeli also found that tuber- 
culosis is very rare in the first twelve months of life, uncommon up to the age of 
five years, but so frequent from five to fourteen years that it was found in one-third 
of all bodies examined. In studying these statistics of Naegeli it must be remem- 
bered that in many of the autopsies tuberculosis was not the cause of death, and 



TUBERCULOSIS 



241 



in some cases was present in such a very slight degree that only careful search 
revealed its presence. Burrell believes that about 70 to 80 per cent, of all persons 
who reach the age of forty years have or have had some form of the disease. 

The far greater frequency of tuberculosis in cities as compared to country dis- 
tricts and villages is shown by the statistics of Paris, in which the number of cases 
per thousand is 4.9; whereas in 662 villages in France it is only 1.81. 

Notwithstanding these facts it is interesting to note that in many parts of the 
world tuberculosis has undergone a most remarkable decrease in its frequency, 
although the mortality rate of 1 in 7 still holds true for many cities. In New 
York the mortality has decreased from 4.6 to 2.6 per thousand in ten years, and 
a similar fall of about 40 per cent, has occurred in Philadelphia in that time. Abbott 
has shown that in 1853 the mortality of pulmonary tuberculosis in Massachusetts 
was 42 per 10,000 inhabitants, whereas in 1895 it was 21.8 per 10,000 inhabitants. 
The decrease in the entire United States has been from 254.4 per 100,000 in 1890 
to 190.5 per 100,000 in 1900, and in 1910, 160.3 per 100,000. Hiller has shown that 
at the present rate of decrease the disease will be extinct in Prussia in 1927 and 
in England about 1947. In Prussia the mortality fell from 31 per 10,000 in 
1886 to 19 per 10,000 in 1901, and in England it has fallen 50 per cent, in the last 
forty years. In New York City the decrease in sixteen years equals 40 per cent. 



Fig. 50 





30 


o 

-'- 

30 


!- 
00 


OO 

oo 


oo 
oo 


© 

OO 

:/0 


OO 
OO 


oo 

30 


OO 
OO 
30 


oo 


13 
OO 


OO 
00 


00 


00 
OO 

OO 


CO 
OO 

OO 


© 

O0 
30 


iH 
OO 


Oil 

5o 


o3 

OO 


To 


13 

CO 
OO 


O 

OO 
OO 


c- 

30 


OC 
OO 


o 

OO 
OO 


© 

OO 


OO 


© 

OO 


to 
© 


-H 
© 


32.5 






























































32 






/ 


/ 


\ 




















































31.5 


\ 




/ 






\ 






h 












































31 




V 








\ 




/ 




\ 










































30.5 






























































30 






























































29.5 






























































29 






























































28.5 






























































28 






























































27.5 
































\ 






























27 
































\ 


y 




























2G.5 






























































20 


































\ 




























25.5 


































> 


\ 


























25 




































\ 


























21.5 






































\ 
























21 








































V 






















23.5 








































V 


\ 




















23 










































\ 




















22.5 












































V 


















22 












































\ 


















21.5 






























































21 






























































20.5 






























































20 






























































19.5 






























































19 





























































































































Annual death rate from pulmonary tuberculosis per 10,000 inhabitants in Germany from 

1'875 to 1903. (Locke.) 



A very great difference in frequency is found in different races. Thus, in the 
United States the death rate in those of English descent is 15 per 10,000, whereas 
for the Irish it is 43, and 59 for the colored race. 

Occupation also makes great differences; thus, the death rate among trades- 
people is 17 per 10,000, among barbers 33 per 10,000, book-keepers 40, and stone- 
cutters 54 per 10,000. 

The average age at death from pulmonary tuberculosis is thirty-five years, but 
the actual incidence of the disease is from fifteen to thirty-five years. 

The relative frequency of the different forms of tuberculosis is difficult to deter- 
16' 



242 DISEASES DUE TO A SPECIFIC INFECTION 

mine. Statistics of deaths from tuberculosis in Ireland from the years 1891 to 
1901 show the following figures as to the relative frequency: 

Pulmonary tuberculosis 21.35 per 10,000 

Tuberculosis of the mesenteric glands 2.2" 

Tuberculous meningitis 2.25 " " 

Other forms of tuberculosis 2.3" " 

Some difference exists, however, between the frequency of primary and secondary 
lesions. Thus, Heller, of Kiel, found but 1.45 per cent, of primary intestinal 
tuberculosis, but 37.8 per cent, in which the principal lesion was abdominal. 

Pathology and Morbid Anatomy. — As already stated, when discussing the etiology 
of tuberculosis, the bacillus enters the body usually through the respiratory mucous 
membrane, or through that of the alimentary canal. It is possible, however, for 
infection to take place through the skin, but this is usually followed by a localized 
lesion and rarely by visceral disease. The results which accrue from the entrance 
of the bacillus vary greatly with the virulence of the micro-organism, the vital 
resistance of the individual and the organ or part in which the primary localiza- 
tion of the bacillus takes place. The effect of the bacillus upon the local tissues 
is to cause an accumulation of cells in the immediate neighborhood, followed in 
favorable cases by repair or, under less promising conditions, by necrosis. This 
aggregation of cells, composed of lymphoid, endothelioid, and, it may be, giant cells, 
and containing the bacillus, is the histological or rather anatomical characteristic 
of the disease, and is called a tubercle. 

In the great majority of instances the pathological process which is induced is 
inflammatory in type, and, as already stated, the lungs and their adjacent lymph 
nodes are the parts which are usually affected in adults, whereas in young children 
the gastro-intestinal tract and its adjacent glands are commonly involved, either 
alone or with the structures just mentioned. When the collection of the cells is 
small the growth is said to be a miliary tubercle, because it is approximately the 
size of a millet-seed; but when a tubercle becomes large enough to be called 
a nodule its growth to these proportions is accomplished by the coalescence of 
a number of miliary tubercles. This growth usually is limited, in the miliary 
tubercle or nodule, by the fact that an exudate takes place, as part of the inflamma- 
tory process which the bacilli produce, which prevents the spread of the bacilli to 
adjacent areas, and so limits the field occupied by the micro-organisms. 

As the disease progresses this exudate becomes organized and is finally devel- 
oped into a dense fibroid or cicatricial tissue, which acts as a protective barrier 
against the spread from that particular area of invasion. This barrier in a great 
number of cases remains effective and in a sense imprisons or restricts the pro- 
duction of poisons and lessens their dissemination. Within this limited zone of 
action the bacterial products cause necrosis and in the dead tissue the germ is sup- 
pressed or actually destroyed. After the local necrotic process is complete the 
necrotic contents are more or less fully absorbed and only a cicatrix remains to 
mark the site of the original lesion, or if this does not take place the caseous and 
degenerated mass undergoes calcification. In either instance a natural process 
tends to bring about a cure. 

If for any cause this protective barrier is removed by absorption while the 
imprisoned bacilli are still alive, or if the wall which is formed is incomplete, the 
bacilli escape and speedily infect adjoining or distant areas, being conveyed by 
the lymph or blood streams. Such is the explanation of those cases in which a 
patient who has suffered from some acute infection, like pneumonia, typhoid 
fever, or influenza, speedily develops tuberculosis during convalescence, although 
the acute illness may, by confining him to a healthful and well-ventilated room, 
have protected him from any recent infection. 



TUBERCULOSIS 243 

In still other cases the protective barrier of surrounding exudate is not formed 
and the amalgamation of tubercles produces a nodule which undergoes necrosis 
and softening and its bacterial contents become diffused into the surrounding 
tissues, thus spreading the infection. In still a third type of cases the lesions con- 
sist in a diffuse exudative process, with little or no tubercle formation, and as a 
consequence we find that it is possible for the entrance of the tubercle bacillus to 
be followed by a tuberculous pneumonia or pulmonary consolidation, tuberculous 
serositis, or lymphadenitis, the lesion not containing the characteristic tubercle. 
In other words, in certain instances the tuberculous inflammation is so intense 
and the poison formed by the bacilli is so abundant or virulent, or the resistance of 
the soil so inadequate, that no attempt at protection is made, but instead there 
occurs a profuse exudative process which is extremely liable to undergo necrosis, and 
this results in rapid breaking down not only of the exudate itself, but of the involved 
tissues as well. 

Under certain admittedly unusual conditions the tubercle bacillus becomes 
distinctly pyogenic and, rapidly developing in the lung, produces not only the 
degenerative and necrotic changes peculiar to tubercle formation, but fills the air 
vesicles with pus, serum, and dead epithelial cells and leukocytes, a state in which 
the part involved speedily goes on to widespread destruction. It is also to be 
recalled that in nearly all cases of tuberculous disease infection by other pyogenic 
organisms, such as the staphylococcus and streptococcus, aids in producing local 
inflammation and pus, and leads to the formation of toxins which cause local and 
general impairment of vitality. 

In some cases, on the other hand, the bacilli, in the presence of the resistance 
offered, do not seem capable of originating an acute inflammatory process, nor do 
they cause the formation of tubercles with caseation, but produce a condition in 
which an excessive formation of connective tissue occurs, which prevents the 
rapid spread of the disease and constitutes a form of infection called chronic hyper- 
plastic tuberculosis in the intestine or in the lung which is closely allied to fibroid 
phthisis, so called; but this fibroid process is by no means entirely dependent 
upon the presence of the bacillus tuberculosis, since other causes may produce it. 

It is fully established that the noxious action of the tubercle bacillus in the human 
organism is due to its poisons, a number of which have been described. The early 
coagulation necrosis and subsequent caseation are clearly the result of bacillary 
toxins. The tendency to fibrosis seen in many cases has been thought to be due to 
a sclerogenous toxin and the frequent cheesy disintegration, so commonly present, 
to a caseogenous poison; it is probable, however, that the same noxious agent in 
some individuals induces caseation and in those more resistant to its action a 
fibroid or fibrocalcareous change. Progressing caseation may be looked upon as 
an evidence of low resistance, while fibrosis, with or without calcification, indicates 
strong reparative and antagonistic powers on the part of the affected tissues. 

With these preliminary remarks we may proceed to a discussion of the various 
manifestations, pathological and clinical, which are to be met with in persons 
affected by this disease. 

Acute Miliary Tuberculosis. — By acute miliary tuberculosis is meant a con- 
dition in which a single organ, or a number of organs, or perhaps the whole body, 
is infected by the Bacillus tuberculosis, causing the formation of innumerable 
tubercles of the type already described. It arises not by the inhalation of dust 
laden by bacilli, but by the escape of bacilli in large numbers from some infected 
focus, as, for example, a caseous lymphatic gland. The escape takes place into a 
bloodvessel, and in a few hours at most the bloodvessels of the neighboring parts, 
or perhaps of the entire body, are swarming with bacilli, so that in a very brief 
space of time the lungs, the liver, and other parts are found studded, or, as it has 
been well expressed, "stuffed," with miliary tubercles. The caseous gland or 



244 DISEASES DUE TO A SPECIFIC INFECTION 

primary cheesy nodule which gives origin to this acute secondary infection is 
usually so situated that it is adherent by inflammatory products to a vein, com- 
monly the pulmonary vein or one of its branches, or to the thoracic duct, or the 
superior cava. By a process of extending necrosis the soft contents of the gland, 
laden with tubercle bacilli, break into the vessel or duct. Sometimes an active 
tuberculosis of the wall of the bloodvessel is present, so that tubercles may be 
found in the intima. Councilman has observed a tuberculous aortitis apparently 
resulting from infection through the vasovasorum. 

Weigert has divided the results of this vascular invasion by the bacilli into 
three classes: (1) that in which all the organs of the body become filled with 
tubercles of the miliary type; (2) that in which the disease, though widely dis- 
seminated, nevertheless appears in multiple but widely separated foci; and (3) that 
in which the tubercles are not so numerous, their growth is more chronic, and 
their size causes them to be classed as nodules. This is manifestly an artificial 
division which is not closely adhered to under natural conditions, for the process 
may represent all these types in one case, while in other instances it may be im- 
possible to tell to which class the case belongs because the lesions shade into one 
another. 

Symptoms. — The symptoms of widely diffused miliary tuberculosis are to be 
carefully studied because they simulate those of enteric fever and other typhoid 
states so closely that not rarely an erroneous diagnosis is made. The chief mani- 
festations may be said to be those of profound toxemia without any localized 
lesion to explain the illness, which begins with the general wretchedness common 
to the early stages of all acute infections and which is followed by fever, rising each 
evening to 102° or 103°. The pulse is unduly rapid, and there are often profuse 
sweats. In such cases there are three symptoms which, while not pathognomonic 
by any means, are nevertheless of some value in separating this condition from 
typhoid fever. The fever is often irregular, sometimes breaking with a profuse 
sweat. In other cases it is higher in the morning than at night. The pulse is often 
exceedingly rapid in the early stages, a phenomenon which, as a rule, is not ob- 
served in typhoid fever. The temperature does not resist cold sponging in the first 
week as does that of typhoid fever, but, on the contrary, falls with great rapidity 
to below normal. Later there is the absence of rose spots to lead one to a current 
opinion, and careful examination of the lungs may reveal some area of infiltration 
or softening, or of dulness on percussion which should arouse suspicion. 

Additional differential factors are as follows: There is absence of the Widal 
reaction. This reaction, however, often does not appear in typhoid fever until 
after the tenth day. Tubercle bacilli may, by spinal puncture, be found in the 
cerebrospinal fluid, and in some instances the ophthalmoscope will reveal tubercles 
in the choroid. Rarely the bacillus can be demonstrated in the blood or urine. 
Enlargement of the spleen, the diazo reaction in the urine, the presence of active 
diarrhea or severe constipation, and the fever are not differential points in favor 
of typhoid, for they all appear in miliary tuberculosis. Unlike typhoid fever, 
herpes labialis may be present in acute miliary tuberculosis. 

In other instances the disease has a much more abrupt onset. The patient is 
seized with a chill followed by high fever, or rapid pulse, profound prostration, and 
copious sweats. Emaciation proceeds with remarkable rapidity. The aspect of 
the patient is profoundly toxic or septic and his expression anxious. The tongue 
is dry and the cheeks flushed. 

When miliary tuberculosis involves the lungs the pulmonary symptoms are 
chiefly those of diffuse acute bronchitis, although careful examination may reveal 
at one apex, or at both, some impairment of resonance due perhaps to an ancient 
infection. The general symptoms are distinctly asthenic, as already described, 
and added to them there are fine rales over the greater part of the chest and a degree 



TUBERCULOSIS 245 

of dyspnea far out of proportion to the lesions which can be discovered. The 
respirations may be unduly rapid. The cyanosis is very pronounced, the cough 
constant, and the patient may seem surprisingly ill considering that no cause can 
be discovered. The sputum may be rusty or blood-streaked, or a true hemoptysis 
may develop. Auscultation may reveal pleural friction due to tuberculosis of the 
pleura, and as the case progresses widely distributed rales may be heard in the 
back and front of the chest. In these cases great mental anxiety is often a marked 
symptom unless the disease attacks a child, when the patient usually lies limp and 
apathetic and perhaps stuporous. 

These patients usually die in from one to three months, but cases are occa- 
sionally met with in which death ensues as early as the fourteenth day. In still 
other instances the case becomes less fulminating in character, the symptoms mod- 
erate, and the patient passes into ordinary subacute pulmonary tuberculosis. 
Acute tuberculous bronchopneumonia is more frequently seen in children than in 
adults. 

Diagnosis. — The diagnosis is not difficult in the pulmonary form if there is a 
history of an old tuberculous lesion elsewhere, or if the marked cyanosis as com- 
pared to the apparent limited area of disease is considered. Here again the 
presence of tuberculous foci may, if found, show that an acute condition is imposed 
upon an older one. The physician must not be led into the belief that the lungs 
are normal because he is able to elicit a clear and resonant percussion note on the 
chest wall, for a compensatory emphysema often is present in these cases. 

When the miliary process chiefly or entirely involves the meninges the symptoms 
are of course cephalic in large degree, and we have that grave state known as 
acute tuberculous meningitis present. (See Tuberculous Meningitis and Tuber- 
culosis of Serous Membranes.) 

Spinal puncture to determine the cause of the disease is a most valuable aid. 
If tuberculosis is present the cerebrospinal fluid will be turbid and occasionally, 
if it is placed in a centrifuge, the bacilli can be found, or some of the fluid may be 
injected into a guinea-pig, which will develop tuberculosis, if this be the cause of 
the illness. 

From typhoid fever of the meningeal type tuberculous meningitis is separated 
by the presence of spots and by the Widal test. Again, the diagnosis of tuberculous 
meningitis may be confirmed if a focus of primary tuberculosis can be found in the 
other organs, as in the lungs, the bones, or the mesenteric glands. 

Prognosis. — The prognosis is always fatal, although cases said to have recovered 
have been reported. 

Treatment.— The treatment consists in the use of nutritious food and stimulants 
and in the relief of restlessness by chloral or the bromides. 

Glandular Tuberculosis. — Glandular tuberculosis, or tuberculosis of the 
lymphatic glands, is the condition which was formerly called "scrofula," before 
Koch demonstrated the existence of the tubercle bacillus. It is now known 
that no such disease exists as scrofula, or scrofulosis, in the sense of a separate 
entity. 

Tuberculosis of the lymph glands is often a very mild form of the infection and 
the mortality from its presence is very low. Indeed, it may be said that if the 
infection does not escape to other parts of the body life will not be seriously 
jeopardized. 

In studying this state it must be recalled that one of the important functions 
of the lymph nodes is to arrest and perhaps destroy such micro-organisms as may 
endeavor to enter the general system. As soon as pathogenic germs enter a healthy 
gland one of several processes takes place. In a strong individual with great 
vital resistance the gland becomes enlarged and active in an evident endeavor to 
destroy the invaders. In this it may succeed, or the few bacilli which escape 



246 



DISEASES DUE TO A SPECIFIC INFECTION 



Fig. 51 



are caught and destroyed by adjacent glands. If the infection is virulent 
and the vital resistance is below par, the battle is more prolonged, the inflamma- 
tion in and about the gland is more active, and the general system may be saved 
by the additional safeguard of a wall of protective tissue thrown around the in- 
fected gland to protect the rest of the body. In still other cases the glands go 
on to caseation and the necrotic contents escape externally or even internally. 
It is a noteworthy fact, however, that this so-called pus is usually sterile or con- 
tains bacilli in such small numbers as to be demonstrable only by inoculation ex- 
periments. Again, if the infection wins the battle and the gland undergoes casea- 
tion, it is still possible for the area to be surrounded by a fibrous barrier which walls 
up the caseous mass and its bacilli and protects the body even though the gland 
is destroyed. 

When the protective processes fail the bacilli pass the lymph nodes, or a caseous 
gland in juxtaposition to a bloodvessel breaks, and general tuberculosis ensues as 
already described. 

Tuberculous infection of the lymph nodes takes place in four chief areas: the 
cervical glands, the mediastinal glands, and the mesenteric and retroperitoneal 
glands. In the first class the infection takes place through the tonsils, in the naso- 
pharynx, or because of the presence of bad teeth or a break in the gums. Koenigs- 
feld, as a result of elaborate experiments with human and bovine bacilli, concludes 
that the tubercle bacillus can pass through the unwounded skin. He believes that 
clinical evidence supports the view that this is the method of infection in not a 
few human beings, including cases of " scrof ulosis" in children. The mediastinal 
glands suffer by the entrance of the bacillus through the mucous membrane of 

the larynx, bronchial tubes, or smaller 
bronchioles, while the abdominal lymphat- 
ics receive their infection from the intes- 
tines. 

The diagnosis of cervical adenitis is not 
difficult, although occasionally, when the 
disease is bilateral and the swelling is 
great, the possibility of Hodgkin's disease 
may have to be considered. 

The involvement of the mediastinal 
glands by tuberculous infection results in 
a spread of the disease to the retroperi- 
toneal lymphatics or in the growth of the 
tissues affected to such a degree that 
lymphatic tumors may be formed which 
cause serious symptoms by pressure. Thus, 
the recurrent laryngeal nerve may be 
pressed upon and laryngeal spasm result, 
or the superior vena cava or pulmonary 
vein suffers from compression, and in a 
similar manner bronchial obstruction may 
ensue. More important, however, than 
the pressure symptoms are possible perforation by ulceration of the bronchi or 
trachea, or even of the bloodvessels, with rapid diffusion of the infection all 
through the body (Fig. 51). So too, it is possible for bacilli to enter the lung, 
to pass to the lymphatics, to cause disease in these glands, and finally cause 
pulmonary tuberculosis, pleural tuberculosis, or pericardial tuberculosis by softening 
and rupture into these parts through the adhesions which are formed. 

In diseases of the retrobronchial glands auscultation over the upper end of the 
sternum, when the head is well thrown back, may reveal a tracheal hum, and 




Contents of a caseous gland escaping into the 
right bronchus. (T. Fisher's case.) 



Tuberculosis 247 

careful percussion may elicit some dulness. The x-rays often give valuable 
assistance in diagnosis. 

When the mesenteric and retroperitoneal glands are involved, producing what 
is called "tabes mesenterica," the child is anemic, poorly nourished, has consti- 
pation alternating with diarrhea, and presents an enlarged abdomen ("pot-belly"). 
The size of the belly as compared to the rather wasted arms, legs, and thorax is 
noteworthy, and careful palpation may occasionally reveal enlarged glands deeply 
situated in the abdominal cavity. This condition is to be separated from tuber- 
culosis of the peritoneum and from consumption of the bowels, for both of these 
structures are usually free from the disease in these cases, although they may be 
infected by softening of the glands themselves. These lesions probably exist in 
a far larger proportion of cases than is generally thought, and end by a process of 
fibrosis and calcification, for the involvement of these glands is met with in many 
cases at autopsy when death is due to another cause, and when no suspicion of 
tuberculous infection has been present. 

Treatment of Glandular Tuberculosis. — Tuberculosis of the retrobronchial glands 
and of the retroperitoneal glands can be treated only by sunshine and fresh air 
with residence by the sea, and by the internal use of tonics, of syrup of the iodide 
of iron and cod-liver oil to combat anemia. 

Persistent enlargement of the cervical glands demands their surgical removal, 
not their incision, but their excision, because, as has already been stated, a tuber- 
culous focus is always a threatening focus. On the other hand, it cannot be denied 
that large numbers of very healthy adults bear scars showing that they have had 
cervical adenitis in early life. In these cases the battle between vital resistance and 
tuberculous infection has been won by the individual. 

Tuberculosis of the Serous Membranes. — Tuberculosis of the serous mem- 
branes may be divided into the acute and chronic forms. The acute is further 
subdivided into (a) an acute serofibrinous form, macroscopically identical or 
indistinguishable from serofibrinous serositis arising from other causes; (b) an 
acute miliary tuberculous serositis due to the invasion of the serous membrane 
by tubercle bacilli and the formation of miliary tubercles. The two forms just 
mentioned may be distinct or coincident. The chronic tuberculous serositis may 
be (a) fibrocaseous or (b) fibrohy aline. The former results from the formation of 
tuberculous exudates, in which extensive caseation gives rise to cheesy accumu- 
lations of various sizes surrounded by granulations or more fully organized fibrous 
tissue. Marked calcareous change is frequently associated with this form. The 
fibrohyaline type is characterized by marked thickening, and the formation of 
adhesions by newly developed fibrous tissue of a peculiar grayish, translucent form. 
Both the chronic forms may occur together, and the caseous masses may be 
enclosed by hyaline fibrous tissue of the type just mentioned. 

Minot states that Robert Whytt, of Edinburgh, in 1768, first accurately 
described this condition, although he had no clear conception of its cause. 
Guersant, in 1827, reported that the pathological appearances of the membranes 
were of so peculiar a type that he suggested the name "granular meningitis. " 
In 1830 Papavoine described the disease as a true tuberculous lesion, and the 
condition of moderate hydrocephalus which existed with the meningitis was recog- 
nized as having its origin in the tuberculous infection. It was reserved for W. 
W. Gerhard, of Philadelphia, in 1833, to show not only that this type of meningitis 
was tuberculous, but that it was practically in every instance secondary to some 
tuberculous lesion elsewhere. 

Acute Meningeal Tuberculosis. — Meningeal tuberculosis is an inflammation of 
the pia mater produced by an infection of this membrane with the Bacillus tuber- 
culosis and accompanied by an effusion of lymph, it may be the formation of pus, 
and the development of tubercles. These tubercles are usually very minute, but 



248 



DISEASES DUE TO A SPECIFIC INFECTION 



occasionally are large from the amalgamation of several tubercles into one. They 
are most profuse at the base of the brain, hence the name basilar meningitis, and 
extend upward on its sides following chiefly the vascular pathways. In some 
instances, however, the pia mater on the convexity of the brain contains more 
tubercles than exist at the base. Nearly always at the base there is a copious 
exudate of lymph which produces a pearly, gelatinous appearance. The lateral 
ventricles are distended with fluid. 

.Tuberculous meningitis is twice as prevalent in March, April, and May as in 
other months; probably because an earlier infection of the respiratory and abdomi- 
nal organs, hitherto latent, is made active by the severe weather and indoor life 
of the winter months. 

Fig. 52 



COCOCOCOCOCOCOCO CO CO 

2 2 2 *"S 2 ^2 W 2 ™2 w > > 


45 
























40 
























35 
























30 
























25 
























20 
























15 
























10 
























5 

















































The age incidence in 218 cases of tuberculous meningitis in children. (Holt.) 

Symptoms. — The symptoms of acute meningeal tuberculosis are very char- 
acteristic, whether it occurs in children or adults. It is much more frequently 
seen, however, in children between two and seven years. These symptoms are 
best divided into three stages for study. At first the parent notices that the child 
is unusually peevish and irritable, or in other cases peculiarly languid and indisposed 
to play. There is little restful sleep and the child often has night terrors. The 
appetite is capricious and the bowels irregular. After these symptoms have lasted 
for some days, during which time the tubercles have probably been deposited 
in the pia mater, the well-developed symptoms of the disease appear. Headache 
may be constant and is characterized by sharp exacerbations of pain which cause 
the child to give a peculiar high-pitched scream which is quite characteristic. Sud- 
den attacks of vomiting of an explosive character may occur. At times a fleeting 
delirium may be present. 

It is almost impossible in many of these cases to exclude early typhoid fever, 
for a similar train of symptoms may be presented in its early stages. 

The temperature is usually elevated, rising as high as 102° or 103°. The pulse 
is slow and the respirations are irregular and sighing. Rapid emaciation takes 
place, and if the child be very young, so that the fontanelle is open, there may be 
distinct hydrocephalic enlargement. The patient now lies stuporous or somnolent, 
with the eyes half-closed. Indeed, the appearance may be that of deep sleep 
with sighing breathing. 

In some cases in which the onset of the affection is rather acute, the patient 
suffers from a series of convulsions. I have seen such a case with Dr. Brouwer, of 
Tom's River, New Jersey, while preparing this article, in which the child had as 
many as sixty convulsions in twenty-four hours. 



TUBERCULOSIS 249 

As the exudate increases symptoms of intracranial pressure and signs of inter- 
ference with the cranial nerves appear, so that squint, twitching of the facial 
muscles, and chewing movements of the lips and jaws develop. 

Kernig's sign (see Cerebrospinal Fever) is present in most cases as is also that 
of Babinski. Brudzinski's sign consists in contraction of the muscles of one leg 
when the leg of the other side is passively bent. This is called, also, the contra- 
lateral reflex. Another symptom consists in the fact that when the neck is passively 
flexed on the chest, the child being in the dorsal decubitus, flexion of the knees and 
of the thighs on the pelvis takes place. This is called Brudzinski's neck sign. 

Even as late as this the patient may be aroused and may seem so much better 
for a time that the friends are much encouraged, but a relapse inevitably occurs. 
The child is now too stuporous to be roused, the eyes are filled with sticky secre- 
tion, and the parents find solace in the belief that even if hopelessly ill the patient 
does not suffer. The solace is, however, occasionally rudely dispelled by a shrill, 
piercing cry which, interrupting the profound stillness, is more than usually start- 
ling. As death approaches the pulse becomes very rapid, probably from vagal 
paralysis, the pupils no longer react to light, and the eyeballs are rotated upward. 

The duration of the entire illness is about ten to eighteen days, as a rule, but 
cases may die as early as the end of five days, in a convulsive seizure, or they may 
last for several weeks. 

Diagnosis. — The diagnosis of acute miliary tuberculous meningitis must be 
made with the recollection that the following conditions simulate it: Acute men- 
ingitis not due to tubercle is rare in children, has a more sudden onset, as a rule, 
and ends in a week in most cases. The delirium accompanying it is more marked, 
the febrile movement is sharper, and there is usually no history of tuberculosis 
in the family as there is in the tuberculous case in many instances. Tuberculous 
meningitis often develops very rapidly but rarely in so short a time as a few hours. 

From cerebrospinal meningitis of the epidemic type it is separated by the sudden 
onset of that disease, by the absence of its eruption, and by the fact that no cases 
of cerebrospinal meningitis have occurred in the vicinity. By spinal puncture 
the meningococcus may be obtained in one case and the tubercle bacillus in the 
other, although the latter is not constantly discovered. The fluid in cerebro- 
spinal fever contains polymorphonuclear cells and hyaline leukocytes, while in 
tuberculous meningitis recent studies seem to show that a high lymphocytosis is 
the rule. (See Cerebrospinal Fever.) 

Hemenway found the tubercle bacillus in the cerebrospinal fluid in 135 out of 
137 cases. 

As meningeal tuberculosis is so common in children the tuberculin test of Moro 
may be resorted to. This consists in rubbing into the skin of the abdomen on one 
side an ointment of Koch's Old Tuberculin, 5 c.c. with 5 grams of anhydrous 
wool fat. A piece of ointment about as large as a pea is used and, as a control, wool 
fat is rubbed into the skin of the opposite side. If the patient is tuberculous an 
erythema of the skin develops in twenty-four hours which, if the reaction is severe, 
may become papular and if very severe the papules may be greatly reddened and 
almost nodular. The great advantage of the test is its safety. If the patient is 
very gravely ill of tuberculosis no reaction may occur. 

Some clinicians divide tuberculous meningitis in children into three types: 

(1) The hemiplegic, with localized or general convulsive seizures and finally coma. 

(2) The somnolent, with fixity of the eyes without winking, with occasionally 
wakening and finally deep coma. (3) The most common eclamptic type with high 
temperature ranges, paralysis, hemiplegia, or paraplegia with much rigidity of the 
neck and finally coma. 

The prognosis is absolutely hopeless although Pitfield and others have recorded 
single cases which have recovered. 



250 DISEASES DUE TO A SPECIFIC INFECTION 

Tuberculous Pleurisy. — Tuberculous pleurisy is, in the vast majority of cases, 
secondary to tuberculous infection in other parts. Most commonly the primary 
focus is in the lungs or in the mediastinal glands. In some instances the process 
is the result of a general infection which results in miliary tuberculosis, and in these 
instances it not infrequently happens that the pleura is involved without there 
being any tuberculous process in the lungs. Thus Hodenpyl, in 91 autopsies on 
persons in whom the lungs were free from tubercle, found miliary tuberculosis 
of the pleura in 41, both the parietal and visceral layers being affected. He also 
believes that miliary tuberculosis of the pleura is apt to undergo fibrous changes. 

The tuberculous lesions are of three types. In the first type we find scattered 
patches of tuberculous deposit which are the continuation of a tuberculous pro- 
cess in the lung beneath the visceral layer of the pleura, or similar patches are found 
which are independent of lung involvement, or again patches appear upon the pari- 
etal pleura. In the second type the lesions are simply those of a widespread miliary 
tuberculosis of the pleura, and in the third type, which is representative of a more 
chronic or slow process, there is great thickening of the pleura, partly as the result 
of the organization of formed exudates and also of proliferative changes in the 
primitive serous layers. Throughout this tissue and exudate miliary tubercles, 
or masses of miliary tubercles, appear. These undergo coagulation necrosis in 
some instances. 

The presence of any one of these processes usually results in the out-pouring 
of a certain amount of effusion which is often serous and by no means rarely puru- 
lent. When it is serous it is lacking in fibrin and it may be tinged with blood. 
The physician should recall the important clinical fact, in connection with these 
tuberculous pleural effusions, that whether they be serous or purulent, an examina- 
tion of the fluid will rarely reveal the tubercle bacillus unless in some manner these 
organisms are dislodged from the pleural surface by scraping. In some cases the 
effusion is not due to the bacillus tuberculosis alone, but to an associated infection. 
Thus, in the purulent type the Pneumococcus , Streptococcus, or Staphylococcus 
pyogenes are often found. (See Empyema.) 

Reference has already been made to the fact that the visceral layer of the pleura 
is often infected by a tuberculous process in the lung as a result of direct extension. 
It may be added that in nearly every case an inflammatory area — that is, a local- 
ized pleuritis — exists over the seat of the disease in the pulmonary tissues. This 
condition often gives rise to pain in the chest and not rarely causes adhesions between 
the layers of the pleura. The inflammatory process, while tuberculous in origin, 
is not necessarily tuberculous in character, but it often becomes tuberculous, as 
already stated. 

Sometimes when the tuberculous mass in the lung softens and breaks down, the 
visceral layer of the pleura is perforated and sudden dyspnea and pain ensues, with 
the production of pneumothorax. (See Pneumothorax and Complications of 
Pulmonary Tuberculosis.) Through this opening infection with pyogenic bacilli 
occurs or the Bacillus tuberculosis becomes pyogenic, and as a consequence, pyo- 
pneumothorax develops. (See Pyopneumothorax.) 

Tuberculosis of the Pericardium. — Like tuberculosis of the pleura, pericardial 
tuberculosis is usually secondary to primary infection elsewhere. It may, however, 
be primary. It occurs in two forms : the miliary, in which the small tubercles are 
scattered or profuse, and in a form in which the entire pericardium, both in its 
visceral and parietal layers, is thickened by an inflammatory exudate which is 
associated with the development of tuberculous masses which undergo cheesy 
change. In this type the pericardial space may be nearly obliterated by the adhe- 
sions which are formed between its layers. It is a noteworthy fact that although 
the pericardium is so near the lungs and pleura it is, comparatively speaking, rarely 
infected. Out of 1048 autopsies Wells found tuberculous pericarditis only 16 



TUBERCULOSIS 251 

times and in 4500 autopsies Baginsky found it 15 times. In 1317 autopsies on 
phthisical patients Willigk found tuberculosis of the pericardium 11 times. Leudet 
found it 8 times in 299 autopsies. In 1000 autopsies Osier found 7 cases of tuber- 
culous pericarditis. Ellis has reported from the laboratories of the Jefferson 
Medical College a case in which the heart, the pericardium, and the mediastinal 
tissues formed one large, adherent mass of tuberculous nodules. 

The symptoms presented by tuberculosis of the pericardium may be so slight 
that no suspicion of pericardial disease exists during life, or they may resemble 
those of mediastinopericarditis, or adherent pericardium. (See Adherent Peri- 
cardium.) 

Tuberculosis of the Peritoneum. — Aside from tuberculosis of the lungs, tubercu- 
losis of the peritoneum is the most frequent and most important manifestation of 
tuberculous infection met by the physician. The statistics of Grawitz and Brunn 
show that in 13,422 autopsies tuberculosis of the peritoneum was found 284 times. 

In 2802 autopsies on tuberculous subjects, collected from various sources, the 
peritoneum was involved in 571, a percentage of 20.36. These figures represent 
all ages. Steiner found the peritoneum affected in 92 out of 800 cases of tuber- 
culosis occurring in children, or in 11.5 per cent. 

As to the relative frequency of the disease in adults and children Aldibert's 
statistics, based on 326 cases, are of interest. Of these 326 cases, 274, or 84.05 
per cent., occurred in adults and the remaining 52, or 15.95 per cent., occurred 
in children. It is in a very large proportion of cases secondary to tuberculous foci 
elsewhere. The combined statistics of Munstermann, Borschke, and Pribram, 
comprising 437 cases of tuberculous peritonitis examined postmortem, showed that 
only 3 were primary. 

A tuberculous family history is present in 53 per cent, of cases. The disease 
is much more common in the female than in the male; according to Nothnagel, 
90 per cent, of the cases are females. Konig's statistics make it 78 per cent. The 
proportion of tuberculous peritonitis at autopsy is about 3 per cent. 

Tuberculous peritonitis is of especial interest not only because of its frequency 
and gravity, but because it is, in one type at least, more readily cured than any 
other well-developed form of internal tuberculosis. It occurs in three chief vari- 
eties, viz., as miliary tuberculosis, as a chronic tuberculosis with large nodules and 
adhesions, and as a still more chronic form with fibroid changes. The relative 
frequency of the different forms of tuberculous peritonitis is shown by the following 
facts: In 46 cases which came under the observation of Munstermann, 25 were 
exudative, 21 were plastic, and 8 were chiefly caseous. Of the 21 plastic cases 8 
were fibrous. Herringham found fibrous adhesions in 18 out of 50 cases. Borschke 
found the miliary form in 16 out of 226 cases which came to autopsy. 

The miliary form is usually secondary to infection of the mesenteric and retro- 
peritoneal glands, but occasionally in women the infection comes from the Fallo- 
pian tubes, or in males from the bladder or other part of the genito-urinary appa- 
ratus. The miliary tubercles are scattered widely over the peritoneum on both 
its visceral and parietal layers (Fig. 53), and the surface of the liver is often pro- 
fusely peppered by these formations. In these cases there is a serous effusion into 
the peritoneum which in some instances is very profuse, particularly if the case is 
rather subacute in the rapidity of its course. In some instances the symptoms 
come on acutely and give rise to the diagnosis of appendicitis. 

Another mode of its development is well illustrated by a case I saw some years 
since with my associate, Dr. Thornton. A girl about twelve or thirteen years, 
while in apparently good health, was bathing in a pond and playing with a small 
rowboat, the sharp prow of which struck her a severe blow on the epigastrium, which 
made her nauseated and faint. She speedily began to lose weight and strength, 
became distinctly emaciated, and rapidly developed a marked ascites. The 



252 



DISEASES DUE TO A SPECIFIC INFECTION 



abdomen was opened and every peritoneal surface was found literally covered with 
tubercles. The fluid was allowed to escape, drainage was permitted, and perfect 
recovery followed. Undoubtedly the blow on the belly ruptured a tuberculous 
mesenteric or retroperitoneal gland, and so produced general peritoneal infection. 
In such a case no nodules can be found in the belly on palpation, but the presence 
of ascites in a child, or in an adult, without any signs of hepatic disease should lead 
the physician to suspect tuberculosis of this type, particularly if in addition there 
is present some fever of an irregular type, which is commonly moderate, but which 
may rise at times as high as 103° or even 104°. 

Fig. 53 




Miliary tubercles of the surface of the small bowel and mesentery. (Kast and Rumpler.) 



How opening the belly and permitting, drainage cures these cases is not known, 
but the clinical fact that such a result is often achieved is not to be denied, and 
this hohjs true even if this condition develops in adults.. Walter's statistics show 
that 50 per cent, of adults who are subjected to laparotomy recover, and Herz- 
feld's statistics give a recovery percentage of 62 per cent, for children. Marganecci 
gives 85 per cent., von Krencki 71.5 per cent., Thomas 73 per cent. Hall reports 
94 cures out of 110 operations. 

The second, caseous, type of peritoneal tuberculosis with nodules is characterized 
by the presence of caseous masses of tubercle which tend to ulcerate, which are 
associated with seropurulent, or purulent, effusion in moderate amount, and in 
which the belly cavity is not distended by fluid nor the intestines by gas, as in the 
miliary form just described, but is apt to present a peculiar pasteboard rigidity. 
The effusion in these cases is often sacculated by reason of the fact that there are 
formed adhesions which wall off spaces in which the fluid collects. These spaces 
may be between coils of intestine or contiguous mesentery, between the intestine 
and omentum, and between the omentum and the parietal peritoneum. 
- In some instances these sacculations are capable of containing but a few drachms 
of fluid, but in those cases in which fairly large peritoneal areas are separated from 



TUBERCULOSIS 



253 



the general peritoneum by adhesions very large accumulations of fluid may be 
present. If this takes place in the flanks or lower zone of the abdomen, where it 
usually occurs, the symptoms may very closely resemble ovarian cyst, and many 
cases have been operated upon with the idea that ovarian disease was the cause 
of the fluctuating mass. Careful palpation under ether may reveal an irregular 
nodular edge to the growth, or nodules elsewhere may explain the real state. 
Sometimes the masses are not in great numbers, but occur singly, and if the 
intestine be involved, tuberculous ulceration may result and induce a fulminating 
peritonitis. Often the presence of tuberculosis is not suspected until the belly is 
opened. 

Fig. 54 




A case of peritoneal tuberculosis of the fibroid type in a man aged twenty-one years, with great general 

atrophy and scaphoid belly. 

The chronic fibroid type may resemble the nodular type just spoken of, but in it 
the matting of the abdominal contents into a small compact mass is quite extra- 
ordinary, the intestines and omentum being glued together in an adhesive bundle 
which cannot be separated. In these cases the gluing together of coils of intestine 
results in intestinal obstruction. In this type the belly is often remarkably sca- 
phoid and the degree of general emaciation extraordinary. Some idea of its degree 
may be gathered from the illustrations shown in Figs. 54 and 55. 

The symptoms of chronic fibroid peritoneal tuberculosis are characteristic. In 
addition to the general emaciation it will often be found that the skin over the abdo- 
men looks and feels peculiarly rough and scurf -like, or as if there was marked " goose- 
flesh" over this part. In addition it is often stained a curious dirty yellow or is 



254 



DISEASES DUE TO A SPECIFIC INFECTION 



light brownish in hue. The abdominal wall is not only hard, but the abdominal 
muscles are readily felt by the finger-tips, while deep palpation reveals nodules 
or gives the sense of abdominal vacancy as if the patient had been eviscerated. The 
temperature range is not markedly febrile, and often is subnormal, ranging from 96° 
in the morning to 99° at night. 

Fig. 55 




Extreme emaciation in a woman, due to thoracic and peritoneal tuberculosis of the fibroid type. 



It is not, however, in these well-advanced forms of the disease that the physician 
has difficulty in making a diagnosis, but in those cases in which there is general 
impairment of health without marked general emaciation; and it may be with- 
out distinct abdominal symptoms save obstinate constipation, with occasionally 
attacks of active purging, or in those instances in which the patient is still hale 
and robust, but suffers from some abdominal distress. These cases often present 
a distinct abdominal tumor, or tumors, composed of tuberculous nodules, or of 
nodules combined with thickened knuckles of intestine which may be so firmly held 
by adhesions of exuded lymph that gas and feces produce a tumor that cannot be 
readily dispelled by pressure. 

Sometimes a tumor is met with in the epigastric area extending across the 
abdomen at this level, or just above the umbilicus, formed by a peculiar rolling 
of the omentum as a workman would roll up his apron and stow it under his belt. 
A similar condition is sometimes found in carcinomatosis of the peritoneum, but 
such a roll is usually due to tuberculosis. 

When the mesenteric glands or retroperitoneal glands are gravely infected, a 
single nodule or several nodules may be easily palpated. When multiple they are 
usually tuberculous, but where it is single a careful exclusion of malignant growth 
must be made by finding a tuberculous focus elsewhere, or by the tuberculin test. 

Treatment of Tuberculosis of the Peritoneum. — The treatment of the subacute 
or chronic forms of peritoneal tuberculosis consists in operation. The first thing 
to be looked for at operation in peritoneal tuberculosis in the female is the Fallo- 
pian tubes, for they are the cause in the majority of cases. If diseased they must 
be removed, for such tubes will persistently infect the peritoneum. 

The operative treatment is most successful, as a rule, when the state is char- 
acterized by sufficient effusion to keep the intestinal coils apart, and so prevent 
adhesions. The operation consists in a single opening of the peritoneal cavity 
and a free entrance into it of atmospheric air. Any attempt to remove the tuber- 
culous masses is useless, unless a single mass can be excised without damaging the 
tissues and without the danger of setting free bacilli to cause infection elsewhere. 
In sacculated cases the sac should be incised, drained, and packed with iodoform 
gauze. In the chronic fibroid type operation will not be productive of much good, 
for it cannot result in the loosening of the shrivelled omentum or of the cicatricial 
contractions about the intestines, but in these cases celiotomy may arrest the 
disease. When there are sacculations with accumulations of fluid or pus, the 



TUBERCULOSIS 255 

operation is of value in that it evacuates these collections and may arrest the 
process, but it does not promise complete cure as in the cases with large ascites. 
(For statistics see page 252.) 

The medical treatment consists in active feeding with easily assimilated food- 
stuffs and in the use of cod-liver oil. If anemia is marked the syrup of the iodide 
of iron may be given in alternate weeks with the oil, and I have certainly seen good 
results follow the use of nightly iodoform inunctions over the abdomen, a mixture 
of olive oil and iodoform in the proportion of 10 grains to the ounce being used. 
Iodoform suppositories, 10 grains each, may also be employed. 

Pulmonary Tuberculosis. — Pulmonary tuberculosis, or pulmonary phthisis, as 
it is sometimes called because it causes such emaciation or wasting, is the most 
prevalent disease to which man is susceptible. It affects, as a rule, young adults 
or adolescents (see Frequency of Tuberculosis), but it may occur at any period 
of life, being comparatively rare in the first five years of existence and in the period 
of well-developed old age. 

As a result of infection of the lung by the Bacillus tuberculosis we find three 
types of pulmonary disease: the miliary, the chronic or caseating, ulcerative type, 
and the so-called fibroid type. Of these the second form is by far the most common 
and the most important from the clinical stand-point. The infection takes place 
as a primary process through the entrance of the bacillus by the respiratory passages, 
or secondarily as a result of the transference of the bacillus from some primary 
focus by the bloodvessels or lymphatics. 

Much discussion has arisen as to the mode by which the first focus of tuberculosis 
in the lung is produced. Birch-Hirschfeld proved that, in many cases at least, 
the bacilli gain their primary lodgement in a bronchiole, where the lung is least 
able to get rid of foreign matter by coughing, and that, from a primary tuberculous 
lesion at this point the rest of the lung becomes infected. Aufrecht also proved 
that the primary infection sometimes takes place through the circulation, to which 
the bacilli gain access by the tonsils and the alimentary canal, the pulmonary focus 
being due to a plugging of a vessel by their presence. 

Whether the means of infection be respiratory or vascular, the ultimate lesions 
are often the same; but the early lesions differ, and the prognosis may be governed 
to some extent by the finding of a primary focus elsewhere which is responsible 
for the pulmonary lesions. 

The early lesions of pulmonary tuberculosis, due to infection by inhalation (aero- 
genous infection), are found chiefly in the wall of a bronchiole and in the alveoli 
grouped around it and forming lobules. Either by extension from this infected 
lobule or by the fusion of a number of similarly affected lobules, large tuberculous 
masses are speedily formed. They are also characterized by the extension of the 
tuberculous infection to the tissues around the bronchioles, giving rise to an extend- 
ing bronchopneumonia which is nodular in its character owing to the primary 
lobular limitations. 

The early lesions of the form of tuberculosis of the lung which is due to infection 
by way of the bloodvessels or lymphatics are found in the walls of the alveoli — that 
is to say, in the connective tissue between the alveoli and in the interlobular capil- 
laries. The disease may be well scattered through both lungs in either instance, but 
in the first type the patches are larger, involving, it may be, a lobule at a time, 
whereas in the second form they are diminutive and more of the nature of miliary 
tubercles as observed elsewhere. This we would naturally expect from what has 
been said of the cause of miliary tuberculosis. After the disease has existed some 
time the areas of tuberculous deposit in either case may attain the same size. 

The discovery that there is a primary seat of tuberculosis, which has given rise 
to the pulmonary lesions, requires a graver prognosis because it indicates that there 
is more than one focus, and because such a primary lesion which has caused pul- 



256 DISEASES DUE TO A SPECIFIC INFECTION 

monary disease by infection through the vessels may have caused other foci of 
infection elsewhere by the same means. Again, the disease is more apt to be 
generalized throughout the lung in this case than in the inspiratory form of infection. 

Tuberculous infection of the lung, therefore, produces the following changes 
in the pulmonary tissues : The gray and yellow tubercles, which differ in no way 
from those tubercles already described as occurring elsewhere, become amalga- 
mated and form caseous masses, with, sooner or later, the characteristic softening 
of the growth; if the tubercles do not undergo necrosis and fail to coalesce, the 
accompanying low-grade irritation or inflammation may lead to fibroid changes. 
Along with these changes in the tubercles themselves there is always associated a 
considerable amount of inflammation, which often results in the formation of an 
exudate which fills the air vesicles just as it does in croupous or catarrhal pneumonia. 
Side by side with the development of the tubercles in the lungs, and of the pneu- 
monic exudate, there develops in the interstitial tissues themselves a process 
which is tuberculous and which causes thickening. This is the so-called tuberculous 
infiltration of Laennec. The lung, therefore, becomes solidified, partly as the 
result of the tuberculous growth, and partly as a result of the inflammation caused 
bv the bacillus. 

Sooner or later a large part of the infiltrated area undergoes caseation. Around 
this focus or area of active tuberculous process inflammatory changes occur, which 
may cause the neighboring parts of the lung to present lesions like those of catarrhal 
pneumonia. On making a section of such an area the lung presents a smooth, 
homogeneous surface, as does a piece of Castile soap or cheese (Figs. 56 and 57), 
but if the process is not far advanced in caseation it may show a peculiar gelatinous 
appearance, the so-called gelatinous pneumonia. 

The fourth condition, which is noteworthy, is the lack of bloodvessels in the 
diseased portion of the lung, for no new ones are formed with the morbid growth 
and the ones naturally present are occluded by the disease which involves their 
coats and causes thrombosis; the resulting thrombus in turn undergoes caseation 
so that the vessels disappear in the tuberculous mass. These vascular changes 
possess great interest for this reason, and also because by this means the tubercle 
bacillus may enter the blood and infect other points, or by a process of ulceration 
of the vessel wall hemorrhages may occur. 

All tuberculous lesions in the lungs are, therefore, very similar in character; 
all manifest a disposition to undergo similar reparative or degenerative changes, 
the alterations being differences in degree rather than in kind. 

When the restrictive efforts of the affected organ are inadequate caseation 
extends until a bronchus is reached, through which the products *of necrosis are 
removed by drainage and expectoration. Air takes the place of the material 
removed, and so a cavity is formed, the walls of which are lined by broken-down 
tubercle-containing material, which continually softens (caseation) and melts 
down, thereby enlarging the cavity. This cheesy material is loaded with bacilli 
in far greater numbers than they exist in the solidified part of the lung. The 
cavity is also infected by the pathogenic bacteria inhaled in the air, and these aid 
in the destructive local process and increase the general toxemia. 

It is interesting to note that the smaller bronchioles are usually closed by tuber- 
culous infiltration as the disease progresses and only the larger ones remain patulous. 
These communicate with the cavities by small lateral orifices as the tube courses 
along the wall of the excavation, or open into the cavity like the small papilla of 
a duct. The walls of the bronchial tubes which provide drainage for the cavities 
are often the site of tuberculous ulceration. 

Tuberculous cavities are of two classes, moist or secreting, and dry. The first 
is that met with in the acute types of the disease and it often increases in size very 
rapidly. The contents of this cavity are usually composed of caseous matter, 



TUBERCULOSIS 



257 



broken-down lung tissue, pus cells, and tubercle bacilli, and the walls of the cavity 
suffer from active ulceration. 

The dry cavity, on the other hand, is found in the chronic cases which often 
last for years; efforts at repair smooth the wall, in which fibrous tissue develops, 
and it not rarely happens that by the fibroid process already described as occurring 
in this disease the size of the cavity is greatly decreased. These cavities contain 
but little material beyond a small amount of pus, and from their walls hemorrhage 
may rarely occur as the result of erosion of large vessels. Secondary cavities are 
due to the spread of the infection by the vessels or bronchi, and follow the secondary 
caseation process already described. 

Fig. 56 




Caseous consolidation in the upper lobe and bronchiectasis in the lower lobe. (Kast and Rumpler.) 

We have now passed over the stage of pulmonary infection, consolidation, 
caseation, and disintegration, and come to the study of the processes often instituted 
in reparation. This is not a part of the tuberculous process. The small-cell 
infiltration and exudation in the inflammatory zone surrounding the area of infection 
sometimes escape speedy involvement in the tuberculous process, and instead 
of degenerating rapidly aid in the production of fibrous tissue. At first it is 
immature and imperfect in character, but as time passes it becomes firm, dense, 
and fully-formed fibrous tissue. If the tuberculous focus is small it may be com- 
pletely encapsulated by this fibrous covering, with the result that the caseous 
mass becomes calcareous or is gradually absorbed so that only a puckered scar 
results. 

When a cavity heals its walls undergo cicatricial contraction, but it is probably 
never obliterated unless it has been exceedingly small before the healing process 
began. 
17 



258 



DISEASES DUE TO A SPECIFIC INFECTION 



In regard to the distribution of the cavities Ewart has collected the following 
interesting statistics. In 791 cases cavity occurred at the apex in 282 cases, in 
the dorso-axillary region in 227, in the mammary region in 189, in the sternal region 
in 61, and at the base in 32. 

The growth of fibrous tissue is most marked in those parts of the lung which 
ordinarily possess the greatest amount of connective tissue, as in the interlobar 
and interlobular portions of the pulmonary tissues. 

Fig. 57 




Caseous consolidation above. Red hepatization below. (Kast and Rumpler.) 

If a large cavity is present bands of fibrous tissue may persist, and, stretching 
across it, form trabecular (Fig. 58). At times these trabecular consist largely of 
good-sized bloodvessels which have not been closed by the tuberculous process. 
If they are perforated by ulceration, so violent a hemorrhage may occur as to 
cause death, even though the process of advancing cicatrization is endeavoring 
to limit the progress of the disease. At times the lesion in the bloodvessel develops 
into an aneurysm, and this may rupture, causing hemoptysis. 

Finally, we find still another process designed to arrest the disease and save the 
patient, namely, thickening of the pleura which protects the pleural cavity from 
pneumothorax and which, as it undergoes fibroid change, contracts and so acts 
as a sort of fibrous capsule of the entire diseased lung. 

Fibroid tuberculosis of the lungs is a very chronic condition, already described 
from the pathological stand-point, and characterized by marked overgrowth of 



TUBERCULOSIS 



259 



fibroid tissue in the affected organ. A somewhat similar state exists when no 
tubercles have been present. The primary areas of tuberculous invasion become 
invested by fibrous tissues so that tuberculous bronchopneumonia becomes gradu- 
ally changed into one of fibrous overgrowth, with shrinkage of the parts so that 
the lung becomes much decreased in size and even the chest may be sunken and 
deformed. These thoracic changes are, however, more marked in those cases in 
which the visceral pleura is also involved in the cicatricial or fibroid process. The 
disease loses many of the symptoms of ordinary pulmonary tuberculosis, and while 

Fig. 58 




2 cm. 

Left lung, superior lobe and upper part of lower lobe, the former containing a number of communicating 
caverns, brought about by tuberculous infiltration, caseation, and evacuation of the contents through 
the bronchi: A, aneurysmal dilatation of an artery spanning one margin of a large cavity; B. communica- 
tion with another cavity; C, C, thickened and adherent pleura between the two involved lobes. The 
pleura over both lobes is thickened, and at the autopsy the cavity had been obliterated by universal 
adhesion; D, the pointer from the letter D leads to a small group of tubercles in which caseation is just 
beginning; E, a fused group of tubercles, further advanced than at Z>. 



the constricted cavities may contain bacilli and the bronchial tubes provide copious 
material for expectoration, the process of general wasting goes on very slowly and 
the strength does not decrease with any speed. Such conditions are usually seen 
in patients of middle life and may last for ten to twenty years. Death finally 
comes from dilatation of the heart or from an acute complicating pneumonia or a 
hemorrhage from an ulcerated bronchial vessel. 

Symptoms of Pulmonary Tuberculosis.— The onset of this, the most common 
type of the disease, is often such as to mislead the physician. In some cases there 
is no cough, but only a slight rise of evening temperature preceded by chilly sensations. 



260 DISEASES DUE TO A SPECIFIC INFECTION 

If the cases in which these symptoms have given rise to the diagnosis of " malarial 
poisoning" could be gathered together they would be a "multitude which none 
can number." In many instances this error has been a deserved reproach to 
the physician who made it, because he has not searched for tuberculosis as a cause 
but has simply prescribed quinine. 

• Another type of onset is found in those cases which present insidious pleural 
effusion. (See Pleurisy with Effusion.) In still a third series the primary symp- 
toms are laryngeal. As these lines are written I am sending a case of active tuber- 
culosis of the lungs to New Mexico. He was told by several skilled laryngologists 
that his husky voice was due to gout of the larynx, whereas if they had examined 
his chest marked signs of phthisis would have made the diagnosis evident. All 
cases presenting signs of persistent hoarseness should cause the physician to search 
for tuberculosis, syphilis, papilloma of the larynx, and aneurysm of the aorta. 

In the fourth type the very earliest sign of the disease is spitting of blood. There 
can be no doubt that in the vast majority of instances the bringing up of blood 
from the bronchial tubes means tuberculous infection. The only other causes 
which are at all frequent in the production of hemoptysis are acute pneumonia 
or pulmonary infarction due to cardiac lesions. It not infrequently occurs that 
hemoptysis in the stage of onset is scanty and associated with no demonstrable 
physical signs, the lesion being situated in such a position that it readily perforates 
a vessel. (See p. 261.) 

The symptoms of pulmonary tuberculosis may be divided for study into those 
which are complained of by the patient, those which can be readily observed by 
the physician, and those which can be demonstrated by the aid of physical diagnosis. 
It must be remembered, however, that the severity of the symptoms of all kinds 
varies to an extraordinary degree in different cases and at different times in the 
same case. It is necessary, therefore, in speaking of the symptoms to adhere to 
the description of the three types of the disease named when discussing its path- 
ology. At the outset, however, it may be said that two symptoms are present in 
all cases at some period, namely, loss of flesh and fever. 

It may be said of the fever of tuberculosis that it is usually moderate, varying 
from 100° to 102°, although at times it may reach 103°. When the temperature 
reaches higher than this it is probably not due solely to the tuberculous infection, 
but to septic or hectic fever, depending upon associated staphylococcic, pneumo- 
coccic, or streptococcic infection. In all instances in which the fever is high it is 
prone to run a very uncertain and aberrant course, save that it is high at night and 
low in the morning, as in nearly all fevers, particularly that due to sepsis. It is 
very easily broken, as a rule, by the use of any antipyretic medicine, but this 
effect of drugs is, of course, very temporary. 

The loss of weight depends upon several causes for its existence. The loss of 
appetite, the cough, which is exhausting and sleep-destroying, the sweats, the 
disorders of digestion, and the anemia are all active factors in decreasing flesh. 
Last, but by no means least, as a cause of loss of weight, is to be considered the 
toxemia of the disease itself. 

The rapidity of loss of flesh is sometimes remarkable, amounting to as much 
as four or five pounds a week. This rapidity of loss is a good guide to the activity 
of the tuberculous process, for if it be rapid the outlook as to the progress of the 
patient's illness is gloomy. On the other hand, gain in weight is correspondingly 
encouraging in that it indicates a very slow, or arrested, progress of the disease. 

A third symptom, often of very great annoyance to the patient, is siceating, which 
is particularly prone to occur at night. These sweats vary greatly in severity, 
and seem to occur because of the relaxation of sleep, but in many cases their true 
cause is the hectic or septic state of the patient. If they are not severe enough to 
exhaust the patient or disturb his rest, they are to be regarded as an effort to 



TUBERCULOSIS 261 

diminish toxemia, but if they become so profuse as to be called colliquative they 
are deleterious. At times the sweat follows a sharp rise of septic temperature. 
It is hardly necessary to add that profuse night sweats, while a common symptom 
in well-developed phthisis, are by no means pathognomonic of this disease. 

Aside from the loss of flesh, fever, and sweats, the most constant symptom of 
pulmonary tuberculosis is cough. It varies in its character and in its degree in 
different cases of the subacute or chronic form of the disease. In the early stages 
it is apt to be worse on going to bed or on getting up in the morning, and in 
these stages is usually annoy ingly unproductive and persistent. As the disease 
advances and the process of softening begins to take place in the consolidated 
part of the lung, the cough becomes less dry and more productive. When cavities 
are formed, marked increase in morning cough is very prone to occur in order that 
the cavity may be well cleared of the accumulations which have occurred in it 
during the night. Cough is to be regarded as a useful attempt on the part of the 
system to keep the lungs clear. Only when it provokes hemorrhage or is so excessive 
as to cause exhaustion, loss of sleep, or vomiting is it to be regarded as an evil. 

Aside from the general symptoms of tuberculosis already described, patients 
with pulmonary tuberculosis often have severe pain in the chest, which is due to an 
extension of the inflammation to the visceral layer of the pleura. They also suffer 
from dyspnea on exertion partly because of the diminished area of lung and lessened 
ability of the blood to carry oxygen, partly from cardiac feebleness, and partly 
because the general nervous system and the muscles are so feeble that any exercise 
leads to exhaustion. 

The sputum is composed of mucopurulent material from the associated chronic 
bronchitis, or if the lung is beginning to undergo softening the expectorated material 
is thin, with small, pale and greenish-looking masses in it — the so-called " nummular 
sputum/' Sometimes when a cavity is being emptied or there is a marked bron- 
chorrhea the sputum is very purulent. 

The quantity of sputum varies greatly. The average amount in an active 
case varies from 1 to 4 ounces a day, but I have known a patient with several 
cavities to raise a pint or more in twenty-four hours. 

Complications. — A frequent symptom of the ulcerative type of pulmonary tuber- 
culosis is hemoptysis, but a large number of cases pass through all stages of the 
disease without bringing up a particle of blood. It is absent, according to West, 
in from 20 to 30 per cent, of cases. Hemoptysis is more than three times as frequent 
in males as in females. The quantity of blood lost varies from a mere streak in 
the sputum to 3 ounces in the average case. Occasionally it amounts to 4 or 6 
ounces, but a little blood "goes a great way," and patients will state that they have 
spit a quart when only a few ounces have been raised. It is rare for as large an 
amount as a pint to be coughed up in twenty-four hours. Very rarely a large gush 
causes death by suffocation. Sometimes the hemorrhage is concealed and unaccom- 
panied by blood-tinged sputum. If of a dribbling type it may inundate a large 
part of the lung or even fill a cavity and cause death without any external manifes- 
tation; such cases are rare. A free hemorrhage nearly always means the presence 
of an ulcerating cavity. The blood in hemoptysis may come from the pulmonary 
vessels or from the bronchial vessels, but it is usually from the former. Flick, 
Ravenel and Irwin believe that hemoptysis is usually due to pneumococcus 
infection. 

All ages may suffer from hemorrhage from the lungs, but the period from eighteen 
to thirty-five is of course that of greatest frequency. Hoffnung has recorded a 
case in a child of ten months and Powell one in a child at seven months of age. 
The hemorrhage occurs most frequently at night. 

The blood which is expelled in true hemoptysis is usually frothy and is brought 
up by coughing. It is also usually red except in instances of slow oozing into a 



262 DISEASES DUE TO A SPECIFIC INFECTION 

cavity, when it may appear as a dark clot or clots. When the bleeding is profuse 
the blood gushes out of the mouth. Often before the spitting of blood actually 
takes place a salty, or bloody, taste in the mouth is persistently present for some 
time. 

Hemoptysis due to pulmonary tuberculosis is to be separated from hematemesis 
by the fact that the first occurs with coughing and the second with retching or 
vomiting. It is further differentiated by the fact that the blood is frothy and 
filled with mucus and bubbles and is usually bright red in hemoptysis, whereas 
in hematemesis it is usually pure or discolored by contact with the gastric juice. 
In one state the history of pulmonary disease, or the discovery of lesions in the 
lungs, reveals the seat of the hemorrhage ; in the other gastric symptoms are present. 
In hemoptysis the blood is often brought up in small degree for several days, 
whereas in hematemesis it is usually brought up once or twice on one day and then 
the bleeding ceases. 

In this connection it must not be forgotten that hemoptysis, or blood-spitting, 
is not always due to tuberculosis of the lungs. It is sometimes present in the 
stage of onset in acute croupous pneumonia. It is not rarely met with in thoracic 
aneurysm, and its occurrence, unless it be very profuse, does not necessarily mean 
immediate death in the latter type of cases, since it not rarely happens that the 
vessel oozes blood for several days before it finally completely gives way. Some- 
times by the pressure of the aneurysmal sac some small vessel may be eroded so 
that the blood escapes from it alone. Slight hemoptysis occurs in some cases of 
malignant intrathoracic growth, and swollen glands by pressure may rupture a 
neighboring vessel and cause leakage of blood. Again, hemoptysis often develops 
in mild degree as a result of pulmonary infarction. 

Among the other causes of hemoptysis may be mentioned hemorrhage from a 
superficial vessel in a bronchial tube in bronchiectasis, and from the larynx in 
malignant and non-malignant growth or tuberculosis of this organ. Hemoptysis 
is sometimes due to a varicose condition of the veins at the root of the tongue. 

A peculiar form of hemoptysis which lasts in some cases for years is seen in 
Formosa and Japan, due to the presence of the parasite Paragonimus westermanni. 
(See Parasitic Hemoptysis.) 

Although hemoptysis in the great majority of cases indicates pulmonary tuber- 
culosis, it must not be forgotten that this symptom sometimes occurs for years 
without any other signs of the disease appearing. I have one case in mind in 
which the young wife of a student at the Jefferson College had repeated hemorrhages 
during an entire winter without any physical signs being present, and continued to 
have them for many years afterward. Eight years after they began she still 
had them on exertion, but was the picture of health, had no signs of aneurysm or 
tuberculosis, and had gained thirty-five pounds. 

Many of the other complications of pulmonary tuberculosis in addition to 
vomiting, diarrhea, and hemoptysis have already been considered when discussing 
the disease as it affects serous membranes, as in pleurisy and pericarditis. The 
most important is pneumothorax, which follows the perforation of the tuberculous 
lesion into the pleura. It occurs in from 3 to 10 per cent, of all cases, is often 
fatal if sudden in onset, and may cause distressing dyspnea. West says that of 
39 cases, 2 died in an hour, 8 others in twenty-four hours, and 29 out of the 39 
inside of two weeks. The mortality is about 90 per cent. Effusion usually speedily 
develops. I have seen great relief follow gentle aspiration of the air from the thorax, 
but aspiration is to be avoided save when the pressure produces urgent dyspnea. 
Sometimes the pneumothorax develops insidiously without severe symptoms, 
producing what is called "latent pneumothorax." (See Pneumothorax.) 

A still more rare affection seen in some cases of the chronic forms of pulmonary 
tuberculosis is pulmonary osteo-arthropathy (which see). 



TUBERCULOSIS 263 

Diagnosis. — Before the physical signs of pulmonary tuberculosis are dealt with 
the sites of the lesions usually present may be discussed, so that they may be 
examined with particular interest in every case. The apices are the parts affected 
in the vast majority of cases, and it is here that the primary lesion is usually found, 
even if other parts become more severely diseased later on. The process as it 
extends is prone to travel backward rather than forward. No satisfactory explana- 
tion of this fact is obtainable. 

Next to the apices the upper part of the middle lobe on the right side is most 
frequently the site of infection, or the upper part of the lower lobe on the left side 
is diseased. The area of the upper part of the middle lobe on the right side is one 
which is often overlooked, owing to the fact that it is covered by the right scapula. 
Only when this scapula is raised by the hand being placed on the top of the head is 
the spot of impaired resonance exposed at its lower margin. 

Tuberculosis of the bases rarely occurs except after the disease has lasted long 
enough to involve the whole lung. 

Physical Signs. — The two methods of physical diagnosis which give us the 
most information in cases of pulmonary tuberculosis are percussion and auscultation. 
Throughout that period in which there is infiltration or consolidation of the lung 
percussion gives impaired resonance or dulness over all the part affected, unless the 
lesion be deep-seated, in which case light percussion over this part may produce a 
sound which is high-pitched or slightly tympanitic. It is of the utmost importance 
that the physician apply the light percussion test skilfully, as infiltration is the 
first or early lesion, and this is the stage when a cure is usually possible. The most 
important areas to be so tested are the apices, anteriorly, below and above the 
clavicles, with and without forced inspiration, and on the top of the shoulder. 

At the right apex the resonance on percussion, the vocal resonance on auscultation 
and the vocal fremitus on palpation are all greater than at the left apex in most 
healthy persons. With the development of cavity the percussion note over it 
undergoes a change and there is developed a high-pitched tympanitic resonance, 
which careful percussion will show to be surrounded by an area, or ring, of impaired 
resonance representing the surrounding area of infiltrated lung tissue. At times 
in the neighborhood of tuberculous lesions in the lungs hyperresonance is developed 
on percussion, as the result of a compensatory emphysema of the lung. If the 
cavity communicate with a bronchus and the patient takes a breath and holds it, 
with the mouth open, percussion may develop the so-called "cracked-pot sound. " 

Auscultation reveals, in the earliest stages of infiltration, prolongation of expira- 
tion in the part involved. This is a physical sign of very great importance. Again, 
it may reveal some harshness of the inspiratory murmur and both inspiration and 
expiration may be more distinct and rougher than in health. 

Occasionally careful auscultation will also reveal a few very fine rales on forced 
inspiration. In lesions of the apex on the left side such a forced inspiration not 
rarely produces an inspiratory sound which is interrupted by the action of the heart 
three or four times during the act of drawing air into the lung and forced respirations 
followed by a cough may develop rales or cog-wheel sounds not otherwise demon- 
strated. 

It must not be forgotten that negative signs may be as valuable as positive 
ones, and therefore if the infiltration produces an absence of breath sounds at the 
infected spot this may indicate disease as surely as do the more positive signs 
already named. 

If the physician listens carefully over the area of consolidation with his disen- 
gaged ear closed by his finger-tip, and the patient will say one, two, three in a stage 
whisper, the area of consolidation will give greater vocal resonance than the same 
area in the healthy lung. 

With the development of softening the fine dry rales which have been heard at 



264 DISEASES DUE TO A SPECIFIC INFECTION 

first become coarse and moist, and as a cavity is formed they may become even 
bubbling or gurgling. These rales sometimes possess a curious metallic sound. 

As the cavity is formed the vocal resonance over it increases and may become 
startlingly clear, so that when the patient speaks the sound of the voice is trans- 
mitted with great clearness through the chest wall. This is called pectoriloquy. 

Over such a cavity cavernous breathing is often heard, or, if the cavity is a 
small one, the breathing may be hollow, tubular, or amphoric, as if the patient 
were blowing with his lips over the mouth of an open bottle. 

Moist cavities also present on auscultation, in addition to large moist rales, 
metallic tinkling due to the dropping of fluid from their walls. This metallic 
tinkling is to be separated from the metallic tinkling of hydropneumothorax by 
the absence of the physical signs of fluid in a dependent part of the chest, and by 
the fact that such a cavity is near the upper part of the lung and so produces this 
sign in the upper zone of the chest. 

The sounds arising from a dry cavity are blowing or amphoric. When such a 
cavity has existed long enough for marked fibroid change to occur it often happens 
that the chest over the affected part is greatly flattened, and it may be decreased 
in all diameters. Compensatory hypertrophy of the opposite lung causes an 
increase in the size of the chest on that side, and this emphasizes the difference 
between the two sides. Further than this, the contraction process may great^ 
displace nearby organs. Thus, if the left lung undergoes this change, the right 
lung, partly from enlargement and partly from traction, may extend as far as three 
inches to the left of the sternum, the heart may be drawn upward and tilted to 
the left of the nipple as high as the third interspace. Even the stomach may be 
drawn upward. On the other hand, when the right lung is affected by the disease 
the heart may be drawn to the right under the sternum, the liver may be pulled 
upward, and the left lung drawn well over to the right side of the chest. Most of 
these marked changes are due to associated pleural adhesions, and these may cause 
deformity of the entire chest. 

The diagnosis of cavity from bronchiectasis is made by the recollection that a 
cavity is usually near the apex, and bronchiectatic spaces are at the base, as a rule, 
although they may develop as high as the third or fourth rib. If so, they are 
nearer the sternum than is the cavity. Again, in cases of cavity the area around 
the hollow space is usually dull on percussion, whereas in bronchiectasis it is usually 
hyperresonant from emphysema. 

It is to be remembered that tuberculosis may occur as a complication of bronchiec- 
tasis, but that well-developed bronchiectasis rarely occurs in tuberculosis except 
in old chronic cases with much contraction due to fibroid change. 

Palpation. — Palpation over that portion of the chest which is infiltrated by a 
tuberculous process, or in which a cavity has already formed, also presents very 
definite physical signs when the patient speaks, namely, a marked increase in 
vocal fremitus. If the cavity is superficial and of any size it may be possible to 
feel the bubbling rales which are produced by its contents. Hyperalgesia to 
irritation, heat and cold sometimes exists in the skin over areas in the lung affected 
by pulmonary tuberculosis, and this sign may decrease as convalescence is estab- 
lished. 

Inspection. — Inspection of a well-advanced case of pulmonary tuberculosis 
occurring in one .whose configuration is naturally phthisical reveals a very typical 
picture, but in those with well-developed chests very advanced lesions of the lungs 
may be present before any change in the appearance of the chest is manifest. 

The physical signs of acute pneumonic tuberculosis are at first the same as those 
of acute pneumonia. There are bronchial or tubular breathing, dulness on percus- 
sion, and fine crepitant rales. As the disease progresses these signs become modified 



TUBERCULOSIS 265 

to the extent that the rales become coarse and more moist in character, and signs 
of softening are therefore developed. 

In the diagnosis of a case of this character it may not be possible to state accu- 
rately the true cause of the disease for several days, but the following points are 
of some value, namely, the discovery in the history of the patient, or in the body 
at the time, of a tuberculous infection, as of enlarged cervical glands, or of tuber- 
culous masses elsewhere, as in a Fallopian tube or in a testicle or joint; the general 
appearance of the- patient as to nutrition, for the pale, anemic patient with the 
typical slim bones and large joints, large orbital spaces, and delicate features is 
more apt to succumb to the bacillus tuberculosis than to the pneumococcus. On 
the other hand, it is to be remembered that robust and hearty persons may develop 
acute tuberculous pneumonia and die in a short period. The presence of the 
pneumococcus in the sputum is of little diagnostic value, but the discovery of the 
tubercle bacillus will be of great aid in determining the cause of the illness. 

Microscopic Diagnosis. — An examination of the sputum in pulmonary tuber- 
culosis by the aid of the microscope reveals shreds of mucus mixed with particles 
of caseous substance and small round cells, leukocytes, and pus corpuscles. Crystals 
of the triple phosphates, oxalates, and of tyrosin and leucin are often present. All 
these constituents of the sputum are, however, of little importance as compared to 
two others, namely, the presence of elastic-tissue fibres possessing the morphology 
and arrangement of pulmonary reticulum, showing that breaking down of the lung 
is taking place, and tubercle bacilli, the presence of which reveals the fact that they 
are the cause of this condition. The bacilli are indisputable evidence of the pres- 
ence of the disease, but their absence from a specimen of sputum does not exclude 
tuberculosis, because they may happen to be absent from that individual sample, 
or they are absent because the sputum does not come from a part of the lung in 
which breaking down is taking place. Even an old cavity, if it is well drained, 
may not provide bacilli constantly. 

Yellow, elastic fibres are to be sought for by spreading the sputum in a thin 
layer on a pane of glass placed over a blackened surface. A second sheet of glass 
is placed over this and the sputum smeared by moving the upper piece laterally. 
The particles of elastic tissue are usually contained in small masses of yellowish- 
gray material, which, if crushed and placed under the microscope, are found to 
consist of characteristic, double-contoured, interlacing, yellow, elastic fibres, 
having the arrangement of the pulmonary elastica. Elastic-tissue stains are of 
value in the hands of experienced microscopists. As many meats are rich in elastic 
tissue which may lodge in the mouth, the mere finding of such structures in the 
sputum does not justify the diagnosis of "breaking down" of the lung. The 
recognition of pulmonary elastica must be based on the shape and arrangement 
indicated. Occasionally small pieces of calcareous matter are found in the sputum. 

The bacilli are sought for in the following manner: A microscope slide is thor- 
oughly cleansed and dried. From the sputum spread out on a glass plate, or in a 
Petri dish, nummular particles if present are selected, or if absent the thicker 
portion of the sputum is spread in a thin layer over the surface of the slide and 
allowed to dry spontaneously. The dried film on the slide, surface upward, is 
passed three times through the flame in order to fix the thin layer firmly to the 
slide. Cover-glasses may be used instead of slides, but possess no special advan- 
tages. Of the many stains recommended Ziehl's carbol-fuchsin gives satisfactory 
results. It is prepared by dissolving 1 gm. of powdered fuchsin in 10 c.c. of alcohol; 
to this solution 90 c.c. of 5 per cent, aqueous solution of carbolic acid is added; 
the stain is ready for immediate use, and if prepared from proper ingredients 
keeps well. The prepared stain is poured over the slide, which is then heated 
over a Bunsen burner or alcohol lamp until steam begins to rise, when the heat 



266 DISEASES DUE TO A SPECIFIC INFECTION 

is withdrawn. After staining five minutes the excess is poured off and the slide 
freely washed in clean water. It is then flooded with Gabbett's solution, which 
consists of 1.5 gm. of methylene blue dissolved in 100 c.c. of a 25 per cent, aqueous 
solution of sulphuric acid. This is allowed to act for one minute; it is then poured 
off and the slide washed in water; if any of the red dye be retained the application 
of the Gabbett solution is repeated until all macroscopic evidence of the fuchsin 
has disappeared from the thoroughly washed slide, which is then stood on end and 
allowed to dry. Instead of Gabbett's solution, Pappenheim's decolorizer is now 
preferred by many laboratory workers. It is made by dissolving 1 gm. of coralin 
(known also as rosolic acid) in 100 c.c. of absolute alcohol, saturating the mixture 
with methylene blue, and then adding 20 gm. of glycerin. This reagent follows 
the carbol-fuchsin without washing in water. Three to five changes of the fluid 
are used, the film then washed in water and allowed to dry. Pappenheim's method 
has the advantage that in urinary specimens it will better differentiate between 
tubercle and smegma bacilli. 

A drop of immersion oil is placed on the stained film and the specimen examined 
with a one-twelfth-inch immersion lens. If it be desired to preserve the specimen, 
balsam is applied to the dried slide and a cover-glass placed on it. In properly 
prepared films the cellular elements and bacteria, other than the tubercle bacillus, 
will have selected the blue dye; the tubercle bacillus, however, will appear red on 
the bluish background. 

Tubercle bacilli are found so constantly in many cases of tuberculosis in the 
feces that the stools should always be examined whenever lack of sputum prevents 
the case from being readily diagnosticated. In acute miliary tuberculosis Rosen- 
berger found them constantly in the stools. The presence of tubercle bacilli 
in the stools does not necessarily indicate the presence of intestinal ulceration. 

X-Rays. — A valuable aid in determining the presence of consolidation of the 
lung in tuberculosis is the use of the fluoroscope or x-ray photograph, for a very 
distinct opacity often reveals such a lesion. 

Tuberculin. — Tuberculin is used in three ways as a diagnostic agent : By hypoder- 
mic injection; by instillation into the eye and by applying it to the broken or un- 
broken skin. When used hypodermically in the hands of inexperienced men it has 
been well said that the use of tuberculin is like looking for a leak in a gas main with 
a lighted candle; and Lawrason Brown well says that none of the indications of 
the test as yet devised, differentiate clearly clinical tuberculosis that demands 
vigorous treatment form non-clinical tuberculosis that requires only a God-fearing 
life. 

In the diagnosis of pulmonary tuberculosis there can be no doubt that tuberculin 
when properly employed is a valuable agent, although I believe that in the majority 
of instances it should not be used, since careful examination of the patient and 
consideration of his history will in most instances reveal the presence of tubercu- 
losis, or point to its presence with such a degree of certainty that the patient 
should certainly be sent away for his health on the ground that he is a fair mark 
for a tuberculous infection, and that his lung is in such a condition that he is at 
all times liable to the rapid development of a true tuberculous process. It is 
thought by some that the reaction which is produced may actually increase the 
rapidity of the tuberculous process. 

Old tuberculin, which is used hypodermically, for diagnostic purposes is 
usually given to adults in the dose of yV to 5 milligrams, and if tuberculosis 
is present it causes a reaction in the form of a rise in temperature of two or three 
degrees within a few hours. If the dose is larger than 0.0001, susceptible persons 
may have a violent reaction. If the patient fails to react to the smaller doses, 
before deciding that the tuberculin test has proved him free from tuberculosis, 
doses of 2 m£. or 3 mer. or even more should be given at intervals of a week, but 



TUBERCULOSIS 267 

a reaction is not positive proof of tuberculosis, for it is to be remembered that the 
tuberculin reaction sometimes occurs in persons who have syphilis and rheumatoid 
arthritis. It is thought by some that the reaction which is produced may actually 
increase the rapidity of the tuberculous process. 

The use of tuberculin for diagnostic purposes has a larger field in cases of suspected 
renal or abdominal tuberculosis than it has in the diagnosis of pulmonary lesions, 
in which the physical signs can usually be demonstrated. 

In order that a careful record of its effects may be obtained the temperature 
of the patient should be taken after the injection at intervals of every two hours 
for six hours, and after that every hour for twelve hours. Before the test is made 
it must be determined that the patient is afebrile by a careful record of his tempera- 
ture for several days, as otherwise the usual fever may be mistaken for a reaction. 
The subcutaneous diagnostic use of tuberculin is contra-indicated if there are active 
signs of disease and these also render its use unnecessary as a rule. 

In addition to fever, when the test is positive there is usually backache and pain 
in the limbs so that the patient may feel as if suffering from an attack of grippe. 
As a rule the reaction begins in from six to twelve hours, reaches its acme in from 
twelve to twenty-four hours, and the patient recovers by the end of thirty-six 
hours. Rarely the reaction may persist for as long as twelve days. 

It has been urged against Tuberculin R. that there is a possibility of its containing 
living bacilli which may infect the patient. For this reason many clinicians employ 
a tuberculin prepared by filtration and subsequent concentration of sterilized 
bouillon cultures, whereby a germ-free produce is assured. (See Treatment.) 

The opthalmotuberculin test depends upon the fact that when a 1 per cent, solution 
of tuberculin, prepared by precipitating it with alcohol and washing it with water, 
is dropped into the eye of a patient who has tuberculosis in any part of his body 
an inflammatory reaction develops in the conjunctiva so that this membrane 
becomes infected and red. For this test tuberculin is made up in tiny tablets, 
each of which contains 5 milligrams. This tablet when dissolved in 0.33 c.c. of water 
(or 5 minims) represents in each minim 1 milligram or a single dose for the test. 
As with the injection method so with this, a reaction is not absolutely positively 
diagnostic. There are two important facts to be recalled about this test. First, 
that if tuberculin is dropped into the eye and fails to produce reaction it is not 
possible to use the same eye for a subsequent test with a larger dose, since the eye 
has become sensitized to tuberculin by the first application. Second, it is generally 
considered by opthalmic surgeons that this test may cause dangerous ocular inflam- 
mation if the patient is very susceptible. 

The cutaneous method of von Pirquet consists in abrading the epiderm of the 
arm, or elsewhere, as in vaccination, in two adjacent spots. Upon one of these 
abraded areas is placed a drop of old tuberculin, 25 per cent, strength. The other 
abraded area is treated by a drop of 50 per cent, glycerin in water containing 
one-tenth per cent, of carbolic acid and is used as a control spot. If the reaction 
is positive the area which has received the tuberculin becomes reddened after 
about three hours. This redness reaches its height in twenty-four hours and is 
nearly gone in forty-eight hours. A slight papule may also be felt or seen. In 
cases of delayed but more severe reaction the redness may not appear for two or 
three days and may persist for twenty-one days or more, the papules being distinct 
and constant. The part may itch and the axillary glands become a little swollen 
if the arm is the limb used in the test. If these various changes do not occur the 
test is negative. The objection to this test in adults is that many who are not 
suspected of having the disease react. If the patient is exceedingly ill from tuber- 
culosis these reactions may fail, particularly in miliary tuberculosis and tuberculous 
meningitis. Von Pirquet also states that it is often negative in the first week of 
measles. (For the Moro test see Tuberculous Meningitis.) 



268 DISEASES DUE TO A SPECIFIC INFECTION 

Prognosis. — It is not long since it was almost universally thought that subacute 
pulmonary tuberculosis was an utterly hopeless and incurable disease. At present 
we know that it is in many instances a curable affection, even when it is not 
possible to obtain the very best conditions for cure. Further, we know that 
hundreds of persons have the disease and get well without even knowing that they 
have had it. It is manifest, however, that only those cases can recover in which 
the disease is not far advanced and in which the vital resistance of the individual 
can be maintained at such a level that the protective processes of combat and 
repair, already described may be carried out to completion. 

The degree of vital resistance of the patient is of very great importance in deciding 
the prognosis. Often the most powerfully built individual falls a victim to rapid 
phthisis while his comparatively feeble comrade manifests the most remarkable 
vitality. Additional factors in determining the outlook in an individual case are 
the maintenance of the body weight, the absence of anemia (but red cheeks do 
not necessarily mean good blood), and the presence of a good digestion, particularly 
in respect to starches and fats. A good family history is not as important a factor 
for good as a bad history is important for evil. 

Considerable work has been done to determine the value of Arneth's blood 
picture as a prognostic sign in the way of estimating the reaction of the patient. 
Arneth makes five divisions of the polynuclear leukocytes based on the lobes of the 
nucleus, from one irregular lobe up to five distinct lobes. He finds the average 
number of these five types in each hundred cells in healthy persons to be 5, 35, 41, 
17, and 2, respectively. The postulate is that the fewer the lobes the younger 
and less efficient the cell. A shift to the left, that is an increase in number of the 
first two groups (the sum of which is the Arneth index), is regarded as an unfavorable 
sign. Not all observers are agreed upon the value of this method, which may be 
partly due to personal equation in grouping the leukocytes. It appears worthy 
of further testing in cases under treatment; as possibly being corroborative of the 
clinical picture. 

A large number of statistics as to the curability of this disease by climate and 
feeding and by out-door life are now obtainable, and some statistics will be found 
discussed under Treatment. 

F. C. Wood believes that the diazo reaction can be used to aid in determining 
the question of prognosis, stating that if no reaction occurs and the kidneys are 
intact the outlook is favorable, but that if the urine reveals a strong and persistent 
reaction the outlook is evil. 

The average duration of life in a case of pulmonary phthisis is limited to two 
years. 

Marriage should be forbidden for either sex if suffering from tuberculosis, even 
if it be in a mild form. The woman who is tuberculous may survive her first 
pregnancy only to pass into a hurried decline after the birth of her child or during 
lactation. Several pregnancies almost always destroy her. The man not infre- 
quently loses nervous vigor by marriage, and this is the more prone to occur, as 
it is notorious that tuberculous men are cursed with a degree of sexual desire which 
is in excess of that of health. 

The prognosis of hemoptysis so far as its causing immediate death is concerned 
is favorable. Patients rarely die during, the hemorrhage unless it takes place in 
those who are already very feeble and anemic. Rarely the hemorrhage is so profuse 
as to cause death by suffocation. West gives the proportion of deaths from this 
cause as but 1 or 2 out of every 100 cases that die of this disease, whereas 60 per 
cent, of tuberculous cases are supposed to suffer from hemoptysis at some period 
of the malady. 

The secondary effects of hemorrhage may, however, be disastrous, for if the 
neighboring part of the lung is inundated with blood and with bacilli, the bronchioles 



TUBERCULOSIS 269 

in that part become filled with the extravasation and a traumatic tuberculous 
pneumonia speedily ensues. 

Treatment of Pulmonary Tuberculosis. — The treatment of pulmonary tuberculosis 
in its subacute or chronic forms may be considered in several parts. 

1. Its treatment by proper diet, proper exercise, and rest. 

2. Its management by suitable out-door life, and particularly by climate. 

3. The employment of drugs to control or modify symptoms which are severe 
enough to demand attention. 

4. The use of tuberculin as a curative remedy. 

5. The avoidance of the use of drugs with the idea that they can cure the disease; 
for he who tries to cure pulmonary tuberculosis by drugs does not know the morbid 
anatomy of the malady. 

It is of vital importance in the treatment of pulmonary tuberculosis that the 
disease be recognized at the earliest possible moment and that curative measures 
be immediately instituted. The possibility of cure depends solely upon the limita- 
tion of the lesion, and this is difficult to accomplish in direct proportion to its 
size and the degree to which degenerative changes have advanced. 

Diet. — There can be no doubt that the proper nourishment of the patient is 
the most important matter demanding the attention of the physician; for tuber- 
culosis is not only a disease in which emaciation progresses rapidly, but it is one 
in which the outlook depends entirely upon the ability of the patient to carry out 
protective processes through which alone he can hope to recover his health. Under 
these circumstances it is evident that the physician must do everything in his 
power to keep the digestion in the best possible order, to administer foods which 
are easily digested and readily absorbed, and, equally important, to prescribe 
no drugs or foods which by disordering the stomach will interfere with the function 
of this important viscus. It must also be remembered that the digestion of food 
requires nervous energy just as does the performance of any other vital function, 
and care must be taken that food is not ingested at a time when, by reason of 
exercise or other cause, a considerable quantity of nervous energy has been recently 
expended. The physician is, therefore, in the difficult position of knowing that 
the patient must take large quantities of nutriment if recovery is to be expected, 
and at the same time be careful that the digestion is not overburdened by the too 
frequent administration, or too free employment, of nutritious articles. If the 
patient's digestion is moderately strong, he may follow a line of diet about as follows : 

Before getting up in the morning he should receive a teacupful of hot milk, which 
should be sipped and not gulped down in one or two large swallows. After taking 
this, he should rest in bed for fifteen or twenty minutes; should then bathe, or be 
bathed, and clothed, and for his breakfast have wheaten-grits, oatmeal, or some 
of the more modern cereal preparations which are known to possess real nutritive 
value. If his appetite is good he may also have at this time a tender chop or a 
small piece of steak, and if accustomed to the use of tea or coffee, these beverages 
may be allowed unless it is found that they increase nervous irritability. In some 
instances the patient may desire to take an orange or some other fruit with his 
breakfast, and to this there can be no objection. The meal should be adequate, 
but not large enough to be heavy. 

Half-way between his breakfast and his mid-day meal the patient should receive 
some light luncheon, consisting of a cup of broth, a piece of toast, a glass of koumyss, 
or a sandwich made of scraped beef; or, if he tires of this, one made with toast and 
anchovy or caviar. Often an egg, cooked or raw, may be taken between meals 
with advantage. If desired, a glass of sherry or some red wine may also be taken 
at this time; or, in its place, Scotch or rye whiskey may be given. 

The dinner should be the heaviest meal of the twenty-four hours, and should 
be taken between twelve and two o'clock. It should consist of a nutritious and 



270 DISEASES DUE TO A SPECIFIC INFECTION 

somewhat stimulating soup which is easily digested and absorbed; one of the clear 
soups being preferred rather than a puree, unless it is known that the patient readily 
digests thickened and rich soups. This may be followed by a small piece of fresh 
fish, great care being taken that the fish is really fresh, and then by a hearty course 
of any one of the roast or broiled meats, accompanied by two or three wholesome 
vegetables, such as potatoes, string beans, asparagus, spinach, carrots, macaroni, 
and similar substances. With this meal it may be well for the patient to take a 
little sherry wine or whiskey and water, particularly if he is accustomed to stimu- 
lants with his meals. Some plain, nutritious dessert like cornstarch or rice-pudding 
may also be taken. 

During the afternoon a light luncheon should be given him, somewhat similar 
to that which has been taken in the middle of the forenoon, two or three hours 
after his dinner. In the evening another light meal should be taken, which should 
consist of arrow-root or an egg cooked in some simple form, or a few stewed oysters 
or milk-toast may be used, and again before going to bed at night a cup of broth, 
a glass of koumyss, a cup of hot milk, or some curds and whey may be given. 

The patient who is able to take the quantity of food which has just been described 
is, of course, one whose digestion is in fairly good condition. But if careful attention 
is paid to the digestive tract by the administration of aids to digestion, such as 
pepsin, pancreatin, and taka-diastase, if the bowels are moved regularly by the 
use of proper laxatives, and if, above all, the patient is required to conserve his 
nervous energy in order to expend it upon his digestive apparatus, it is quite remark- 
able what large quantities of food may be taken, even by the consumptive who 
otherwise seems quite feeble. 

The actual quantity of the food at each feeding must be varied from day to 
day with the patient's appetite and with the conditions which may arise. If the 
patient has passed a restless and feverish night, the quantity of food at each 
feeding should be small; whereas, if he has had a restful night, and therefore has 
been able to gain nervous energy, larger quantities may be given. So, too, limited 
quantities should be ordered when the tongue is at all foul, and larger quantities 
ordered when it is comparatively clean. It is of vital importance that these daily 
variations should be made in the diet, for the digestive apparatus of no one is 
prepared day in and day out to take exactly the same quantity of food, and digest 
it satisfactorily. Both the physician and the patient must remember that profes- 
sional advice as to food and digestion is much more important for the patient than 
advice as to the treatment by drugs. 

Exercise. — The majority of cases of pulmonary tuberculosis do not require 
much exercise provided they are supplied with sufficient fresh air. Patients, 
however, differ very greatly in regard to this matter. Some of them seem capable 
of taking moderate exercise with great advantage, and others cannot take any 
exercise without suffering either from a disordered digestion or from a restless night 
caused by inordinate fatigue. In many instances the patient's health can best 
be preserved by giving him fresh air, and supplanting exercise by massage and 
gentle Swedish movements. Of course, these remarks do not hold true of those 
cases in which a small area of the lung is involved, with almost no impairment of 
the general health and muscular strength. These patients should take healthy 
exercise, being careful to avoid excessive fatigue, and they should be impressed 
with the idea that exercise in sufficient degree to approach exhaustion is not only 
bad on general principles, but actually diminishes their ability to prevent the 
spread of the infection in their lungs. The whole question of exercise must, there- 
fore, be gauged in each case by the real strength of the individual rather than by 
his ambition to be up and about. 

Climate and Out-door Life. — In these two factors we have a great aid in 
the treatment of pulmonary tuberculosis, although, of course, these agents must 



TUBERCULOSIS 271 

be prescribed with the same care that governs our employment of ordinary 
remedies. There can be no doubt whatever that an out-door existence is capable 
of curing pulmonary tuberculosis under certain circumstances, even when the 
climate is by no means theoretically suitable for pulmonary cases. This is a matter 
of importance when it is remembered that a very large proportion of consumptives 
find it impossible to travel great distances to obtain those climatic conditions 
which are most favorable to them. 

At every modern resort for consumptives every measure is taken to keep the 
patients for many hours each day in the open air, the essentials being that they 
shall be exposed to sunlight, and, if possible, to the direct rays of the sun, and 
be protected from high winds. These conditions can be obtained by the erection 
of suitable sheds facing the sun, and providing wind guards which will place the 
patient in a quiet atmosphere. Even should the patient be unable to go to the 
country for fresh air, good results have been found to follow this plan of treatment 
while he remains in a city residence, either in a suitably arranged room or in a 
tent or shed erected upon the roof of his house. 

The climate to which the patient should resort, if it is possible for him to travel, 
should, in the great majority of instances, be one which is found at an altitude vary- 
ing from 3000 to 6000 feet. There are two great essentials in such a climate: first, 
that there shall be an unusual number of hours of sunshine in the course of the 
year, and, second, that the atmosphere shall be dry. A third point of importance, 
but by no means an essential one, is that the atmosphere shall be quiet, in order 
that there may be little dust. The temperature is of comparatively little import- 
ance, provided it is not accompanied by humidity, for it is quite remarkable how 
patients suffering from this disease often thrive in temperatures which in winter 
are far below the freezing point, and in summer are often as high as 90°. At those 
altitudes of from 5000 to 6000 feet which are suited to this class of patients the 
atmosphere is so clear that the sun's rays are not interfered with, and even if the 
thermometer shows that a zero temperature is present, the patient, if properly clad 
and protected from wind, can very frequently lie out-of-doors all day, warmed by 
the heat of the sun. This is beneficial to an extraordinary degree. 

A high altitude is advantageous for the tuberculous patient, not only for the 
reasons which we have given, but also because the rarity of the atmosphere requires 
that he use all possible portions of the lung tissue, and this being the case, he 
gradually expands and calls into functional activity all those parts of the lung 
in the neighborhood of the tuberculous lesion which have a tendency to become 
functionally inactive. This development of active circulation of air and blood does 
much toward aiding nature in walling off the tuberculous focus and preventing 
its further spread. A high altitude is also advantageous because it seems to increase 
the quantity of hemoglobin in the blood. Whether it increases the number of red 
blood cells is still a matter of debate, some asserting that the increased number 
of corpuscles, found in the superficial bloodvessels after a patient has been some 
weeks at a high altitude, depends more upon an altered distribution of blood than 
upon any actual increase. 

Of the high-altitude resorts which are most popular because of their excellent 
climate for consumptives may be mentioned Colorado Springs, Colorado, certain 
parts of Arizona and New Mexico, and parts adjacent in America, and the so- 
called Engadine, in Switzerland, of which the most celebrated places are Davos, 
Pontresina, and San Moritz. 

A high, dry climate is contra-indicated in tuberculous patients who are suffering 
from tuberculous laryngitis, since the dry air increases the laryngeal irritation. 
It is also contra-indicated in patients who have dilatation or degeneration of the 
heart muscle, and great care should be taken to determine the state of the heart 
in alltuberculous patients before sending them away from home. A persistently 



272 DISEASES DUE TO A SPECIFIC INFECTION 

high pulse rate is a distinct contra-indication to altitudes. If valvular disease 
exists, and there is a tendency to failure of compensation, a high altitude is also 
contra-indicated; but where compensation is adequate, the mere presence of a 
murmur does not necessarily contra-indicate resort to an altitude, provided the 
patient is cautious not to overexert himself. 

Emphysema associated with pulmonary tuberculosis usually contra-indicates 
a high altitude. 

It has been taught by some that a tendency to hemoptysis also renders a high 
altitude inadvisable, but very eminent phthisiologists, on the contrary, have 
asserted that a tendency to hemorrhage does not contra-indicate health resorts of 
this character. My own personal feeling is that the patient who has a tendency 
to hemoptysis should approach a high' altitude very gradually in order that his 
heart and lungs may become accustomed to the altered atmospheric conditions, 
and certainly, for the first few weeks after his arrival, should rest constantly. 

Still another contra-indication to such an altitude, unless perchance the climate 
is very mild and the temperature fairly constant, is renal disease of any kind, or 
tuberculosis of the genito-urinary tract. Should any of these contra-indications 
exist, the climate of choice is one which is represented by San Diego, California, 
where the air is pure, where sudden changes of temperature do not occur, and where 
a flood of sunshine is constantly obtainable. 

In those cases which have a great deal of secretion, excessive cough, and exces- 
sive expectoration, dry climates, such as are found near Phoenix, Arizona, and 
Silver City, New Mexico, are the climates of election. 

For those who are unable to take a long journey, and for those who are not 
thought to be suitable cases for high altitudes, the Adirondacks in the neighbor- 
hood of Saranac Lake, New York; White Haven, Pennsylvania; or Asheville, 
North Carolina, can be recommended. These altitudes are in the neighborhood 
of 2500 feet. Lower altitudes which have been found advantageous for these cases 
exist at Thomasville, Georgia, and Lakewood, New Jersey, where the curative 
elements are the sunshine and pure air. 

It is interesting to note, in regard to the treatment of pulmonary tuberculosis 
by fresh air, proper diet, and moderate or high altitudes, that a large percentage 
of cases can be cured. Thus, Trudeau reported, at the Adirondack Cottage Sani- 
tarium, where the altitude is less than 2500 feet, cures in 72 per cent, of incipient 
cases and 17.8 per cent, in advanced cases; and Clapp and Bowditch, of the 
sanatorium at Rutland, report cures in 72.5 per cent, of incipient cases and 46.11 
per cent, in advanced cases. 

Still more recently Trudeau has presented the results obtained by an analysis 
and study of all the cases under his observation in seventeen years. Of the 1500 
cases under consideration, which have been discharged from two to seventeen 
years, 434 could not be traced, leaving 1066 which have been traced. Of these 
1066, 46.7 per cent, are still living, 31 per cent, are known to be well at present, 
in 6.5 per cent, the disease is still arrested, 4 per cent, have relapsed, 5.2 per cent, 
are chronic invalids, and 53.3 per cent, are dead. As to the influence of the stage 
of the disease on the permanency of the results obtained, he found 66 per cent, of 
the 258 incipient cases discharged are well at present. Of the 563 advanced cases 
28.6 per cent, are well, and of the far-advanced cases 2.5 per cent, only remain 
cured. Thus we learn that 31 per cent, of all cases discharged from two to seven- 
teen years ago have remained well, and that 66 per cent, of the incipient cases dis- 
charged during the same time continue well at present. Surely these results 
are encouraging and he has shown us the way in a great work. Thirty years ago 
physicians were of the opinion that cures did not take place from pulmonary tuber- 
culosis in more than 2 per cent, of cases. 

Sea voyages, which at one time were very popular in the treatment of tuber- 



TUBERCULOSIS 273 

culosis of the lungs, are no longer regarded with much favor. The possibilities of 
seasickness, bad weather, and of consequent close confinement are naturally not 
looked upon with favor, when we consider that free feeding and fresh air are abso- 
lutely essential for these patients. Further than this, the atmosphere at sea is 
never dry, but always more or less damp. Again, there are practically no comfort- 
able sailing ships at the present time, and steamers make such rapid voyages that 
the patient is not long enough at sea to be materially benefited. 

Before the physician decides to send his patient away from home for the climatic 
treatment of his disease, he should determine whether such treatment really offers 
fair chance of benefit; for it is a vital mistake to exhaust the strength and finances 
of the individual in a vain endeavor to arrest an inevitable process. If it is decided 
that the disease has advanced so little that such a trip can promise good, the next 
question which arises is as to whether the patient is strong enough to stand the 
journey, and, again, if he can stay away long enough to be benefited; for in all 
instances it is useless for a patient to leave home with any expectation of returning 
in less than six months or a year, and usually he had better give up the hope of 
returning except for a visit, if he wishes to preserve his health after the climate 
has done its good work. It is also a grave mistake to send such patients far from 
home unless they can be accompanied by some relative or friend, as homesickness 
exercises a deleterious influence upon vitality. 

Drugs. — I have already mentioned the use of the various digestants when speak- 
ing of the diet. The ever-present anemia of many of these patients is to be 
overcome by the careful administration of iron and arsenic. Arsenic for 
many years has had the reputation of being a drug of great value in tuberculosis. 
Iron is also very useful, but it should not be given in the large doses ordinarily 
employed. As I have repeatedly pointed out, the quantity of iron in the body is 
exceedingly small, not more than about 30 grains, and therefore the administration 
of 2 or 3 grains of reduced iron two or three times a day provides in twenty-four 
hours far more iron than can possibly be utilized, and at the same time tends to 
produce constipation and so disturb digestion. Most cases will do better if they 
are given in the neighborhood of yw to i grain of reduced iron three times a day. 

Strychnine may be used in moderation as a bitter and as a nervous tonic, but 
it is a mistake to use it as a circulatory stimulant, as it is only an irritant to the 
nervous system, and produces fictitious strength. Quinine cannot be given in 
doses which are adequate to control hectic fever, and if any attempt of this kind 
is made it disorders the stomach and produces headache; 2 or 3 grains, twice or 
thrice a day as a bitter tonic, are quite sufficient for the average patient. 

The syrups of the hypophosphites and lactophosphates have been popular with 
the profession for many years. In many instances the improvement which follows 
their use depends upon the iron or strychnine which they contain, and too fre- 
quently these syrupy preparations disorder the stomach and spoil the appetite. 
If it is desired to administer calcium, potash, and soda to such patients, it is better, 
in the writer's experience, to give an elixir of the glycerophosphates in the dose of 
a dessertspoonful three times a day to an adult. 

When the heart is weak, particular care should be taken in regard to rest, and 
digitalis may be given, but it should be used in small doses over a long period of 
time rather than in full doses for a short period. It is quite remarkable what good 
results follow the use of 2 or 3 minims of a physiologically tested tincture of digi- 
talis three times a day. These doses, maintained for some time, produce a true 
improvement in the heart muscle and do not disorder the stomach; whereas, 
larger doses soon upset the cardiac balance, and almost certainly disturb digestion, 
and even produce vomiting. 

For the control of night sweats no remedy equals camphoric acid in my experi- 
ence, given in the dose of 15 to 20 grains, two or three hours before the time that 
18 



274 DISEASES DUE TO A SPECIFIC INFECTION 

the sweat usually comes on. The best way to administer it is in cachet or capsule, 
or dissolved in a little brandy. The difficulty in the use of atropine for this pur- 
pose is that it checks other secretions and sometimes by so doing renders the cough 
more dry and annoying. 

Fever, as a rule, requires treatment only if it becomes excessive. The patient 
may be sponged with tepid water and alcohol, and even cool water may be used. 
But care must be taken that the temperature does not break rapidly and become 
subnormal. The use of the coal-tar antipyretics is entirely inexcusable. They 
diminish vital resistance, are apt to produce profuse sweats, and increase cyanosis 
and dyspnea when the pulmonary lesions are well developed. 

The use of creosote or of any of its derivatives, with the idea that they are 
beneficial for pulmonary tuberculosis, is based upon an utterly erroneous view of 
the disease and of the action of these drugs. When bronchitis is present as a com- 
plication their value as stimulating expectorants is worthy of consideration, and 
under these circumstances, by improving the condition of the bronchial mucous 
membrane and aiding expectoration, they may eventually help the patient, but 
they certainly do not exercise any influence upon the tuberculous process itself. 
Worse than this, in many instances they do not even act as expectorants, unless 
given in doses so large as to disorder the stomach. The number of unfortunate 
consumptives whose struggle with their disease has been lost through disorder of 
the digestion arising from the administration of expectorants is not comforting 
to contemplate. 

Cough is to be controlled by the use of such cough sedatives as heroin in the dose 
of y4 to y 1 ^ of a grain three or four times in twenty-four hours. A very useful plan 
of treatment under these circumstances is the administration of the elixir of terpin 
hydrate and heroin in the dose of a teaspoonful every four hours. In some instances 
cannabis indica is useful as a cough sedative. In still other cases, if the cough seems 
to be due to a dry and irritable condition of the bronchial tubes, quiet and sleep 
is obtainable if there is disengaged in the air of a room, from a bronchitis kettle, 
steam which arises from water into which is poured creosote, oil of pine, and oil 
of eucalyptus, equal parts, to the extent of J to 1 drachm. Care should be taken 
that the patient does not go out-of-doors into the cold atmosphere after inhaling 
the warm, steam-laden atmosphere. 

When a laryngeal tuberculosis develops, these steam inhalations are often exceed- 
ingly valuable. 

Sometimes an excessive cough at night can be stopped by giving the patient 
a drachm of Hoffmann's anodyne, or a little spirit of camphor. In other instances 
morphine in the dose of 2V to y^- °f a grain is required, but opiates are to be carefully 
avoided if other measures of relief are sufficient. 

When the cough depends upon the accumulation of large quantities of material 
in the bronchial tubes or in cavities, it is of vital importance that it should not 
be arrested by the administration of drugs ; for it is an effort on the part of nature 
to get rid of materials which, if they are retained in the lung, will greatly increase 
septic poisoning. This is particularly true of morning cough, which, though it 
is often exceedingly annoying, is really an effort to empty a cavity which has be- 
come filled during the night. Such coughing can frequently be aided by placing 
the patient in such a position that the cavity will readily drain into its supplying 
bronchus. 

Whenever the physician in the treatment of pulmonary tuberculosis is tempted 
to employ a drug, the question of its influence upon the stomach and digestion 
should be carefully decided, even though the indications for the use of the remedy 
which exist in other portions of the body seem very clear and conclusive. Thus, 
the use of cod-liver oil in the treatment of pulmonary tuberculosis is undoubtedly 
to be commended, provided the patient can digest it, and at the same time 



TUBERCULOSIS 275 

take ordinary food. Even a healthy man cannot exist on cod-liver oil alone; and 
it is a vital mistake to impair the appetite and digestion by giving full doses of this 
sometimes valuable drug. Any sign of indigestion of the oil, as in eructations, or 
in the passing of oily stools, should be the signal for stopping its use at once. The 
digestion of good food does more for a patient's vitality than the digestion of 
good oil. 

Serum Therapy. — An endeavor has been made to treat tuberculosis by means 
of antitubercle serum, but so far the results which have been obtained have not 
been encouraging. 

Antistreptococcic serum has been used on the ground that nearly all cases of 
tuberculous cavity are infected by the streptococcus as well as the tubercle bacillus, 
and that if the former malign organism were removed, or its toxins antagonized, 
the patient could the better combat the original cause of the illness. If strepto- 
cocci are found in the sputum in large numbers it may be used to aid the patient, 
but otherwise its use is futile. 

Tuberculin. — The employment of tuberculin as a specific remedy for pul- 
monary tuberculosis has not as yet received general professional endorsement. It 
is true that a very large number of physicians who are especially engaged in the 
treatment of tuberculous patients have written papers in which they have highly 
praised the employment of this substance, and that statistics are numerous which 
tend to show that it produces advantageous results. It must be admitted, therefore, 
that at times it does good. But, on the other hand, it is a good rule in practice to 
follow the majority in the use of new remedies; for new remedies which really are 
advantageous are taken up and constantly employed by everyone. Probably the 
conclusions as reached by Trudeau, in regard to tuberculin, represent the real facts 
of the case when he says: "My experience with tuberculin treatment at the 
Sanitarium thus far has led me to believe that when carefully tried, in suitable 
cases, it has proved apparently free from danger, and that it has seemed to have 
some favorable influence in bringing about the healing of the lesions, probably by 
inciting the formation of fibrous tissues." 

The tuberculin which should be employed is that which is prepared by the more 
modern methods. It is now made and marketed by a number of reliable concerns, 
and it can be obtained both in this country and abroad. This remedy is not one 
which is suitable to all cases and should only be given by an expert in its use. 

Before speaking of the use of tuberculin it is important that its several forms, as 
used today, should be understood. A very large number of products have been 
made and given this name but practically only three are generally used. The 
first of these is that originally proposed by Koch in 1890; it is often called "Old 
Tuberculin." This is prepared from pure cultures of tubercle bacilli made upon a 
5 per cent, glycerin-bouillon medium. This culture medium is evaporated to one- 
tenth of its bulk and then filtered through porcelain to remove all bacilli. Old 
tuberculin is, therefore, a product which contains all the educts of the bacilli in 
a 50 per cent, solution of glycerin. The dose varies from yoVo to y^ of a milli- 
gram for curative use. The second form is called "Tuberculin R." (T. R.), an 
abbreviation of the words "Tuberculin Residuatum." Tuberculiji residuatum is 
prepared in the following manner: 

The live virulent germs are dried thoroughly and then ground in a ball mill for 
a considerable time. The resultant dry powder is taken up with sterile water and 
centrifugalized. The supernatant clear liquid, which is called Tuberculin T. O., 
is thrown away. The remaining portion, the residue, is the material from which 
T. R. is now made. This is done by repeatedly grinding and extracting with water. 
The process of drying, grinding, taking up in water and centrifugalizing is repeated 
until there is no residue left. The united extracts of this T. R. residue constitute 
the Tuberculin R. of commerce. In T. R. two ends are supposed to have been 



276 DISEASES DUE TO A SPECIFIC INFECTION 

accomplished, viz.: (1) The removal of the toxic and otherwise deleterious con- 
stituents of the germs; (2) the bringing into solution of the immunizing substance. 
The dose of the T. R. is always measured on the basis of the amount of dry germ 
material in it — each cubic centimeter of the dilute product contains toVo" °f a 
milligram. The doses used vary with the different workers. Koch recommends 
5^0- milligram to 20 milligrams, but the modern tendency is to use smaller doses. 
Wright, of London, uses 3-2V "o to -g-g-o milligram; some begin as low as to -J "00" an d 
gradually increase the dose. The T. R. is always administered hypodermically and 
if aseptic precautions are observed will be absorbed promptly and without local 
trouble. This is a much more powerful preparation than old tuberculin and is 
the one commonly used for curative purposes. The object is to develop a gradual 
resistance to infection, and a reaction such as is sought when tuberculin is used in 
diagnosis is always avoided, if possible. It appears on the market in glass bulbs, 
holding 1 c.c. of normal salt solution which also contains Tinny °f a milligram of 
"T. R." 

The third tuberculin, often called Koch's new tuberculin, or Bacillen 
Emulsion (B. E.), is a finely powdered virulent culture of tubercle bacilli, the 
strength being 5 milligrams of dried powder in each cubic centimeter of gly- 
cerin and water equal parts. This is also a very powerful product and is often 
used for curative purposes. The beginning dose is usually tttW °f a milligram. 
The use of these products should not cause reaction. If it occurs the dose must be 
cut down and a further use postponed until no trace of a reaction remains. The 
treatment must be continued for months and the doses are increased as time goes 
by. Usually in the absence of reaction the injection is given twice a week. 

The dose is injected into the tissues of the back by means of a sterilized syringe 
on every alternate day. It is desirable to avoid reaction, and all febrile movement 
that may be induced by one injection must have disappeared before another 
dose is given. After repeated doses the patient may be able to stand very large 
doses without any reaction and with good effect. 

When vomiting complicates pulmonary tuberculosis, its cause must be discovered. 
If it follows excessive cough, the cough must be controlled in the manner already 
described. If it arises from gastric irritability, 2 to 5 grains of subnitrate of bis- 
muth and 1 to 2 grains of oxalate of cerium may be given an hour before meals. 
In other instances, where the stomach is depressed rather than irritated, 1 or 2 
drops of Fowler's solution before meals is advantageous. 

The treatment of hemoptysis consists in the administration of a hypodermic 
injection of f of a grain of morphine if the patient shows great mental perturbation 
because of the hemorrhage. It does not have any direct influence upon the flow 
of blood, but by producing nervous quiet it relieves the patient's mind and so 
quiets the circulation. If the flow of blood is profuse, the patient should be allowed 
to occupy that position in which it is most easy for him to rid his bronchial tubes of 
fluid. I have seen relief produced by permitting him to lie flat on his chest with 
his head resting on the edge of the mattress in such a way that the blood readily 
flowed from his mouth without violent efforts at coughing. 

When hemoptysis is recurrent artificial pneumothorax is to be considered (see 
below) . 

A multitude of measures have been recommended for the control of the hemor- 
rhage. Manifestly, none of them can exercise much power for good. No one 
would think of attempting to control the hemorrhage from a ruptured varicose 
vein in the leg, or from a small artery on the surface of the body, by the internal 
administration of any drug of which we have knowledge. Such indirect st t yptics 
as tannic and gallic acid are useless. When the hemorrhage ceases after the admin- 
istration of these, or other styptics, by the stomach, it is evident that the arrest 



TUBERCULOSIS 277 

must be due to the natural clotting of the blood rather than to any effect of drugs. 
That this is the correct view of the case is still further emphasized by the fact that 
the pulmonary bloodvessels are very poorly supplied with vasomotor nerves and 
with muscular fibres, and therefore drugs which act by contracting bloodvessels 
cannot exercise any powerful influence in this area. Finally, absorption is so slow 
from the stomach that it is incredible that styptics can exercise a material effect 
before the hemorrhage destroys the patient or is stopped by clotting. If the cir- 
culation is bounding, a dose of chloral or aconite may be given as a circulatory 
sedative. Nitroglycerin hypodermically is also of value and amyl nitrite may be 
given by inhalation to diminish the blood pressure in the lung by dilating the 
systemic vessels elsewhere. 

The use of adrenalin by the stomach is of doubtful value, first, because, as 
just pointed out, the pulmonary bloodvessels are poorly supplied with muscular 
fibres upon which the adrenalin can act, and, second, because when adrenalin is 
placed in the stomach it is decomposed. The use of astringent substances in 
atomizers is equally futile. All of the fluid strikes against the pharyngeal wall, 
and may run down into the stomach, but it does not reach the lungs. 

Some practitioners haVe recommended the application of ice upon the perineum 
in cases of hemoptysis, believing that in some reflex manner it diminishes hemor- 
rhage from the lungs, and others have applied a small ice-bag over the cavity from 
which the hemorrhage takes place. There is much more danger of these measures 
adding to shock by chilling the patient than there is chance of their doing good. 
As already stated, hemoptysis rarely produces death as the immediate result of the 
loss of blood, and remedies which receive credit for arresting the flow are probably 
unworthy of the confidence imposed in them. 

Artificial pneumothorax, induced by the injection into the pleural cavity of 
nitrogen gas or air, has become a recognized therapeutic procedure in pulmonary 
tuberculosis, provided the disease is well advanced, is progressive, is largely or 
entirely unilateral and, still more important, provided that adhesions do not exist 
to such an extent as to prevent an adequate collapse of the lung to be caused by 
the procedure. The advantages gained are: an arrest of the disease in the lung, 
a diminution in the cough and expectoration, and often a decrease, or disappear- 
ance, in the systemic symptoms. This method of treatment has also proved of 
distinct value in persistent or repeated hemoptysis, as the collapse and inactivity 
of this lung permits arrest of the hemorrhage. A special apparatus, whereby the 
rapidity and force of the flow of gas or air is controlled is needed, provided with a 
gauge by which the operator can determine the pressure in the chest. Such an 
apparatus is now manufactured by several instrument makers. The quantity 
of gas injected depends, of course, upon the size of the chest and the condition of 
the patient during the injections. Any evidence of shock, great oppression or 
collapse necessitates the immediate arrest of the procedure. Commonly about 200 
to 300 c.c. of nitrogen gas are used every other day, as a considerable amount of gas 
is absorbed. The question is not so much one of how much gas as of how much is 
needed to collapse the lung and cause nearly complete pneumothorax. This is 
determined by the usual methods of diagnosing pneumothorax and by the aid of 
the arrays. The frequency of repetition of the injection and the length of time 
they are resorted to depend upon the maintenance of pulmonary collapse. Nitrogen 
gas is used because it is less rapidly absorbed than ordinary air. Under rigid 
asepsis a needle attached to a rubber tube leading to the apparatus is inserted in 
the fifth or sixth intercostal space in the midaxillary line, the patient lying on the 
unaffected side. After it is in place it must be quietly moved about, as one would 
move a probe, to determine that there are no adhesions, before the injection is 
attempted. Death rarely has resulted from this method when proper cases have 
been selected and proper precautions taken. Indeed some patients very far ad- 



278 DISEASES DUE TO A SPECIFIC INFECTION 

vanced in the disease and apparently near death have been greatly benefited. It 
is rather to be tried in desperate cases with cavity formation and profuse expectora- 
tion than in mild ones. In urgent, persistent hemoptysis air may be injected by 
producing a positive pressure in an ordinary aspirating apparatus if no special 
apparatus is at hand. 

Tuberculosis of the Alimentary Canal. — Tuberculosis of the alimentary canal 
may occur in any of its parts from the tonsils to the anus, and, while its develop- 
ment is a comparatively rare primary form of the infection, it is nevertheless met 
with in sufficient frequency to make it of importance. In an analysis of 5142 
autopsies, William Hunter, the Government Bacteriologist of Hong Kong, found 
that this condition was rarely present in children under five years, notwithstanding 
the very great prevalence of tuberculosis among the Chinese. 

Tuberculosis of the Tonsils. — The tonsils may contain tubercle bacilli, on their 
way to the infection of neighboring lymphatic glands, or they may be actually 
tuberculous themselves, containing in their substance miliary tubercles or caseous 
foci. These lesions are more frequently met with in children than in adults, and 
may depend upon auto-infection — that is, the tonsils may be infected by tubercu- 
lous sputum which is expectorated (secondary), or they may become infected by 
the entrance of tubercle bacilli in dust by the nose or mouth or perhaps in the milk 
of tuberculous cows (primary). Koplik has recently made an interesting report 
on this subject in the American Journal of the Medical Sciences. 

Even more important than tuberculosis of the tonsils is tuberculosis of the so- 
called third or pharyngeal tonsil, constituting the "postnasal adenoid." As is 
well known, these growths are not rarely tuberculous. From these adenoids the 
bacilli may pass through the lymphatics and so cause tuberculosis of the media- 
stinal and bronchial lymph nodes. 

Tuberculosis of the Pharynx and Esophagus. — The pharyngeal wall is not uncom- 
monly the site of miliary tubercles, in the course of chronic pulmonary tuberculosis, 
and even more commonly tuberculous ulceration extends from the larynx and 
epiglottis to the pharynx and adds greatly to the discomfort of the patient. Tuber- 
culosis of the esophagus is exceedingly rare, but some cases have been recorded. 
It may complicate general miliary tuberculosis, being a part of the systemic infec- 
tion, or it may arise from the swallowing of tuberculous sputum, or, again, from 
the extension of the disease from a tuberculous lymph node or vertebra. The 
ulceration may lead to perforation from within or the reverse. 

Tuberculosis of the Stomach. — Tuberculosis of the stomach rarely occurs, prob- 
ably because its juices protect it from infection. When it does occur, it appears as 
a miliary tuberculosis due to circulatory infection, or as single or multiple tuber- 
lous ulcers involving the mucous membrane. These ulcers are usually the result 
of a process starting from an ulcerating gland which becomes attached to the 
stomach and so causes disease by the extension of the inflammatory process. Van 
Wart has reported an instance of solitary tubercle in the muscular layer of the 
stomach which is believed to be unique. 

Tuberculosis of the Intestines. — Tuberculosis of the intestines is a much more 
common condition, and in the great majority of instances is secondary to infection 
elsewhere. Primary intestinal tuberculosis occurs usually in children, and as 
the result of the ingestion of milk which is infected by the specific bacillus. This 
primary form has been denied an existence by such excellent men as Leube and 
others, but so many other pathologists, of whom Bollinger may be taken as a leader, 
have observed it that its existence is proved. 

The secondary or common type of intestinal tuberculosis is usually the result 
of pulmonary tuberculosis, and arises from the swallowing of tuberculous sputum. 
When the pulmonary lesions have lasted for a long time intestinal infection will 
be found at autopsy in a large proportion of cases, about 25 per cent. Statistics 



TUBERCULOSIS 279 

have been published by certain pathologists giving over 50 per cent. The lesions 
are found chiefly in the ileum (80 per cent, of the intestinal cases) just before it 
joins the cecum, or in the ileum and colon 45 per cent., in the colon alone 3 per 
cent, and in the rectum 7 per cent., according to Frerichs. These statistics as 
to the relative frequency of the various lesions hold true of the disease, as it ap- 
pears in children as well as adults, even when the malady appears as a primary 
affection. 

Tuberculous infection of the intestine primarily involves the lymph nodes of the 
bowel, causing them to become swollen by reason of the characteristic cell prolifera- 
tion which the tubercle bacillus always produces. The solitary glands project 
markedly above the surface as yellowish-white masses which finally undergo casea- 
tion and softening, and then the mucous membrane covering them breaks down, 
forming an ulcer which is surrounded by somewhat overhanging edges. The ulcers 
are not very numerous; at times only one node may be involved. If the agminated 
glands, or Peyer's patches, are infected, separate caseous masses develop, several 
ulcers form, and finally coalesce, forming a large necrotic surface of very irregular 
outline. It is interesting to note that this condition is quite different from the pro- 
cess in enteric fever, in which disease the glands are affected generally and the 
individual agminated mass is uniformly infiltrated. Tuberculous ulcers of the 
agminated glands usually extend transversely across the gut because the process 
does not remain confined to the patch, whereas the lesion of enteric fever extends 
longitudinally. 

The overlying serosa is commonly thickened, often contains distinct tubercles, 
and at operation the diagnosis of tuberculous ulcer may be made without opening 
the bowel. Fibrosis and thickening, with associated contraction may cause stricture 
and symptoms of obstruction; perforation is not common and is usually overlooked. 

Tuberculosis of the cecum in the neighborhood of the appendix may give rise 
to the belief that appendicitis or tumor of the bowel is present. (See Symptoms.) 

When the rectum is affected the ulceration is preceded by infiltration and casea- 
tion in the submucosa, it often encircles the bowel, and the tissues near the seat 
of the ulcer are frequently dotted with small, yellowish or whitish, tubercles which 
add to the area of the ulcer as they undergo degenerative change. They also give 
rise to tuberculous infection of the peritoneum and perirectal tissues and to tuber- 
culous abscesses and fistula?. 

With the distinct and specific lesions just described tuberculous disease of the 
bowel presents an associated condition of acute and chronic catarrh or, in other 
words, a true enterocolitis. 

Of recent years much has been written of chronic hyperplastic tuberculosis of 
the intestine. In this form the intestinal wall is greatly thickened, the lumen 
commonly narrowed and sausage-like. Distinct cylindrical segments of the in- 
volved tissue may be recognized through the thin abdominal walls. Neoplastic 
masses which may attain the size of a fetal head occasionally develop, and polypoid 
growths may occur on the interior of the bowel. The condition is most common in 
the ileocecal region, and is rarely restricted to the small intestine, but may involve 
one or more parts or the whole of the colon, causing strictures with interposed 
dilated areas, although actual dilatation is rare. The stenosis may be almost 
complete. Histologically there is marked hyperplasia of the connective tissue of 
the intestinal wall, and the great thickening, sometimes attaining 5 cm., is due 
largely to this cause. Caseous areas and even typical tubercles may be absent. 
The newly formed tissue is often but scantily supplied with bacilli. 

Symptoms of Intestinal Tubekculosis. — The symptoms of intestinal tuber- 
culosis consist chiefly in the manifestations met with in most cases of enterocolitis. 
The patient complains of looseness of the bowels, or diarrhea, and a considerable 
amount of colicky pain. With these signs there is wasting and decrease in strength. 



280 DISEASES DUE TO A SPECIFIC INFECTION 

The tongue may be coated, but it is often unduly clean and the normal roughness of 
its mucous membrane is replaced by a raw-beef appearance. Palpation of the abdo- 
men may reveal tenderness at certain points, which is now, however, very well 
marked, and auscultation will show an excessive amount of peristaltic movement 
and rumbling. At times the appetite may be excessive owing to the fact that the 
diarrhea causes starvation of the tissues, which is recognized by the system and 
shown in a desire for more food. At such times, in particular, the stools may 
contain undigested particles of food. There are, however, no symptoms in this 
early stage that can be considered typical, and the presence of tuberculosis else- 
where may be the chief reason for believing that the alimentary canal is involved. 

When ulceration occurs the presence of mucopus, blood, and, more important, 
the discovery that tubercle bacilli are in the stools make it possible for us to state 
positively the cause of the disease. If the disease develops farther, as it is prone 
to do if life is prolonged a sufficient length of time, the peritoneal coat of the intes- 
tine is involved and gradually a general adhesive peritonitis, such as was described 
in the article on peritoneal tuberculosis, is produced, with its characteristic thick- 
ening of the peritoneum and cicatricial contraction of the omentum and mesentery. 
This produces constrictions in the intestine, which may be due to the peritonitis 
or to the ulcerative process inside the bowel. 

In some cases the inflammatory process produced by tuberculosis of the caput 
coli is so intense that pain in the region of the appendix may give rise to the belief 
that an acute appendicitis or appendicular abscess is present. In a case known to 
be tuberculous the possibility of this condition is manifest, but in one which has 
a small and unrecognized tuberculous focus elsewhere, as in the lungs, operative 
procedures for appendicitis may be hurriedly resorted to when no necessity for 
them exists. 

So, too, the finding of a mass in this region, without sharp pain, may mislead 
the physician into a diagnosis of malignant growth if the rest of the body be not 
well investigated for a tuberculous focus. Such a mass may be differentiated 
from carcinoma by the fact that there is a focus of tuberculosis elsewhere. If 
the growth be slow it is probably tuberculous; whereas if rapid it is probably 
cancerous, for cecal tuberculosis may last two years and cecal cancer rarely lasts 
longer than eight months. Further than this, if the patient is below thirty years 
of age tuberculosis is more likely than cancer; whereas after forty years the reverse 
is true. The tumor when outlined by palpation, in tuberculosis is elongated and 
the thickened intestine can be felt, whereas in cancer it is usually sharply circum- 
scribed and the rest of the bowel cannot be outlined. Fever is usually present in 
tuberculosis and absent in cancer. The presence of tubercle bacilli in the stools 
will, of course, decide the diagnosis, and even if they cannot be found, the presence 
of a tuberculous focus elsewhere, in a person below forty years, should be considered 
as pointing strongly to this bacillus as the cause of the growth, but if active pul- 
monary changes are present it is to be recalled that nearly all such patients have 
virulent tubercle bacilli in their stools. 

At times the tumor found at the ileocecal region results in obstruction of the 
ileocecal valve, and the colon becomes greatly distended with gas, appearing as 
a large mass in the sides and in the epigastrium. In other cases the colon undergoes 
atrophy, and can be felt through the emaciated belly wall as a narrow, thickened 
band. I have seen the entire colon in a case of this character shrunken to such 
an extent that it was smaller than the ileum. In doubtful cases resort may be had 
to tuberculin to determine the true nature of the mass. 

Prognosis in Intestinal Tuberculosis. — The prognosis in intestinal tuber- 
culosis is not as grave as in pulmonary tuberculosis, as far as early death is con- 
cerned. In the majority of instances the patient dies of the primary focus before 
the state of the bowel is grave enough to cause death. Such cases often last for 



TUBERCULOSIS 281 

several years and have periods of improvement followed by relapse, and are char- 
acterized by gradual loss of vitality. If death is caused by the intestinal state, 
it comes as a direct result of profound feebleness and exhaustion. 

Treatment of Intestinal Tuberculosis. — The treatment of intestinal 
tuberculosis, as in tuberculosis of the lungs, consists to a great extent in the main- 
tenance of the greatest degree of nutrition and vitality that is possible, and this 
can only be accomplished by an out-door life, plenty of sunshine, the avoidance of 
fatigue, and the use of such foods as are easily digested in the stomach or in the 
duodenum, so that the greater part of the nourishment will be absorbed before 
the lower part of the ileum is reached. In those cases in which excessive peristalsis 
rapidly carries the contents of the small intestine to the large bowel before absorp- 
tion can occur, it is needful to insist on small quantities of food being taken at a 
time, and to order that no water be taken at meals. It is also essential that the 
patient shall immediately after taking food lie down and rest, in order to apply all 
the nervous energy possible to the process of digestion and to prevent stimulation 
of the bowel to active movement. For the purpose of arresting peristalsis and 
diarrhea the salicylate of bismuth in the dose of 10 to 15 grains three or four times 
a day may be given, or salol and the subnitrate of bismuth may be used. Another 
valuable drug is eudoxine in the dose of 10 to 20 grains three times a day in cap- 
sule, or bismuth subgallate may be given in the same dose. In some instances iodo- 
form may be given in keratin-coated pills in the dose of 5 grains four times a day 
to exercise the influence of this substance on the tuberculous lesions ; or if the dis- 
ease is in the rectum or colon, 20 grains may be injected dissolved in 4 ounces of 
olive oil, or 5 to 10 grains may be given in suppository. Some relief and comfort 
can also be obtained by the use of a hot-water bag over the abdomen and by 
painting the belly wall every few days with tincture of iodine. 

Tuberculosis of the Liver. — Tuberculosis of the liver occurs as part of a general 
miliary tuberculosis, and as a form characterized by the formation of fairly large 
aggregations of tubercles in which the nodules may be as large as a walnut. Tuber- 
culosis of this organ is practically always secondary to disease elsewhere. (See 
Tuberculosis of the Peritoneum.) 

The miliary form is characterized by the formation of miliary tubercles which 
are intralobular or interlobular in position. They may even be in the walls of 
the biliary ducts, and vary in size from those so small that they cannot be seen 
with the naked eye to others which are several millimeters in diameter. When the 
tubercles are massed together so that they form small nodules, the cells of the liver 
are of course destroyed, the surrounding cells suffer coagulation necrosis and infil- 
tration with spheroidal cells, and tubercle bacilli may be found in large numbers 
in the cheesy masses. 

Tuberculosis of the Genito-urinary System. — Tuberculosis may involve any 
part of the genito-urinary tract, and is by no means rarely met with in the testicle, 
the Fallopian tube, the bladder, and the kidneys. 

Tuberculosis of the Testicle. — When tuberculosis appears in the testicle it develops 
in one of two forms. In one of these the onset is abrupt and accompanied by 
acute inflammation, and in the other type the disease develops slowly, with no 
inflammation and without pain. When the acute inflammation of the first type 
disappears the testicle presents irregular nodules, which also develop in the chronic 
form. In a large proportion of cases the disease is secondary to lesions elsewhere, 
but it may be primary, particularly if it begins in the epididymis. Verneuil believes 
with others that infection may occur during coitus if tuberculous disease of the 
uterus exists, but that state is very uncommon. Babes has found tubercle bacilli 
in the vagina. 

In nearly all cases, whether the disease be primary or secondary, the lesion begins 
in the head of the epididymis, forming nodules which undergo caseous changes. 



282 DISEASES DUE TO A SPECIFIC INFECTION 

The infection spreads to the vas, which becomes thickened and nodular, and to 
the testicle, the vaginal tunic of which is infected. In more than three-fourths 
of the cases this secondary infection of the testicle takes place. 

When primary infection of the testicle occurs the tubercles also produce nodules, 
which soften and may form a sac of cheesy matter. Sinuses may form after adhe- 
sion to the scrotum has taken place and discharge externally. 

Symptoms of Tuberculosis of the Testicle. — In the form of the disease 
characterized by sudden onset the symptoms closely resemble those caused by 
gonorrheal orchitis, for sickening pain and swelling are present. Instead of sub- 
siding in the course of a week or ten days, the swelling persists, although the pain 
disappears; but before many days have passed softening occurs and the so-called 
abscess is formed, escaping by one or more sinuses. The swelling is often bilateral, 
and in some instances massive caseation does not take place, but hydrocele 
develops. In the chronic painless form there is gradual enlargement, usually of 
one testicle, with the development of one or more nodules and a sense of weight. 
In place of caseation a fibroid process may develop. 

Diagnosis. — The diagnosis of acute tuberculosis of the testicle can be made 
only after care has been exercised to exclude the possibility of injury, metastasis 
in mumps, gonorrhea, syphilis, and the orchitis of some of the acute infectious 
diseases such as typhoid fever. A previous history of gonorrheal orchitis is, how- 
ever, of importance, for this condition predisposes to tuberculosis of this part. 
The absence of any of these causes, the presence of tuberculous lesions else- 
where, as in the seminal vesicles or prostate, or in organs farther removed, and 
the fact that the patient is in young adult life, all favor the diagnosis of this 
disease being present. The development of suppuration and the finding of the 
bacilli in the cheesy pus will, of course, decide the diagnosis. 

The chronic type must be separated from sarcoma and from the thickening 
following gonorrheal orchitis. The absence of any recent history of gonorrhea, or 
of urethral discharge, and the presence of an irregular tumor which increases in 
size, all point to tuberculosis as the cause. The finding of the bacilli proves tuber- 
culosis, but the presence of the gonococcus does not prove the absence of tuber- 
culosis, for obvious reasons. If hydrocele is present the injection of some of the 
fluid into the peritoneal cavity of a guinea-pig may decide the diagnosis by produc- 
ing tuberculosis in that animal. 

Treatment. — In most cases it is far safer to remove the gland. The palliative 
treatment consists in the ordinary hygienic measures used in tuberculosis and, if 
the disease is localized, in incision and drainage with iodoform gauze; or in other 
cases, after the abscess is evacuated, the cavity may be injected with iodoform in 
glycerin or in olive oil to the extent of 15 drops. In other cases a few drops of this 
mixture may be injected into the gland at different points every three or four days, 
care being taken that antisepsis is preserved. 

Tuberculosis of the Bladder. — This condition may be either primary or secondary, 
and when secondary it may be due to infection through the bloodvessels from a 
distant point, or by direct extension from the prostatic urethra, which is diseased 
through infection of the prostate gland, which is affected in 97 per cent, of cases 
of genito-urinary tuberculosis according to Kazywicki. In other instances the 
tuberculous lesions are transferred from the kidney by the ureter to the bladder. 
In still other instances the infection passes from the vas deferens or epididymis 
or seminal vesicles to this viscus. Primary vesical tuberculosis is quite rare, and 
when it occurs is due to infection from tuberculous female genitals (Fournier). 
In many instances a case of tuberculosis of the bladder which is seemingly primary 
is really secondary to an unrecognizable infection of the kidney. The renal con- 
dition in other instances may be known to exist during life, but it may develop 
so synchronously with the vesical lesions that it is difficult to tell which organs 



TUBERCULOSIS 283 

were first affected. In many other cases the primary lesion may really exist in 
the prostate or in the seminal vesicles. 

The bladder, when affected by tuberculosis, develops grayish miliary tubercles 
in its epithelial lining, which can rarely be seen through the cystoscope as small 
gray spots, which, like all other tuberculous growths of small size, tend to amalga- 
mate and form patches which in turn may ulcerate, and so destroy the mucous 
membrane. The ulcers may be single or multiple, and, like tuberculous ulcers 
of the bowel, may have irregular outlines with the base covered by greenish or 
grayish pus. Sometimes they are deep, at others superficial, and in the severe 
cases they may penetrate the walls of the bladder and cause abscesses, which in 
turn may perforate the rectum, the vagina, or even the tissues in the suprapubic 
area. The chief lesions are usually in the area of the trigonum. Tubercle bacilli 
may be found in the pus in the urine. 

Symptoms. — The symptoms of tuberculosis of the bladder are usually not well 
marked in the early stages, and the onset of the malady may be so gradual that 
the disease is well developed before it is recognized. At first nothing more than 
a little vesical irritability may appear, and the urine remains clear and normal in 
appearance. The microscope may, however, reveal a few red blood cells, and later 
distinct hematuria develops, which is characterized by the appearance of a few 
drops of clear blood at the end of urination. As soon as the mucous membrane 
of the bladder becomes eroded infection is prone to occur and cystitis develops, 
and with the appearance of cystitis pain comes to be a prominent symptom, asso- 
ciated with tenesmus and a constant desire to urinate, which exhausts the patient 
and prevents sleep. The earliness with which these symptoms develop depends 
upon the seat of the disease. If it be in the trigonum, they arise promptly; if 
elsewhere, they may be postponed for months. Retention of urine may follow 
ulceration, or in other cases as the neck of the bladder ulcerates incontinence is 
produced. 

Often the symptoms vary greatly in severity; from grave severity at one time 
to almost complete relief at another. Fever is often absent. 

Diagnosis. — The diagnosis of vesical tuberculosis depends upon the presence 
of these symptoms and the finding of the bacillus in the urine, or by inoculation 
of a rabbit or guinea-pig with the urine, with the subsequent development of the 
disease in that animal; but the failure of either of these tests does not exclude 
tuberculosis. Hematuria is rare, but pyuria is constant, and pyuria without the 
presence of ordinary pus-producing germs is very suggestive. Failure to find 
tubercle bacilli does not negative the diagnosis. The cystoscope usually decides 
the diagnosis. If gonorrhea, stone in the bladder, stricture of the urethra, or a his- 
tory of the use of irritating drugs can be excluded, and if no spinal disease exists 
to cause secondary bladder trouble, tuberculosis should be suspected. The pres- 
ence of tuberculosis elsewhere, of course, suggests that this disease is the cause 
of the bladder trouble. 

Treatment. — For the general plan of treatment in these cases reference must 
be made to treatises on genito-urinary disease. The bladder must be soothed by 
alkaline diuretics if the urine is acid, hyoscyamus may be given for vesical irri- 
tability, and if the disease is active iodoform in olive oil may be injected into the 
bladder every day, using a 10 per cent, solution. The bladder should be care- 
fully emptied before the iodoform is injected. In other cases corrosive sublimate 
1 : 5000 may be employed by injection. In severe cases perineal drainage is to 
be resorted to. 

Tuberculosis of the Kidneys. — With regard to the pathway by which the bacillus 
reaches the kidneys two views have generally been held. Hematogenous infection 
is admitted. Until recently an ascending infection has been thought not uncom- 
mon, but there is at present a decided tendency to doubt that infection travels 



284 DISEASES DUE TO A SPECIFIC INFECTION 

from below upward; it has been shown by many observers that tubercle bacilli 
are occasionally present in the urine of tuberculous patients, even when subsequent 
examination at autopsy discloses no tuberculosis of the genito-urinary organs, and 
hence it is not necessary to invoke ascending infection to explain renal lesions 
secondary to tuberculosis elsewhere. 

Tuberculosis of the kidneys appears in an acute and chronic form. The former 
is of the miliary type and is associated with the signs of tuberculous infection 
elsewhere, and cannot be treated separately from the general state. The chronic 
form may arise as a primary lesion, or, far more commonly, as a secondary process 
due to disease of the lower genital tract. When the disease is primary the bacillus 
probably gains access to the kidney through the blood; this type is that usually 
met with in children. But the form ascending from the genitals is that met with 
in adults, as a rule. Males are more frequently affected than females. The disease 
is most frequent between twenty-five and forty years of age, but it has occurred 
in an infant at the breast and in very old men. The lesions are often bilateral. 

The pathological process is primary, and secondary renal tuberculosis is quite 
different. In the primary form, in which the infection comes by the blood, the 
bacilli, resting in the vessels of the tufts and tubules, form small tubercles, which 
gradually undergo necrosis and so cause a spread of the disease to other parts 
of the kidney, particularly the calices and the pelvis. The necrosis of tuberculous 
nodes gives rise to areas of softening or abscess cavities, and these are filled with 
cheesy material which rarely contains blood and urine, although lime salts are 
frequently present in the dead tissue. Not only tubercle bacilli but pyogenic and 
other micro-organisms are often present. The capsule of the kidney is thickened 
and may show scattered tubercles. The size of the organ is considerably increased 
by the growth of the tubercles and the associated inflammation, forming the so- 
called massive tuberculosis of the kidney. Finally, the kidney may be shrunken. 

As the tuberculous process in the pelvis of the kidney increases the ureter is 
usually infected, and as a result is often partly occluded. This produces a reten- 
tion of urine in the kidney and so a secondary hydronephrosis develops, or it may 
be a pyonephrosis. Sometimes in the early, and much more frequently in the 
later stages of the affection the tissues surrounding the kidney become more or 
less affected and a perinephritic tuberculosis may appear from rupture of a softened 
area through the capsule of the kidney. 

When that form of renal tuberculosis which is secondary to tuberculosis in the 
lower genito-urinary tract develops, the ureter is first involved, and thence the 
pelvis of the kidney. The disease then attacks the tips of the pyramids and so 
gradually the entire gland is involved, but to a less degree than in the form first 
described. Pyonephrosis is very common in these cases, and obstruction in the 
flow of urine is usual. 

Symptoms. — Often no symptoms appear until the pelvis of the kidney is diseased, 
when pain becomes a marked symptom. This pain may be dull or acute, as if 
due to a renal calculus, with the characteristic radiation of the pain to the penis 
and inner side of the thigh. The urinary symptoms are frequent urination, slight 
incontinence, and, later, distinct signs of cystitis develop. These symptoms often 
mislead the physician into a diagnosis of disease of the bladder. Before the pelvis 
of the kidney is affected the urine may be normal, but afterward it contains pus and 
blood, the pus coming from this area or from the necrotic ulcerating tubercle. 
Attacks of violent' pain, arising from acute hydronephrosis due to blocking of the 
ureter by cheesy masses, may occur, followed by a free flow of purulent urine as 
the obstruction gives way. Tubercle bacilli can usually be found in the urine, but 
care must be taken that the smegma bacillus is not mistaken for the specific bacillus, 
and as indicated above, the demonstration of the tubercle bacillus does not prove 
that the infection is in the genito-urinary organs. 



TUBERCULOSIS 285 

The associated symptoms are those of anemia, debility, and loss of flesh. A 
lumbar tumor may also appear. 

When the case is grave the question of operation must be considered, and it is 
important to discover if the disease is bilateral or unilateral before operating. 
This may be done by ureteral catheterization. 

Tuberculosis of the Fallopian Tubes, Ovaries, and Uterus. — The frequency of 
tuberculosis of the Fallopian tubes is notable. It forms the largest part of all 
statistics involving the female genitalia, for, as stated below, the ovary and uterus 
are rarely affected. Tuberculosis of these parts was recognized and reported as 
early as 1744 by Morgagni. In 1886 Hegar published an important paper on this 
subject which marked an epoch in its study. To illustrate the great frequency 
of tuberculosis of the female genital tract the statistics of eight European patho- 
logists may be cited. In 8627 cases of tuberculosis in females, this disease had in- 
fected the genitals 208 times. These relative proportions are probably too small. 

Unlike tuberculous disease elsewhere, tuberculosis is quite frequently a primary 
lesion in these parts, the infection being received in some cases frOm the male 
during coitus (Verneuil, Cohnheim), but in the majority of instances taking place 
through the blood or lymphatics. According to the statistics of Schramm, Spaeth, 
Mosler, and Frerichs, genital tuberculosis is found to be primary in about 18 per 
cent, of cases of genital tuberculous disease. 

Genital tuberculosis is most common during the period of sexual life. Patho- 
logically the condition under these circumstances is like that of an ordinary salpingi- 
tis, the tubes being thickened and filled with cheesy material. Because of the inflam- 
mation associated with the tuberculous process the fimbriated extremity of the 
tubes becomes adherent to the ovaries and the uterus may become infected. This 
condition may develop in children as well as in adults, and it is usually bilateral. 
True abscess of the tube may arise from this cause and a tuberculous parametritis 
and peritonitis often start from this nidus. In some cases a miliary tuberculosis 
of the tube develops. 

The ovary is rarely involved, but when this occurs it is always a secondary 
infection from an infected tube or other adjacent parts or from the blood. The 
uterus is affected only in very rare instances. 

Prognosis. — The prognosis in tuberculosis of the female genitalia is more favor- 
able than would be imagined, provided an early diagnosis is made and operative 
treatment resorted to. It is, of course, more favorable in these instances if the 
lesion be a primary one, for if severe disease is present elsewhere, operation may 
be contra-indicated and general recovery impossible. 

Treatment. — The treatment is entirely surgical. 

Tuberculosis of the Heart. — The heart very rarely becomes tuberculous but myo- 
cardial changes, due to the disease elsewhere, are not uncommon, consisting chiefly 
in fragmentation of the myocardium, brown induration and interstitial myocarditis. 
Fatty degeneration also occurs. The pericardium suffers from tuberculosis in the 
pulmonary form of the disease only slightly more frequently than the heart muscle 
Norris found it recorded only thirty-one times in 7646 cases of pulmonary tuber- 
culosis. General endocarditis arising from this cause is exceedingly rare. Some- 
times a general endocarditis arises from an associated terminal infection. An 
endocarditis producing mitral stenosis is, however, more common but is not directly 
due to tubercular infection, but to toxemia. Ferrend and Rathery have reported 
a case of tuberculous vegetative endocarditis following primary tuberculosis of 
the spleen. Tubercle bacilli were found in these vegetations and in the clotted 
heart blood. 

Tuberculosis of the myocardium is very rare. In 1902 Anders collected 71 
cases of tuberculosis of the myocardium, and reported one of his own, which were 
all he could find in literature. Out of 3999 autopsies reported by Valentin and 



286 DISEASES DUE TO A SPECIFIC INFECTION 

Sangelli this condition was found in only nine instances. Weigert, however, states 
that he has found minute tubercles in different portions of the heart in nearly all 
his autopsies on patients who died from acute miliary tuberculosis. 

Tuberculosis of the Thyroid Gland. — Fraenkel and Chiari in 480 autopsies on 
tuberculous subjects found the thyroid gland affected thirteen times. 

Tuberculosis of the Brain and Cord. — Tuberculosis of the meninges of the 
brain and cord has already been mentioned when discussing the tuberculous infec- 
tion of the serous membranes. The tissues of the brain and cord are, comparatively 
speaking, very rarely affected. When tuberculous lesions occur in these parts 
they are practically always secondary to tuberculous lesions elsewhere, but there 
are a few exceptions to this rule. Thus, Demme has recorded a unique case of 
tuberculous tumor of the cerebellum in a child of twenty-three days, and he has 
also had a case in which infection seemingly took place through the nose. 

When tuberculous tumors develop in these parts of the nervous system they 
appear as solid or caseous, rounded masses, which resemble the ordinary tuber- 
culous growth as it is seen elsewhere. They vary in size from a millet-seed to an 
orange. When incised they are caseous, fibrocaseous, or hyaline and calcareous, 
or all of these changes may be found associated. The surface of the growth is 
sometimes soft and translucent, and the adjacent brain-tissue may be filled with 
miliary tubercles, which, coalescing with the main growth, in this way increase 
its size. The growth does not undergo the rapid changes usually met with else- 
where. Sometimes these nodules become encapsulated by fibrous tissue just as 
does the ordinary tuberculous growth in the lung, or rapid softening in the surround- 
ing tissues develops and suppuration takes place. 

These tuberculous growths do not tend to infiltrate the surrounding tissues. 
They generally occur in the brain tissue itself, and while it has been asserted that 
they always spring from the pia mater, this view is of doubtful value. As they 
often project above the surface, the cerebrospinal fluid is readily infected. One- 
third of these tuberculous growths occur in the cerebellum, in one of its hemispheres 
or in the middle lobe. After the cerebellum, the cerebrum is the most common 
site, and after this Gowers gives the following order: the pons, the cerebral ganglia, 
the quadrigeminal bodies. As a rule, more than 1 growth exists: but sometimes 
2 and sometimes as many as 10 or 12 are present. Thus, Trevelyan found them 
multiple in 17 out of 33 cases, which is a smaller proportion than is usual, and the 
largest number in any one case was 4. In a case reported by Middleton there 
were 20, and in a case reported by Homen there were 12. West and Henoch have 
each reported a case in which there were 12 tuberculous tumors. There are a 
few cases recorded in which recovery has taken place notwithstanding the presence 
of a tuberculous tumor in the brain, and without operation. (For literature see 
Trevelyan's article in the Lancet for November 7, 1903.) The symptoms and 
treatment of tubercle of the brain are discussed under Brain Tumor. 



HODGKIN'S DISEASE. 

Definition. — Hodgkin's disease is a condition in which there is marked swelling 
and overgrowth of the lymphatic glands, both internal and external, with a moderate 
degree of anemia which is in no way peculiar to this malady. The spleen is usually 
enlarged. The overgrowth of the lymph nodes and lymphatic tissues generally 
is closely allied to malignant lymphadenoma. Another name for the disease is 
" pseudoleukemia." 

History. — Although a difference between this state and scrofulous enlargement 
of the lymph nodes had been made prior to 1830, it was not until Hodgkin in 1832 
described cases seen at Guy's Hospital that it was generally recognized. In 



HODGKIN'S DISEASE 287 

1856 Wilkes, in London, and Bonfils, in France, still further illuminated the 
subject. 

It was not until Virchow completed his work on the histology of the blood that 
Hodgkin's disease became clearly differentiated from leukemia of the lymphatic 
type. The fact that changes of a peculiar character exist in the lymph nodes 
was not known until 1897, when several investigators, notably Fischer, described 
them. 

Etiology. — Within the last few years the view that Hodgkin's Disease was a 
peculiar condition due to infection by the Bacillus tuberculosis gained a number of 
adherents, and there are without doubt certain facts connected with the malady 
which tend to substantiate this view. On the other hand, Dorothy Reed, Longcope 
and Simmons have published careful investigations to prove that Hodgkin's disease 
possesses definite pathological characteristics peculiar to itself. In 1913 Negri 
and Mieremet described a pleomorphic organism obtained from the enlarged 
nodes in cases of the disease to which they gave the name of Corynebacterium 
granulomatis maligni. Later Bunting and Yates isolated it in pure culture from 
three cases, found it in two others not in pure culture, and stained it in the intestinal 
lesions of a sixth. They suggest for it the name of Corynebacterium hodgkini. 
Billings and Rosenow recently report finding this organism in 12 cases, in pure 
culture in 3, with a staphylococcus in the others. They describe it as a Gram- 
staining, non-acid-fast, polymorphous, diphtheroid organism, growing on blood 
agar, blood serum, and ascites-dextrose agar. These findings appear significant, 
though actual proof that this organism is the cause of Hodgkin's disease has not 
yet been adduced. The disease is more frequent in males than in females, and in 
adults than in childhood. 

Pathology and Morbid Anatomy. — The changes which are most marked are en- 
largement of the lymphatic glands at first in limited areas and later all over the 
body. The cervical and inguinal glands are usually the most prominent, and the 
outlines of the neck may be completely obliterated. At autopsy the retrobronchial 
and retroperitoneal glands may be found enormously increased in size, forming a 
mass as large as the arm, and pressing on adjoining tissues such as the thoracic 
duct and the bloodvessels. The affected nodes are discrete and regularly enlarged. 
Their consistency varies. Sometimes they are firm and dense, at others so soft 
as to fluctuate. The cut surface of these glands is translucent, gray, or more rarely, 
yellowish, and the tissues of the glands bulge forward. An overgrowth of lymphoid 
tissue may take place at the apices of the lungs and lead to a diagnosis of tuber- 
culosis. Death may be due to pressure on the thoracic bloodvessels, and perhaps 
to pulmonary infiltration and exudation. Osier asserts that infiltration of the 
lung does not occur in this disease, and that when such an infiltration does take 
place the disease is true lymphosarcoma. There is also enlargement of the spleen 
with overgrowth of the lymphoid bodies, which are grayish white in appearance, 
and consist of lymph follicles held together by a reticulum of connective tissue. 
The marrow of the long bones may be lymphoid or purulent in appearance, as it is 
in some cases of myelogenous leukemia. The liver and kidneys may also be 
enlarged and contain lymphoid masses. 

The characteristic microscopic lesions of Hodgkin's disease are an early increase 
in the lymphadenoid tissues with a proliferation of endothelial cells, the formation 
of uninuclear and multinuclear giant cells, thickening of the reticulum, and lastly 
an overgrowth of the connective tissue of the lymph nodes to the development 
of which the increased density of these masses is due. Eosinophile cells in most 
cases are present in very large number in the lymph nodes and in the bone- 
marrow. Not only is the disease characterized by these changes in the pre-existing 
lymph nodes, but there is a constant formation of new nodes which soon become 
similarly affected. 



288 



DISEASES DUE TO A SPECIFIC INFECTION 



The blood changes are most variable. In some cases they are moderate, in 
others severe, in that the red cells may be decreased in number, but even when 
the patient is at death's door there may be fully 3,000,000 cells present. The 
red cells are not altered in a manner which is in any way characteristic. The 
changes consist solely in a diminution in number to a moderate degree, and in a 
reduction of the amount of hemoglobin. The leukocytes are not increased as in 
true leukemia, but are often actually diminished. Pinkus thought a relative 
increase of the lymphocytes constant, but this change was present in but 1 of 
Longcope's 7 cases, although a very large proportion of the white cells may be 
of this variety. Occasionally the increase of white cells may rise to the number 
seen in certain inflammatory states, as from 30,000 to 40,000. In the later stages 
the blood picture may assume all the characteristics of an intense secondary anemia. 

Fig. 59 




Hodgkin's disease. 



Symptoms. — The symptoms of pseudoleukemia are those of ordinary severe 
secondary anemia, with shortness of breath and palpitation of the heart on exertion. 
The enlarged masses of glands in the neck and groins may be very characteristic 
in appearance, associated as they are with pallor and puffiness of the face. When 
the internal glands are primarily and chiefly involved the diagnosis from tuber- 
culosis may be difficult because the pressure may cause consolidation with patches 
of dulness on percussion, and because a distinct febrile movement is often present. 

These masses by producing pressure may give rise to paroxysms of cough or of 
pain or constant dyspnea. When the inguinal glands are affected edema of the 
lower extremities may develop, and shooting pains may be felt in the legs. After 



LEPROSY 289 

the glandular masses become very large, superficial sloughing may occur, and there- 
fore the resemblance to a suppurating tuberculous mass may be increased (Fig. 
59). I have seen an actinomycosis of the neck produce similar symptoms. Bronz- 
ing of the skin may occur. Moderate fever is often present. It may be low and 
regular or high and irregular in type. Occasionally it has an intermittent char- 
acter with sharp exacerbations, so that it resembles intermittent or remittent 
malarial fever. Jaundice due to pressure on the bile-ducts may appear. 

Additional symptoms met with in some cases are murmurs in the great vessels, 
produced partly by the anemia but chiefly by the pressure caused by the growths. 
Deafness due to closure of the Eustachian tubes by growths in the pharynx and 
unequal pupils due to pressure on the cervical sympathetic, may be present. 

Diagnosis. — From true leukemia pseudoleukemia is to be separated by the 
absence of the large excess of leukocytes, and the lack of the leukocytes peculiar 
to that disease. From enlargement of the lymph glands due to tuberculosis it 
is to be separated by the test with tuberculin (see Tuberculosis), and by the fact 
that tuberculosis rarely produces enlargement of the cervical glands on both sides 
and in both groins, and by the absence of a tuberculous focus elsewhere. When 
doubt exists a part or all of an enlarged mass of glands may be excised and examined 
microscopically to determine the character of the disease. 

In many cases the clinical diagnosis is most difficult. I have seen the most 
eminent clinicians mistake this malady for tuberculosis. Very rarely a form of 
multiple lipoma distributed in the lymph-node areas closely resembles Hodgkin's 
disease; the picture may further be confused by the presence of glandular and 
calcific masses in fatty tumors; such a case has been observed in the Jefferson 
Medical College Hospital; Chantemesse and Podwyssotsky figure such a case 
under the name adenolipomatosis. 

Prognosis. — The prognosis in Hodgkin's disease is absolutely bad. Not one 
recovers. These patients have periods of improvement when courage runs high, 
but after all the inevitable progress is downward. Death comes from interference 
with circulation or respiration or by general asthenia. 

Treatment. — The best treatment is the use of arsenic in full doses. Excellent 
results have been obtained in some of these cases by the use of arrays, the parts 
involved being exposed to the rays, repeatedly, over a long period of time. Billings 
and Rosenow report improvement (with one apparent recovery) in several cases 
treated with vaccines made from the organism described under Etiology. They, 
however, used the vaccine as an addition to the a:-rays and other usual methods of 
treatment. 

LEPROSY. 

Definition. — Leprosy is a chronic infectious disease caused by a specific bacillus, 
and is characterized by the occurrence of granulomatous new growths in the skin, 
mucous membrane, peripheral nerves, and viscera. The lesions are partly anes- 
thetic and there is a marked tendency to destructive ulceration and trophic lesions. 

History. — The history of leprosy is as old as the written history of the human 
race. The earliest known records are in two Egyptian papyri of 4260 B.C. and 
2400 B.C. The detailed description of leprosy in the third book of Moses is familiar 
to all. In India and China the earliest writings that unmistakably describe leprosy 
appeared about 700 B.C. The disease appears much later in European history. 
It was not mentioned by Hippocrates, and we may assume that it was unknown 
in his time. It appeared in Greece before 375 B.C. and gradually spread over all 
Europe, its extensions being generally along the track of conquering armies. Its 
extensive distribution in the Middle Ages finally brought about stringent restrictive 
regulations which, beginning in the thirteenth century, served to gradually decrease 
the disease until now it occurs only in isolated centres of infection. 
19 



290 DISEASES DUE TO A SPECIFIC INFECTION 

Distribution. — At present the distribution of leprosy is very extensive, principally 
in tropical and subtropical countries. It is a mistake to consider that leprosy is 
essentially a disease of warm climates. In Europe it appears only in small, scattered 
centres or in isolated cases. It prevails in greatest numbers in Finland, Sweden, 
Iceland, and Norway, particularly the latter. In Russia it is found in forty-nine 
provinces, most frequently in the Baltic provinces of Lifu with 609, and Kurland 
with 201 cases. Isolated cases occur in England, Germany, Brittany, and Italy. 
The total number of cases in Western Europe at present is estimated at 3000. 
The disease is found all over tropical Asia. In British India the number of lepers 
is estimated at 105,000, or one in every two thousand of population. It is believed 
that leprosy prevails in the southern provinces of China more than anywhere else, 
although no accurate figures are available. It is very common in Japan, the number 
of cases being estimated at 23,660 (Souton), and in Ceylon, Persia, Arabia, and 
the Malayan country. In the Philippines there are probably 15,000 lepers. The 
disease is widely distributed in Africa, particularly along the upper Nile and the 
countries bordering along the Red Sea and the Mediterranean. Leprosy was 
introduced into the Sandwich Islands in 1859, and at one time one in thirty of 
the population was affected. 

Much has been said of the early existence of leprosy in America. There is no 
evidence to show that the disease existed prior to the Spanish discovery. The 
so-called evidence of pre-Columbian leprosy in America is entirely too vague to 
justify any deductions. In point of fact it suggests syphilis or sacrificial mutilation 
more strongly than leprosy. At present lepers are found in large numbers in 
Mexico and many countries of South America. In Colombia there are said to be 
seven in every one thousand in the population. There are some cases in New 
Brunswick and British Columbia. Cuba and the Antilles are severely infected; 
the latest figures give 1297 lepers in Cuba. In the United States the disease is 
generally distributed. A recent official report shows that nearly every large city 
has at least one case, the aggregate number for the United States reaching over 
900. The disease occurs in three main foci, namely, one in Louisiana, which has 
existed since 1785, and has lately been estimated as containing about 500 cases; 
another in California, the infection having been brought in by the Chinese, and a 
third in Minnesota, where it has been estimated that there were 170 lepers, the 
number being almost entirely made up of emigrants from the infected districts in 
Norway, from which region infected persons also carried the disease into the Mormon 
settlements of Utah. These settlements in Utah have also been infected from 
Hawaii. 

Etiology. — The specific cause of leprosy is the Bacillus leprae, discovered by 
Hansen in 1871. This bacillus is about the same size and has the same morphology 
as the tubercle bacillus. Like it, it is also acid-fast ; that is to say, when stained 
with an aniline dye it does not decolorize readily in the presence of mineral acid. 
It stains a little more easily than the tubercle bacillus and decolorizes more rapidly. 
It has been grown successfully on artificial culture media in the presence of typhoid 
or cholera organisms. It is found packed in very great numbers inside the leprosy 
cells, but it does not invade the nucleus. It is also found in zooglea masses in 
the lymph spaces, in the granulomatous lesions, and in the infiltrated nerve tissues. 
A number of cases have been reported in which the bacillus has been found in 
the circulating blood. 

Manner of Infection. — There is one case of experimental inoculation on record 
in the person of a Hawaiian convict reported by Arning. Four weeks after inocula- 
tion the disease began to develop with acute pain and thickening of the nerve 
trunks, and a little while after a typical leprous nodule appeared at site of inocula- 
tion. The patient died of the disease in six years. Unfortunately this experiment 
was made in a leprosy country and the man had a leprous family history, so that 



LEPROSY 291 

the evidence derived from it cannot be regarded as absolutely conclusive. There 
can be no doubt that in a large number of instances the bacillus gains admission 
through abrasions of the skin and mucous membranes, and possibly also from the 
friction of infected clothing. 

Corroboration of the idea that the bacilli gain entrance through local lesions is 
found in the fact that where people go habitually without shoes, as in tropical 
countries, the disease first appears in the feet in a large proportion of cases. Ehler 
states that in Iceland the face and hands are most frequently attacked because the 
remainder of the body is so fully protected by clothing. Boinet, in Hanoi, con- 
sidered infected earth to be the probable carrier of the disease to the feet of the 
natives. He found the earth saturated with sputa, crusts, and discharges of the 
lepers. He was able to demonstrate that the soil of the cemetry at Hanoi was 
highly charged with bacilli, but this evidence is of little value, as acid-fast bacilli 
are widely distributed. Carasaquilla believes that leprosy may be conveyed by 
the bite of fleas, and infection by the mosquito must also be borne in mind, since 
the bacilli are sometimes found in the blood and have also been demonstrated in 
mosquitoes. Scabies may transfer the infection. A large proportion of cases are 
undoubtedly infected in sexual intercourse. The contagion of leprosy is, however, 
feeble. 

The immunity of physicians and nurses is proverbial, although several striking 
instances, as that of Father Damien, are on record in which attendants on lepers 
have fallen victims to the disease. It would seem that long intimate contact were 
necessary to contract it. Hutchinson suggests that leprosy may be conveyed from 
person to person by commensal contagion; that is to say, by eating food prepared 
by the sore hands of a leper, and by eating out of infected dishes and utensils. 
Von Bergmann, in a study of 106 cases of leprosy in Riga, found that 60 per cent, 
occurred in people who had lived in intimate contact with lepers. In the workhouse 
at Riga there were 23 cases: 4 who entered with it, 19 who contracted it in the 
house; 9 cases developed in women whose neighbors in the next beds had leprosy, 
but McCoy and Goodhue of the United States Public Health Service in Molokai, 
basing their statistics upon cases exposed not less than five years, found that out 
of 23 Causasian males constantly exposed 3 were infected, and that of 12 Caucasian 
females, none were infected. 

Great significance was formerly attached to the factor of heredity in leprosy, 
but recent studies of the epidemiology of the disease have disproved its importance. 
Boinet cites a case in which grandfather and grandmother were lepers, while the 
father and five children escaped, although living in a leprous community. Children 
of lepers removed soon after birth from the infected districts do not develop leprosy, 
while their brothers and sisters who continue to live in the leper community may 
contract it. None of the children of Norwegian lepers who have emigrated to the 
United States have developed the disease. Tonkin, in a careful study of lepers 
in Algeria, found that only 10 per cent, of the cases had any leprous taint in their 
ancestry; so that 90 per cent.- at least must have derived the disease from other 
sources. He found, further, that less than 10 per cent, of the children of lepers 
developed the disease, which is certainly a low percentage of contagion for persons 
living in close intercourse with lepers, even disregarding the question of heredity. 
There is nowhere a record of a leprous fetus, although one or two cases of infants 
born with leprosy have been reported. 

The disease is exceedingly rare under one year; and, in fact, before the fifth 
or sixth year. It must be recognized as very feebly contagious, therefore, when 
close and prolonged contact is eliminated. Of the various types the tuberculous 
is far more contagious than the anesthetic. 

Many writers have maintained that defective nutrition and diet play an 
important role in this disease. Hutchinson was the foremost exponent of the 



292 DISEASES DUE TO A SPECIFIC INFECTION 

theory that the disease is conveyed by food and that the germs gain entrance to 
the body through the stomach. He believes that tainted fish carry the infection, 
although leper bacilli have never been found in them. This idea of fish serving 
as the medium for the infection of leprosy is not a new one. They have been 
suspected in all ages, and it is true that leprosy occurs chiefly in countries where 
fish forms a staple article of food, and where a large proportion of the inhabitants 
are engaged in fishing. There is nothing inherently improbable in the theory 
that fish may carry the infection, or that a fish diet may represent a common 
additional factor in the development of the disease. As against this theory, Hansen 
maintains that it is necessary to demonstrate the bacilli in fish. He states that 
the people of Norway are using more fish than ever at present, but nevertheless 
leprosy is constantly decreasing. 

Morbid Anatomy. — In tuberculous leprosy the lesions consist in granulomatous 
growths or diffuse infiltration of the skin and mucous membranes. The granulo- 
matous growths are built up of small round and fusiform cells and large vacuolated 
cells, called by Virchow leprosy cells. These cells are probably of endothelial 
origin and are packed full of bacilli. They frequently develop into giant cells. 
The bloodvessels are increased. In diffuse leprous infiltration the same histological 
elements are observed. The new growth invades the bloodvessels, hair follicles, 
and sweat glands. The bacilli are found everywhere, but in greatest numbers in 
the giant and leprosy cells. 

In the macular lesions there is a larger proportion of connective tissue, the 
bacilli are fewer, and none of the large types of cells are seen. In the anesthetic 
type, diffuse or nodular infiltrations are found in the nerve trunks. The nerves 
are firmer than normal and darker in color. The interstitial connective tissue is 
markedly increased and the axis cylinders are atrophied. 

Leprous nodules and infiltrations are found in the liver, spleen, testicle, intestines, 
and kidneys. In the bones osteomyelitis- necrosis, and atrophy are observed, 
the bone being replaced in many instances of leprous mutilations by connective 
tissue. In the larger joints changes occasionally are observed that are very similar 
to the trophic joint changes of tabes. 

Symptoms and Clinical Forms. — Leprosy shows itself under an extreme variety 
of forms. Its beginning is very insidious and at first the progress is very slow. 
Even after a number of years the lesions may be very insignificant and not at all 
conclusive to the casual observer. The incubation period is uncertain, and is 
usually accepted as very long. The average incubation is assumed to be between 
two and three years, although cases are reported in which it is supposed to have 
lasted from ten to twenty-seven years; these prolonged instances must be viewed 
with suspicion as to their accuracy. In many other cases periods as brief as from 
three or four weeks to three or four months are given. It will be recalled that the 
incubation of the Hawaiian inoculation case was four weeks. 

Another disputed point in the symptomatology of leprosy is the existence of 
the primary sore or the leprous chancre, as it has been called. It has been shown 
that all evidence points to direct inoculation as the source of leprosy, and it is not 
unreasonable to assume a primary sore at the point of inoculation of the germ. 
Many observers hold that such a sore does occur, and that in a large majority 
of cases it is located on the nasal septum. Thus, Stickler was able to demonstrate 
ulceration of the septum in 128 out of 153 early cases. 

Leprosy begins with marked prodromata, of which fever is the most common. 
It comes in crises of several days' duration and is usually mistaken for malaria. 
It is entirely analogous to the pre-emptive fever of syphilis. Head and joint 
pains are common as well as general malaise, with frequent drenching and exhausting 
sweats unassociated with fever. Epistaxis is a common and early symptom and 
corroborates Stickler's observation of the existence of a primary ulcer in the nose. 



LEPROSY 293 

After lasting from a few months to two years, an unusually severe attack of fever 
ushers in the primary eruption or macular stage of leprosy. 

Macular eruptions consist in erythematous patches, smooth, shiny, and slightly 
elevated. They occur all over the body, but are more profuse on the face, the 
backs of the hands, and forearm. The supraorbital ridges and malar prominences 
are commonly affected. The hairy scalp is not invaded. The patches come and 
go, although the later crops show a tendency to persist and for the skin to become 
slightly thickened. When the macules invade the hairy portion of the body, the 
hair is lost or becomes white and downy. The macules are anesthetic, particularly 
in the centre of the patches. 

Next follows the stage of development of the leprous nodules or the deposit 
of specific leprous infiltration. Here the disease may be broadly divided into three 
clinical types: first, tuberculous or nodular leprosy, in which the skin and mucous 
membranes are invaded by the specific new growth; second, the anesthetic or nerve 
leprosy, where the leprous deposits take place in the nerve trunk: third, the mixed 
type of leprosy, which combines both of the foregoing and to which class all cases 
ultimately tend. 

Tubercular or nodular leprosy may begin with or without the macular 
stage. The leprous nodules appear under the skin, particularly about the face 
and ears; the nodules are palpable as distinct, tough, flattened masses under the 
skin. They have a peculiar, rubbery consistency, are painless, and freely movable. 
Diffuse infiltration of the skin takes place, and large, flat, leprous patches are formed. 
The leprous lesions grow steadily larger, until on the face large folds and masses 
of tissue are formed, producing the condition known as Leontiasis, or the lion-like 
face of leprosy. New nodules appear and other portions of the body are invaded 
until practically the leprous lesions cover the entire skin surface. In the early 
stages the nodules occasionally diminish in size or may be entirely absorbed. Later 
they break down and extensive ulceration occurs. At this stage the mucous 
membrane becomes extensively involved. The cartilaginous structures of the 
nose are completely lost, and leprous ulcerations of the larynx occur, with loss of 
voice and ultimately cicatricial stenosis, which may cause intense dyspnea. Exten- 
sion of the leprous ulceration into the corneal structures may cause blindness. 
The ulcerations produce horrible and characteristic deformity. 

Death takes place from exhaustion or intercurrent infection. 

Anesthetic Leprosy. — Anesthetic leprosy shows a very different picture from 
the foregoing. The macular stage continues and is marked by increased pigmenta- 
tion and complete anesthesia of the macule. Gradually extensive neuritis is de- 
veloped in the trunks of various nerves, causing pain, severe and neuralgic in 
character, and later large areas of anesthesia or numbness. The superficial nerve 
trunks, the posterior auricular, and the ulnar where it winds about the internal 
condyle, are palpably thickened. Bullous eruptions occur on the hands, feet, and 
elbows, and along the course of the nerves breaking down and leaving extensive 
spreading and destructive trophic ulcers. As a further result of these trophic 
disturbances extensive contractures develop, and fingers and toes slough away. 
In the older cases the areas in the distribution of the affected nerves, which at 
the beginning of the disease were painful or numb, become completely anesthetic 
and the muscles become extensively atrophied. When this condition occurs in the 
hand, a typical claw-like hand of leprosy is produced. The atrophied skin is particu- 
larly prone to injuries and to extensive ulceration. The course of this type of 
leprosy is excessively chronic. 

The mixed leprosy presents a combination of the features of tuberculous and 
anesthetic leprosy. In all cases of extensive tuberculous leprosy the nerve trunks 
eventually become involved, and the evidences of neuritis and trophic disturbances 
are added to the clinical picture. 



294 DISEASES DUE TO A SPECIFIC INFECTION 

Diagnosis. — In advanced cases leprosy could hardly be mistaken for any other 
disease. The lesions are too striking and distinctive. Difficulties in diagnosis 
arise in early undeveloped cases, particularly in the macular and anesthetic types. 
Here, as Manson says, the touchstone of diagnosis is the anesthesia. It should 
be sought for in the centre of macular areas, and in the centre of recent nodules, 
if any exist. Advantage may also be taken of the fact that leprous areas do not 
perspire. Baelz uses an ingenious plan not only for diagnosis, but also for mapping 
out the involved areas. Aniline is rubbed on the skin and pilocarpin is admin- 
istered hypodermically. The leprous areas do not sweat and consequently remain 
unstained. 

The most satisfactory diagnosis consists in identification of the bacilli. For 
this purpose a leprous nodule may be clamped, punctured with a needle, and the 
exuding drop of fluid properly stained and examined. Even in the very earliest 
cases, long before other symptoms appear, leprous thickening can be demonstrated 
in the ulnar or posterior auricular nerves. In doubtful cases the minute fragment 
of one of these nerves should be excised and stained for the bacilli. 

Morrow calls attention to the fact that leprosy and nasal catarrh go hand in 
hand, and that in the large proportion of cases bacilli can be demonstrated in the 
nasal secretion. It has also been shown that where nasal secretion is scanty a 
few doses of potassium iodide will cause a sharp catarrhal flow, in which the bacilli 
may be demonstrated. 

Prognosis. — In the vast majority of cases leprosy slowly tends to a fatal ending 
from exhaustion or intercurrent infection. Isolated cases, however, occur in which 
the disease is arrested or cured. These instances of arrest are more common in 
anesthetic leprosy than in the tuberculous type. Many of these cases survive 
twenty or thirty years, and in a large proportion of these the specific process is 
probably ended, although the extensive damage by nerve involvement and trophic 
lesions remain. Even tuberculous leprosy has been known to disappear. 

Many cases are arrested, and, after a long period of years, death occurs from 
some other disease not associated with the leprosy. These reported cures must, 
however, be accepted with extreme caution. It is probably more fair to speak of 
them as arrests. Mention must also be made of the marked amelioration that 
occasionally follows the removal of a leper from the country in which he has de- 
veloped the disease. 

Treatment. — The treatment of leprosy comprises careful attention to cleanliness, 
provision of good hygienic surroundings, abundance of nourishing food, proper 
clothing, hygienic dwellings, and light occupation. As special remedies gurgun 
oil and chaulmoogra oil have been extensively used. The former has been aban- 
doned. Chaulmoogra oil (oleum gynocardii) may be administered by the mouth 
in doses of 2 drachms, or by the rectum, in an emulsion with hot milk, when it is 
badly borne by the stomach. In some cases this drug seems to have almost a 
specific action. In a few cases apparent cures and in a great many cases very 
marked improvement is observed. The oil may also be administered hypoder- 
mically. 

Unna advises the internal use of massive doses of ichthyol combined with inunc- 
tion of pyrogallic and chrysophanic acid externally. This treatment is supple- 
mented by hot baths. Several cures have been reported following this plan. 
Crocker reports improvement from subcutaneous injection of the bichloride of 
mercury, and De'Luca from intravenous injections of mercury according to Bacelli's 
method. Raynaud reports marked improvement following the administration 
of sodium cacodylate. Roussel reports an apparent cure following the adminis- 
tration of potassium chlorate, and Manson a case of nerve leprosy apparently 
cured by thyroidin. Tuberculin, antivenene, and the iodides have been used and 
do more harm than good. Danielsen recommends salicylate of soda in ascending 



MILK SICKNESS 295 

doses combined with tonics. He believes that it cures leprosy if administered 
early. Baelz uses salicylic acid locally. He treats about one square foot of skin 
at a time by rubbing the diseased area with pumice stone until blood appears. 
Salicylic acid is then applied in a 20 per cent, ointment with lanolin and vaselin. 
This treatment is combined with the oil of gynocardium internally and hot baths. 

Nerve stretching has been recommended and practiced for the relief of the painful 
complications and trophic disturbances of nerve leprosy. 

Prophylaxis. — The only means of limiting leprosy is by isolation. While absolute 
segregation is the ideal and proper measure, it meets with so much opposition, 
and so many cases are concealed, that in the long run better purpose is served by 
adopting a reasonable compromise similar to that followed in Norway. This 
includes caring for indigent lepers in an asylum and allowing those whose people 
are able to take care of them to do so at their homes under proper restrictions. 
The Russian laws isolate only the tuberculous and mixed cases. Although it is 
true that the nerve cases are much less contagious, this regulation must be regarded 
as a mistake. 

FEBRICULA. 

Definition. — Febricula, sometimes called ephemeral fever, is a condition usually 
met with in children, and is undoubtedly a disturbance of the heat mechanism 
of the body produced by the action not of one but of several agents; that is to say, 
many different causes are responsible for it rather than one specific cause. 

Etiology. — The causes of febricula are very numerous. In some instances it is 
probably the result of some infection which is overcome by the protective process 
of the body before it can develop into a full-fledged disease, such, for example, as 
an aborted influenza, or even one of the specific eruptive fevers, or some infection 
entering by the tonsils. Some years ago physicians believed that infectious diseases 
could be aborted in their early stages by proper measures designed to aid nature. 
This view fell into disrepute, but our knowledge of protective processes and of 
antitoxic bodies makes it probably true. In children an ephemeral fever is often 
due to gastro-intestinal catarrh. Sometimes it is due to gastro-intestinal irritation. 

Symptoms. — The patient after a feeling of wretchedness, rarely lasting more 
than a few hours, is found to be mildly febrile, the temperature being about 102° 
to 103° at the most. There may he flushing of the face and even delirium in young 
neurotic children. The pulse and respirations are quickened. The fever usually, 
but not always, ends by lysis in about three days to a week. 

Diagnosis. — The diagnosis of febricula is made in most instances after the patient 
is well, for until then no one can tell that the symptoms are not the early signs 
of one of the acute infectious fevers. The important point is, not to be content 
with a diagnosis of febricula, which is but another way of saying that the condition 
is uncertain, but to search carefully for the real cause. 

Treatment. — This consists in rest in bed, the use of a little calomel followed by a 
saline, and the employment of a mixture of citrate of potassium and sweet spirit 
of nitre to keep the kidneys active. 

MILK SICKNESS. 

Definition. — Milk sickness is a very rare disease which is usually communicated 
to man by milk, or by the butter or cheese made from the milk of cows ill of a 
malady called, when it affects cattle, "trembles," or "slows." When man is 
infected it is given this name and the additional one of "puking fever." This 
disease has been known to exist in the central western states of the United States, 
for a century. It is met with occasionally in North and South Carolina, Kentucky, 
Tennessee, Ohio, Illinois and in Michigan. It is said that the flesh of affected 



296 DISEASES DUE TO A SPECIFIC INFECTION 

animals, if not cooked, may convey the infection. It is important to know that 
the infection may be transmitted from a seemingly healthy cow some time before 
it develops symptoms of the disease. Jordan and Haines have isolated from 
infected animals an aerobic spore-bearing bacillus (Bacillus lactamorbi). They 
also found it in the milk of infected cows and in the soil of regions where animals 
were so infected. Whether this is the specific factor in the disease is not as yet 
determined. 

The disease is now almost never met with, even in animals, and it never occurs 
east of the Allegheny Mountains and rarely, if ever, west of the Mississippi River. 

Symptoms. — The symptoms in the cow consist in refusal to eat, redness of the 
conjunctiva, staggering gait, and muscular tremors, whence the name " trembles. " 
In man, after a day or two of ill-health, the patient is seized with epigastric distress, 
followed by violent vomiting and obstinate constipation, fever, and thirst. Muscular 
tremors also appear. The breath is peculiarly sweet and offensive and the tongue 
swollen. If the disease is severe the patient may develop typhoid symptoms, and 
even become delirious, comatose, or convulsed but there is no fever. In fatal cases 
death may come as early as the fourth day, or be deferred for two or three weeks. 
The more severe the cerebral symptoms, the more grave the prognosis. The 
mortality is about 25 per cent. 

Treatment. — The treatment is purely symptomatic and consists in the use of 
stimulants or sedatives as they may be needed. 

WEIL'S DISEASE. 

Weil's disease, or Infectious Jaundice, is a very rare infectious malady, first 
described by Weil in 1886. It is characterized by the development of fever and 
acute jaundice, and appears usually in the warm months of the year. The victims 
of its onset are usually young and middle-aged adults, and the symptoms are severe 
headache, lumbar pain, and cramp-like sensations in the legs and arms. The mas- 
seter muscles also suffer from severe pains. Jaundice develops as an early symptom, 
and the liver and spleen are found swollen and tender on deep palpation. The 
stools may be putty-colored, as if from obstruction of the gall-ducts. The fever 
may last two weeks, often rises to 103° to 104°, and is characterized by sharp remis- 
sion, as in sepsis. Albuminuria may occur, and even coma may develop. A general 
hemorrhagic tendency may be present. Recovery usually takes place, but con- 
valescence is slow. 

Weil's disease must be separated from bilious remittent fever, catarrhal jaundice, 
and phosphorus poisoning. This separation is readily accomplished if the char- 
acteristic symptoms just described are compared to those presented in the course 
of these conditions. Remittent fever, which is the malady most closely resembling 
Weil's disease, is differentiated by finding the estivo-autumnal parasite in the blood, 
and phosphorus poisoning by the history of the case and the phosphorescent char- 
acter of the vomit, which can be noted if it is examined in the dark. Treatment 
is entirely symptomatic. 

GLANDULAR FEVER. 

Definition. — Glandular fever is an acute infectious disease characterized by a 
moderate febrile movement and a painful enlargement of the cervical lymphatic 
glands. 

•History. — The first accurate account of this disease was published in 1889 by 
Pfeiffer, although it is probable that the condition described some years before 
by Filatow, of Moscow, under the name of idiopathic inflammation of the cervical 
glands, was in reality glandular fever. 

Cases have been reported from different countries on the Continent, and from 



SPOTTED OR TICK FEVER 297 

England and the United States. J. Park West, of Bellaire, Ohio, has reported 
an epidemic in which ninety-six children were attacked, this being the most extensive 
epidemic on record. 

Etiology. — -The specific micro-organism of this disease, if there be one, has not 
been discovered, but that the disease is infectious in nature is shown by the fact 
of its occurrence, as a rule, in small epidemics involving several members of a 
family. The disease generally occurs before puberty, although Galvagni and A. E. 
Roussel have observed it in adults. 

Symptoms. — The onset is sudden and is characterized by moderately high fever, 
restlessness, headache, pain in the limbs, and soreness and pain in the neck, which is 
increased by turning the head or by swallowing. The temperature ranges from 
101° to 103° and may even go as high as 104°. The bowels are usually constipated, 
although in some of the severe cases observed by West copious discharges of thin, 
green feces mixed with mucus took place shortly before the beginning .of conval- 
escence. Abdominal pain is a common symptom, and pressure over the lower 
part of the abdomen, particularly in the midline between the umbilicus and the 
symphysis pubis, often elicits pronounced tenderness. The swelling of the anterior 
cervical glands, which usually begins on the left side and then extends to the right, 
attains its maximutm beween the second and fourth days. The glands are hard, 
easily distinguishable from one another by palpation, and are very sensitive to 
pressure. Suppuration rarely occurs. Examination of the pharynx reveals either 
a normal condition or a slight hyperemia. The liver is always enlarged, and not 
uncommonly there is considerable swelling of the spleen. Acute nephritis is the 
most frequent and most serious complication. The duration of glandular fever 
is variable. European physicians have described a mild or abortive form in which 
the temperature falls to normal on the second or third day, although the cervical 
glands remain swollen several days longer. The average febrile period, however, 
is from seven to ten days. In West's ninety-six cases the average duration of the 
disease from its onset until the complete disappearance of glandular swelling was 
sixteen days. 

Diagnosis. — The occurrence of a sudden febrile attack accompanied by an early, 
painful enlargement of the anterior cervical lymph glands, without any inflam- 
matory involvement of the pharynx, makes recognition of the disease easy. 

Prognosis. — Prognosis is always favorable. Convalescence is rapid, as a rule, 
although in some instances it is retarded by a considerable degree of depression and 
anemia. 

Treatment. — Experience has demonstrated that there is no drug which will 
influence the duration or course of this disease. The patient should be confined 
to bed and a mild aperient given to overcome constipation. 

MOUNTAIN FEVER. 

So-called mountain fever really does not exist as a separate entity. It has 
been proved to be an aberrant form of typhoid fever infection in a number of 
instances, particularly by the United States Army surgeons or those attached to 
the United States Health and Marine Hospital Service. In some cases the infection 
may be paratyphoid. (See Paratyphoid Fever.) In still other instances the fever 
may be due to an anemia depending upon intestinal parasites such as the Anchylos- 
tomum duodenale. Some cases may be "tick fever." (See below.) 

SPOTTED OR TICK FEVER. 

Definition. — Rocky Mountain Spotted Fever, or Tick Fever, is a febrile malady 
chiefly prevalent in the eastern foot-hills of the Bitter Root Mountains in Montana, 



298 DISEASES DUE TO A SPECIFIC INFECTION 

in an area four to ten miles wide and fifty miles long, but it also occurs in all the 
States in the Rocky Mountain area, such as California, Colorado, Idaho, Nevada, 
Oregon, Utah, Washington and Wyoming. It has also been seen in Alaska. Its 
period of occurrence is from the middle of March until the end of July. Herders 
and ranchmen are chiefly infected. 

This form of so-called spotted fever is not to be confused with cerebrospinal 
meningitis. 

Etiology. — This disease is due to a parasite which is probably conveyed to man 
by the bite of some insect. It has been thought that the insect was always the tick, 
male or female (Dermacentor occidentalis), but this is by no means certain, 
although the tick is undoubtedly one of the transmitting agents. 

In the second phase of its development the organism in the red blood corpuscle 
appears to be solitary and distinctly larger than in the first phase. 

Wilson and Chowning thought they had discovered the cause of this disease 
in the blood but Stiles and Craig claim to have proved the non-existence of these 
so-called parasites, the former asserting his inability to discover any structures 
which lead him to a belief in the presence of a protozoon as a cause of the malady. 
Craig believes that the changes seen by Anderson in the red blood cells are not 
due to a parasite, but dependent upon certain alterations chiefly taking place in 
the hemoglobin, such as are often seen during the course of epidemic influenza, 
typhoid fever, measles, variola, and other acute infections. The cause of this 
disease, is, therefore, at present of uncertain character. Rickets has been able 
to transmit the disease to the guinea-pig and monkey by the use of defibrinated 
blood. The organism of Texas cattle fever is incapable of infecting man. 

Morbid Anatomy. — This is not peculiar to the disease. The postmortem con- 
dition is as follows: early rigor, icterus and petechial lesions in the skin, epicardial 
hemorrhages, a soft, flabby heart muscle, greatly enlarged spleen and liver and 
enlargement of the external and internal lymph nodes. 

Symptoms. — The disease makes its appearance in from three to ten days after 
the bite, with chilly sensations, malaise, nausea, headache, and muscular soreness. 
The bowels are constipated, the conjunctiva congested, the urine scanty and albuminous, 
and slight bronchitis occurs. Epistaxis is a constant symptom. The fever rises 
sharply after the chill, but has morning remissions like typhoid fever. The rapidity 
of the pulse is out of proportion to the fever, often amounting to 110 or 140 per 
minute, and there is a very moderate leukocytosis. Respiration is rapid. 

Its acme is reached by the twelfth day, when it gradually falls by lysis for four 
days more, and so convalescence begins. In fatal cases the fever remains high, 
about 104° or 105°, or even 106°. The pulse is usually very rapid and thready, 
and the blood rapidly becomes anemic. 

The rash usually develops about the third day on the wrists, arms, legs, and 
forehead, and later on the back, chest, and abdomen, and consists at first in a 
macular roseola which becomes papular and passes into profuse petechial or purpuric 
eruption. Desquamation may follow. 

Sometimes in the later stage of the eruption it appears like the marks on a 
turkey's egg. Anderson states that slight gangrene of the fingers, toes, and scrotum 
may occur. Albuminuria is a constant symptom. 

One attack develops partial immunity from a second attack. 

When death ensues it occurs as a rule on the sixth to the tenth day. 

Diagnosis. — The' section of the country in which the disease occurs, the history 
of tick bites, and the finding of the changes in the blood are the factors which make 
the diagnosis positive. From ordinary purpura the disease is separated by the 
lack of sore throat and the absence of arthritis. From typhoid fever the diagnosis 
may be quite difficult. In that disease, however, the rose rash appears first on 
the belly on the ninth to the twelfth day, whereas in tick fever it appears as early 



MILIARY FEVER 299 

as the third day, and on the wrists. The discovery of a positive Widal test in 
the blood will settle the diagnosis. Typhus fever breaks out in groups of persons. 
Tick fever always appears sporadically. 

Prognosis. — The disease varies greatly in severity in different regions. The 
disease in Montana is a very grave one, having a mortality of about 70 per cent., 
whereas in Idaho it is as low as 4 per cent. Sometimes the mortality is as high as 
90 per cent. 

Prophylaxis. — Prophylaxis consists in dipping domesticated animals which have 
the tick in solutions which destroy it, as crude oil or tobacco infusion. Regions 
known to be infected should be burnt off. Persons exposed should wear tick- 
proof clothing. If the tick has attached itself cover it with oil, gently remove it, 
and cauterize the spot with carbolic acid. If Ricketts' protective serum can be 
had it should be employed. 

Treatment. — So far as is known quinine seems to act as a specific in this disease. 
Anderson thinks it should be given in the dose of 15 grains every six hours, hypo- 
dermically, and its use continued into convalescence. The heart must be supported 
by stimulants if it is feeble, and the kidneys flushed by copious draughts of water. 



FOOT-AND-MOUTH DISEASE. 

Definition. — This is an acute infectious disease of herbivorous animals, which 
sometimes attacks omnivora and which spreads in epidemic form over large terri- 
tories, causing great mortality in the animals affected. When the disease attacks 
the cow the animal becomes feverish, suffers from swelling of the mucous mem- 
branes of the mouth, and develops blisters on the edges of the tongue and on the 
lips. These blisters become discolored and rupture, leaving ulcers. At times 
similar lesions appear on the teats. The milk of such animals is discolored and 
seems to be thickened as if by mucus. 

The disease is rarely met with in England and America, but at this time a 
widespread epidemic among cattle is present. It possesses interest to us only 
because it is capable of being conveyed to man. This conveyance occurs in the 
case of children by the use of the milk of the diseased cows, and in adults, as a 
rule, by this means or by cheese or butter. 

The symptoms in man are like those of severe stomatitis, associated with fever . 
Recovery in man usually occurs, but a mortality of about 10 per cent, is recorded. 

The cause of the disease has not been isolated. Even a porcelain filter does not 
arrest the organism, if organism it be, that causes the malady. 

MILIARY FEVER. 

Definition. — Miliary fever, sometimes called "the sweating sickness," is an 
acute epidemic disease characterized by fever, profuse sweating, an eruption, 
and a peculiar sense of constriction in the epigastrium. 

History. — The disease was far more prevalent in the seventeenth century than 
it has been since that time, but it still appears in certain parts of the world. Almost 
every country in Europe, including England, has suffered from its presence, but 
it has not, so far as I have been able to discover, ever appeared in the United 
States. 

Etiology. — The cause of the disease is unknown, but it is an acute infection, 
apparently resembling influenza in the manner of its spread, although it does not, 
as a rule, attack large numbers of people throughout a wide area, as does that 
disease. On the contrary, it is very often limited to the population of a single 
town or district. 



300 DISEASES DUE TO A SPECIFIC INFECTION 

Symptoms. — The symptoms of miliary fever are ushered in, as they are in all 
the infectious diseases, by lassitude, headache, and anorexia. This prodromal stage 
may last a day or two, or be so brief as not to be recognized. The patients go to 
bed well, and wake in the morning to find themselves ill and suffering from a drench- 
ing sweat, which persists throughout the illness. The bowels are usually confined, 
the tongue coated, and the pulse but little altered in character for the first few days 
of the illness. A symptom complained of by the patient is one of oppression, 
as if the air of the room were hot and vitiated. The fever is usually high, rising 
to 104° to 105°, and in fatal cases to 107°. On the third day there appears on the 
skin an outbreak of red miliary papules, which often develop a white tip before they 
disappear, and between these are scattered large numbers of pearly vesicles, like 
sudamina, which seem filled with clear fluid. Prior to the appearance of this 
eruption a peculiar pricking or tingling sensation is felt in the skin. When the 
eruption has faded, desquamation sometimes occurs. The entire progress of the 
malady is usually completed in nine or ten days. 

The following facts are also noteworthy, viz.: The sweating is constant, but is 
characterized by paroxysms, in which it becomes still more profuse. The rash 
appears on the mucous membrane of the palate and cheeks. The sudamina, 
or pearly miliary vesicles, although they give the name to the disease, are not a 
constant symptom in all cases. 

Abortion nearly always occurs if a pregnant woman is attacked. 

Miliary fever causes rapid emaciation. 

It is very prone to be followed by a relapse, but the relapse is rarely fatal. 

Prognosis. — Recovery usually occurs. In severe cases, in which the onset is 
fulminating, death may occur as early as the eighth hour after the attack begins. 
These cases have marked nervous symptoms, consisting of convulsions, delirium, 
and coma. Evidently the patient is overwhelmed by toxemia. The mortality 
rate in various epidemics has varied from 5 to 25 per cent. The outlook in children 
is usually good. 

Treatment. — This consists of cold sponging to control excessive fever, the use 
of copious draughts of water to compensate for the loss of water by the skin, and 
for the purpose of flushing the kidneys, and in the administration of stimulants, 
if they are needed, to support the heart. 

VERRUGA (VERRUGA PERUVIANA). 

Definition. — Verruga (a wart) is a chronic, infectious, and inoculable disease, 
characterized by initial fever, rheumatic pains, anemia, and the development of 
granulomatous lesions (warts) on the skin, mucous membranes, and internal organs. 

Distribution. — Verruga is limited to certain high valleys of Peru, on the Pacific 
slopes of the Andes. At present it is principally observed in the valleys of Huaro- 
chiri, Tanyos, Rimac, and Canta, at elevations varying from 3000 to 8000 feet above 
the sea. It is not observed at lower levels. Cases are also reported from the moun- 
tain districts of Ecuador, Bolivia, and Chile. The disease has existed since remote 
times in Peru, possibly in wider extension than at present. It occurred among the 
soldiers of Pizzaro's expedition, and is first mentioned by Zarate in his History 
of Peru (1543). 

Etiology. — Verruga occurs in small epidemics, but is not contagious. Carrion, 
a medical student,' in 1885, proved its inoculability on himself and died of the 
infection. As a rule, one attack of the disease confers immunity. The specific 
cause of verruga has not been established. Nicolle and Le tulle regard it as due 
to a bacillus which in its morphology and staining reaction is identical with the 
tubercle bacillus. The belief is prevalent among the population that the waters 
of certain springs are the cause of the disease. Moisture, heat, and elevation 



VERRUGA 301 

above the sea seem to be necessary factors. Malaria is apparently closely associated 
with the development of verruga; a particularly pernicious type, locally known as 
"Oroya Fever/' being commonly observed with it. All ages and both sexes are 
equally liable. Natives of the verruga zone seem to suffer less severely than 
strangers coming to the valley. For a time this disease was believed to be a form 
of yaws, or frambesia, and, like it, was interpreted as a form of syphilis. Yaws, 
however, is not observed in the internal organs. Furthermore, verruga is observed 
in the domestic animals, including fowls, an observation contrary to any known 
manifestation of syphilis. 

The incubation period is given as ten days to a year. Fifteen to forty days 
(according to Odriozola) seems a more reasonable figure. In the inoculation 
case of Carrion the incubation was twenty-three days. Strong and Tizzer inocu- 
lated a volunteer and the primary lesions developed at the site of inoculation on 
the sixteenth day and increased slowly until the thirty-fifth. Townsend seems 
to have transferred the disease by means of a biting gnat of the Peruvian Andes. 

Symptoms. — Clinically, two stages present themselves, the stage of invasion 
and the stage of eruption. The stage of invasion begins with prodromal symptoms. 
Lassitude, restlessness, and weariness of the legs, lasting for a few days, are followed 
by an evening fever. 

The fever gradually increases in severity, with marked rigors, and may be remit- 
tent or intermittent. In a few days joint pains develop. The joints invaded 
are the smaller articulations of the hands and feet, the knees, and the spine. The 
pain is severe, is worse at night, and is fugitive, passing rapidly from one joint to 
another. Painful contractions of particular muscle groups occur, most frequently 
in the calf-muscles and sternomastoids. Sometimes large muscle groups are 
affected, so that in extreme cases opisthotonos may develop. As the disease 
progresses, anemia and emaciation occur. The skin becomes pale and icteric; 
the liver and spleen become enlarged. Soft bruits are heard over the precordium. 
The fever persists from three to five weeks, when it gradually declines, and, with 
its disappearance, begins the stage of eruption. The eruption usually develops 
after twenty days, or it may be delayed as long as six or eight weeks. In rare 
instances it is observed at the very beginning of the disease. 

With the breaking out of the eruption, all the general symptoms are remarkably 
ameliorated. Beginning first as small, pinkish papules, the lesions become dark 
blue in color, and finally develop into warty excrescences. They appear on the face, 
particularly around the eyelids and nose, on the limbs, about the joints, and rarely 
on the trunk. The palms, soles, and hairy parts of the body are also attacked. 
In size the lesions vary from a millet-seed to growths as large as an apple. They 
may be few or many hundreds in number. These warty growths are exceedingly 
vascular and bleed freely, thus increasing the anemia of the patient. When they 
develop on the mucous membranes and internal organs, dysphagia becomes a 
very common symptom, and hemorrhages occur from the various organs that are 
the seat of the lesions; hematemesis, hemoptysis, hematuria, metrorrhagia, etc. 
After persisting from four to six months, perhaps passing through various recru- 
descences, the lesions subside by involution and desiccation or desquamation, or 
they may ulcerate, or the larger lesions may suppurate. 

Prognosis. — The prognosis is always grave, particularly so in white people, in 
whom 60 to 70 per cent, of all cases die. In natives the mortality is about 10 
to 15 per cent. The early and complete establishment of the eruption is a very 
favorable sign. In delayed or partial eruptions the prognosis is grave. Excessive 
anemia is also an unfavorable sign. 

Treatment. — Treatment is symptomatic. On account of the very general associa- 
tion of this disease with malaria, quinine should always be freely administered. 
Sudorifics and hot drinks are usually employed with the idea of hastening or com- 



302 DISEASES DUE TO A SPECIFIC INFECTION 

pleting the eruption. Descent to lower altitudes not only diminishes the pain and 
abbreviates the disease, but also lessens the tendency to hemorrhages from the 
lesions. Odriozola recommends the removal of all ulcerated verrugas. 

GANGOSA. 

Gangosa is sometimes called Ogo or Rhinopharyngitis mutilans and is an infectious 
disease characterized by destructive ulceration of the soft palate, uvula, hard 
palate and larynx with slight constitutional disturbance and low mortality. It 
occurs in the West Indies and Polynesia and has been best described by Leys of the 
United States Navy and Mink and McLean of the United States Army. Kinder- 
berger, of the United States Navy believes it to be a tertiary stage, or sequel, of 
yaws, combined with an element of hereditary syphilis. 

SYPHILIS. 

Definition. — Syphilis is a contagious disease, due to a spiral organism, the Trepo- 
nema pallidum. It is sometimes called "Lues/' "Pox," or "Lues Venerea" It 
occurs in two forms, the acquired and the hereditary, and is characterized in the 
different stages of its progress by a greater number of pathological changes in the 
tissues of the body than any other known malady. It has been said that he who 
knows the whole pathology of syphilis and tuberculosis knows all pathology. This 
is, of course, an exaggerated statement, but it emphasizes the fact that the disease 
presents lesions in many different tissues. 

The acquired form is usually divided into three stages, called the primary, 
secondary, and tertiary. 

The primary stage is characterized by the development of a chancre or hard 
sore, also called the "initial lesion;" the secondary stage by the appearance of 
eruptions and lymphatic swellings, and by ulceration of the mucous membranes. 
The third stage consists in the growth of tumor-like masses, called gummata, and 
pathological changes in the bones and in the nervous and vascular systems. 

History. — The history of syphilis is not definite. Certain investigators believe 
that it is one of the most ancient maladies, but it was not clearly recognized as a 
separate affection in Europe until 1494. Those who wish to look into this question 
should consult Syphilis in Ancient and Prehistoric Times, by Buret, translated by 
Ohm ann-Dumesnil. 

Distribution. — Syphilis is found all over the world, and in its frequency and 
virulence is not modified materially by climate or geographical conditions, but it is 
worthy of note that the disease is unknown among savage peoples who have not 
come in contact with civilized communities. 

Etiology. — A distinct advance in the investigation of the disease was made in 
1903, when Metschnikoff and Roux succeeded in producing characteristic lesions 
in the higher apes by inoculating syphilitic virus from human beings; this has since 
been many times repeated. Early in 1905 Schaudinn and Hoffmann described a 
small spiral organism which they found constantly in primary and secondary 
syphilitic lesions and which, because of its indifferent staining qualities, they termed 
the Spirocheta pallida. Later they gave it the name Treponema pallidum. Their 
findings have since been confirmed by hundreds of observers in all parts of the 
world. This organism is found in the lesions of primary and secondary syphilis 
and less frequently in tertiary manifestations. Noguchi and others have found 
it in the brain in cases of paresis and in the cord in cases of tabes, thus still further 
implicating syphilis as the cause of these affections. The findings of some observers 
indicate that with proper technique the treponema can be demonstrated in every 
case of paresis. It is found in the artificially produced lesions in apes, and highly 



SYPHILIS 303 

important is its presence in the blood and tissues of infants dead from hereditary 
syphilis. Levaditi has made extensive studies of these cases and finds the organism 
in greatest numbers in the liver, lung, and suprarenal glands respectively. It 
exhibits a preference for the perivascular tissues rather than for the blood stream 
and is found in and without the vessel walls in enormous numbers. Many are 
intracellular, especially in epithelial cells. The organism is 4/z to 15// long, does not 
exceed 0.5// in thickness, and possesses numerous pronounced spirals. It is actively 
motile and has flagella. 

It is important to remember that the spirochete of syphilis must be carefully 
separated from other spirochetal in no way connected with syphilis. This differen- 
tiation requires the skill of one constantly examining spirochetal and some persons 
go so far as to assert that a diagnosis of syphilis is not justified unless two separate 
observers report that the organism present is the Spirocheta pallida. It is not 
difficult to recognize a spirochete on a dark field but it is difficult to differentiate 
it as the specific spirochete of syphilis. It can be grown in pure culture. In films 
it may be stained by Giemsa's and other methods. 

The rapid method by Giemsa is as follows: (1) Fix a thin film for 30 minutes 
in absolute alcohol; (2) Stain for 1 hour in this solution (prepared at the time of 
using) ; Giemsa's solution (Grubler), 10 drops; 1 per cent, aqueous sodium carbonate, 
10 drops; distilled water, 10 c.c; (3) Wash with distilled water. Dry with filter 
paper and examine, with or without mounting in balsam, by the one-twelfth oil- 
immersion objective. The slower method with Giemsa's stain is preferable: 
(1) Dry films in air, then fix in absolute alcohol for 30 minutes. (2) Stain for 20 
hours in Giemsa's solution, 35 drops (1.2 c.c); distilled water, 20 c.c. (3) Same 
as in the rapid method. By these methods the treponema stains a reddish-violet. 

Burri's method of making the containing material opaque is fairly satisfactory. 
A drop of fluid from a chancre or obtained from a lymph node or other lesion is 
mixed with an equal amount of India ink and quickly smeared in a thin film on 
a slide; when dry examine with an oil-immersion objective. The treponema 
appears as a white spiral in a black field. 

In sections of tissue, methods of using the silver salts, as Levaditi's, give the 
best results. These require a week or ten days. 

In the vast majority of cases syphilis is acquired by sexual intercourse, although 
a large number of cases of acquired syphilis, due to non-sexual contact with syphilitic 
persons or their garments when infected by discharges, have been recorded. (See 
Bulkley on Syphilis Insontium.) Obstetricians, midwives, and nurses have often 
contracted the disease through a break in the skin of the finger. Wet-nurses 
have been infected though the nipples by syphilitic infants, and drinking utensils, 
knives, forks, spoons, pipes, and dental instruments have conveyed the poison to 
the mouths of innocent persons. The disease can be transmitted by kissing and 
by the drinking cup. Primary lesions of syphilis have also been produced in the 
mouth by perverted sexual practices. 

The virus of the disease is active in the transmission of the malady throughout 
the primary and secondary stages, and during this time all secretions from the 
lesions of these stages are capable of producing the disease in another person, 
provided that they be brought in contact with a solution of continuity in the skin 
or mucous membrane. Infection does not take place through healthy skin or 
mucous membrane, but the break in the surface may be so slight as to be overlooked. 
The blood of the patient during the secondary stage is capable of spreading the 
disease by inoculation, but notwithstanding this fact it is noteworthy that the 
secretions of the various glands do not contain the poison unless they are contami- 
nated by discharges from local syphilitic lesions. 

The acquired disease is not conveyed by the discharges from syphilitic sores, or 
by the blood of a syphilitic, if five years have elapsed since the date of primary 



304 DISEASES DUE TO A SPECIFIC INFECTION 

infection; indeed, in most cases the virus ceases to be capable of inoculating another 
person at the end of two years after infection. This rule holds true, even although 
the patient may be suffering from syphilitic sores or other active lesions at the time 
of contact. On the other hand, the spermatozoids may indirectly transfer the 
poison from the man to woman by the foetus. 

A person who is suffering, or has suffered, from acquired syphilis is protected 
against a second infection in the vast majority of instances, although a few cases 
have been recorded which seem to throw doubt upon the statement of some syphilog- 
raphers that the protection is absolute. This immunity is developed at once 
after primary infection, as early as the development of the primary lesion or chancre, 
and in some cases even earlier than this. In the case of a person who has inherited 
syphilis from one or both parents the protection against acquired infection is 
absolute, even if no signs of the hereditary disease be present. 

Hereditary syphilis may come to a child through one or both parents. When 
the father only is syphilitic, the term "sperm inheritance" is employed, and when 
the mother only is syphilitic it is called "germ inheritance." A syphilitic male 
may transmit syphilis to his offspring without manifesting at the time of intercourse 
any symptoms of syphilis and without producing in the mother any signs of the 
disease. It is also possible for him to have a healthy child; that is, he may fail 
to transmit the infection. This depends largely upon the stage of the malady, 
its virulence and activity, and the value of any antisyphilitic treatment that may 
have been instituted for the father's benefit before conception, and for the benefit 
of the mother and child after conception. 

A woman suffering from syphilis may or may not bear a syphilitic child, and if 
active antisyphilitic treatment during pregnancy is maintained, the child is likely 
to escape. It is also possible for a mother who contracts syphilis during her preg- 
nancy to give birth to a non-syphilitic child, but it is also possible for the child to 
contract primary syphilis from a mucous patch as it passes through the birth canal. 
It is interesting to note, however, that while the syphilitic mother is not always 
able to confer immunity to primary infection upon her child, so that it cannot be 
infected by the disease before or after birth, it is possible for the syphilitic foetus 
in utero to confer immunity upon its mother, or, to express it differently, given a 
child in utero by a syphilitic father, that child may be syphilitic at birth, but its 
mother may not have been infected during pregnancy, and is protected against 
syphilitic infection subsequently. This is known as Colles' law. That immunity 
to syphilis can be so acquired is proved by the fact that if a syphilitic baby nurses 
at its mother's breast she will not contract syphilis, even if its mouth be filled with 
mucous patches, but if that infant is nursed by an innocent wet-nurse it can produce 
syphilis in that nurse. 

From what has been said so far it is evident that a syphilitic father or syphilitic 
mother may be the parent of a syphilitic or non-syphilitic child. If both parents 
are syphilitic, the probability of the child being infected is twice as great as if 
one parent is affected. 

Prevention. — The prevention of syphilis is one of the great social questions of 
the age that has not been solved. In many cities prostitution has been licensed 
in order that, by governmental and medical control, prostitutes suffering from 
syphilis might be treated and prevented from plying their vocation while capable 
of transmitting the disease. This plan when instituted has not checked the dissemi- 
nation of syphilis, since it continues to spread through illicit intercourse carried 
out with unlicensed women who will not be classed as registered prostitutes. 

Syphilis may also be prevented by forbidding intercourse on the part of persons 
suffering from the disease, and by instructing the non-syphilitic to avoid intercourse 
while any break exists in the mucous membrane or skin of the external genitals. 
Careful regard to cleanliness after intercourse is of some protective value. 



SYPHILIS 305 

A practically sure prophylaxis against infection is the use of 35 per cent, calomel 
ointment. The sooner this is used after intercourse the greater the preventive 
power. It fails if used twenty hours after exposure but rarely if used within six 
hours. The ointment should be well rubbed into the penis behind the foreskin 
with special attention to any abrasions, and left on the part for several hours. 
Several countries now provide soldiers and sailors with prophylactic packages of 
this ointment and insist that it is used. 

Frequency. — It is almost impossible to determine the prevalence of syphilis, 
since the living keep its presence secret and the physician rarely returns a death 
as due to it, but to some indirect result of it. 

In 1874 Dr. F. R. Sturgis estimated that, out of a population of 942,292 in New 
York City, 50,450 were suffering from syphilis. 

In an appendix to Sanger's History of Prostitution, 1892, it was estimated that 
100,000 persons out of a population of 1,800,000 had syphilis. 

Kober believes that there are 2,000,000 syphilitics in the United States. And 
Edsall found that in 1696 cases admitted to the Massachusetts General Hospital 
between 8 and 10 per cent, gave a positive Wassermann reaction. As the blood 
is often negative in old cases the proportion of syphilis in these patients was prob- 
ably higher than the percentage given. 

At the present time the population of Greater New York is about 3,560,000, 
and assuming that the rate of increase of the disease has kept pace with the increase 
in population there would be nearly 200,000 syphilitics in that city. These esti- 
mates are not made, however, on a statistical basis. 

A committee appointed by the Medical Society of the County of New York 
for the study of measures for preventing venereal diseases, addressed a circular 
letter to all the physicians in Greater New York asking them to report the number 
of cases of gonorrhea and syphilis which they had treated from May 1, 1900, to 
May 1, 1901. Of the 4750 physicians to whom the letter was sent, 678 forwarded 
statistics of their cases. The total number of cases of syphilis reported was 7200. 
Assuming that as many cases occurred in the practice of the physicians who sent 
no reports as in the practice of those who forwarded statistics, calculations would 
show that 50,400 cases of syphilis were under treatment in private practice during 
the period of time which the investigation covered. As many patients go from one 
physician to another, it is not improbable that some of the reported cases may 
have figured twice in the statistics; but the committee believed that the number 
which did so was more than offset by the large class of patients who take treatment 
from advertising quacks. 

Of forty-five dispensaries and charitable institutions visited by the committee 
nine refused to give any information. An inspection of the records of the 
remaining thirty-six showed that 7607 cases of syphilis had been treated during 
the year. 

Burre shows by statistics that the morbidity of syphilis among the inmates 
of the licensed houses of prostitution in Paris fell from 30 per cent, in 1873 
to 0.25 in 1902. On January 1, 1873, 1126 public women were registered, and 
during the year 338 cases of syphilis were recorded from among the number. 
On January 1, 1902, 429 public women were registered, and only 1 case of 
syphilis was observed among them during the year. Burre attributes this 
decrease in syphilis to the more general dissemination of knowledge concerning 
the infectious nature of the disease and to the adoption of hygienic measures for 
its prevention, which at present are largely practised by all the licensed prostitutes. 
He also lays some stress upon the matter of obligatory elementary education, 
believing that it may have served to make the prostitutes more intelligent as a 
class than they were thirty years ago. His statistics illustrate very well the fallacy 
of collecting cases and drawing conclusions from them without due care. Surely 
20 



306 DISEASES DUE TO A SPECIFIC INFECTION 

no one supposes that the number of prostitutes in Paris has diminished in the 
proportion of nearly 75 per cent. 

R. W. Taylor stated that most of the cases of syphilis which he saw in hospitals 
were from tenement houses and had not contracted the disease from regular pros- 
titutes, which illustrates the difficulty of preventing its spread by licensing women 
of the town. 

Pathology and Morbid Anatomy. — As already stated, syphilis may in its various 
stages of development affect almost every tissue of the body. Some of these 
manifestations are not distinguishable from lesions resulting from other causes, 
and hence their syphilitic character can only be established, if at all, by the exclusion 
of other factors and the associated presence of recognizable luetic phenomena. 

The primary lesion of syphilis, called the chancre, develops at the point of infec- 
tion, and is usually characterized by thrombotic or proliferative changes in the 
vessels with round-cell infiltration of the surrounding connective tissue, and by the 
formation of connective-tissue cells which are particularly numerous about the 
bloodvessels. As a result of the vascular changes and associated lessened nutrition 
and possibly the action of the syphilitic poison, with or without added infection, 
superficial and usually central necrosis occurs and an ulcer results. 

Soon after the formation of the chancre, just described, commonly in about six 
weeks, the secondary stage develops. The lymph nodes all over the body, but 
notably those adjacent to the initial lesion, become enlarged and inflamed, and 
inflammatory and degenerative or necrotic processes develop in the skin, in the 
mucous membranes, and in the bones and viscera. 

Following this so-called secondary period of the disease there develops the 
tertiary stage, in which the periosteum and the internal viscera suffer from peculiar 
growths of newly formed tissue. A most constant lesion is characterized by the 
formation of a new tissue consisting of spheroidal and polyhedral cells and scattered 
giant cells, poorly supplied with bloodvessels, and having a marked tendency to 
necrosis, especially coagulation necrosis, and hyaline degeneration in their earlier 
stages, and later caseation closely resembling that seen in tuberculosis. The 
growth of this new tissue is usually in circumscribed nodes, and it is in these masses 
that the necrotic and degenerative processes just named occur most markedly 
or are most evident. These " qummata" may grow to considerable size. They 
appear as dirty-white, firm masses which, on section, often are found to be caseous 
at the centre, where the new tissue has undergone necrotic change. 

Syphilis produces grave changes in the bloodvessels, and no other pathological 
process impairs the general vascular system so markedly, except it be renal disease. 
A syphilitic arteritis develops with diffuse overgrowth of fibrous tissue in the 
adventitia, and even gummata may form along the vessels. The arteritis also 
involves the middle coat and even the endothelial lining of the vessels, and so 
narrows or occludes them. This of course diminishes the blood supply to the 
various organs and increases the labor of the heart. The heart muscle also suffers 
from a myocarditis characterized by overgrowth of its connective tissues, and the 
pericardium and endocardium may be thickened for a like reason, but gumma of 
the heart is very rarely produced. The changes in the heart are, therefore, almost 
entirely due to the effects of the disease on the vessels which supply it, and upon 
the changes which occur in the aorta and the peripheral vessels. In other words, 
while arteritis may result in myomalacia cordis the conspicuous change is a fibrosis 
of the heart muscle. The aortitis and general arteritis result in increased cardiac 
and vascular stress. Brooks, from a study of 50 cases, found the myocardium 
diseased in 44 and the aorta in a like number. He emphasizes the point that 
these changes may begin early in the disease instead of being a late manifestation. 

In the secondary stage of syphilis an acute syphilitic nephritis has been described. 
Later on a destructive overgrowth of connective tissue develops in association 



SYPHILIS 



307 



with the vascular changes just described, and gummatous growths occur in the 
kidneys. 

The liver is very commonly affected by the formation of gummata or by con- 
nective-tissue proliferation, which produce grave interference with its function. 
These changes take place in both the acquired and in the hereditary form of the 
disease. This overgrowth of connective tissue occurs in two types. It is developed 
between the lobules, constituting an interlobular or perilobular cirrhosis, and between 
the cellular columns forming an intralobular cirrhosis. In some instances these 
connective-tissue formations consist in large, firm bands which run in various 
directions through the liver and, in contracting, draw in the capsule of Glisson and 

Fig 60 




Nodular syphilis of the liver. (Kast and Rumpler.) 



so cause great distortion of its surface. (See Fig. 60.) Not rarely gummata are 
enclosed by these bands. In the earlier stages and milder forms of syphilitic 
hepatic cirrhosis the changes cannot be considered pathognomonic, but in the 
exaggerated form, just described, typical syphilitic changes occur. As secondary 
lesions of the liver, amyloid disease and atrophy of its parenchyma are occasionally 
observed. (See Cirrhosis of the Liver.) 

The lesions in the lungs consist in gummata which are often surrounded by 
exudative material, as in pneumonia. These gummata may contain a cheesy 
area as in tuberculosis and, by pressure, may cause secondary alterations. A 
second change is overgrowth of fibrous tissue around the bronchi which, associated 
with catarrhal processes involving their mucosa, distorts these tubes, causing 



308 DISEASES DUE TO A SPECIFIC INFECTION 

narrowing at some points and at others bronchiectases. Infarctions may occur 
because of the obliterative changes in the bloodvessels. 

A true syphilitic phthisis presenting symptoms resembling tuberculous pulmonary 
phthisis, but in which tubercle bacilli are not present, may occur, but it is exceed- 
ingly rare. It is true that cases have been reported in which gummata in the lungs 
have, like tubercles, undergone softening of a caseous type, and Wilks has recorded 
an instance in which this process had gone on to the development of a cavity. 
Virchow and Fowler have recorded similar cases. These cases, however, although 
they may produce physical signs of cavity do not present the characteristics of 
pulmonary phthisis in the sense of pulmonary tuberculosis, nor do those instances 
in which bronchiectatic cavities develop as the result of syphilitic fibroid changes 
in the lungs do so, even though the physical signs may be similar. The main 
pathological difference in the two states is this — viz., that in tuberculosis there is 
not only a destruction of the tubercle by softening, but the intervening tissue is 
infiltrated with exudate which soon becomes tuberculous and proceeds to necrosis. 
This does not occur in syphilis. In rare cases syphilis of the lung and tuberculosis 
may be coincident. 

In the hereditary syphilis of infancy a lobar or bronchopneumonia in which 
the pulmonary tissues show red, gray, and white exudates, according to the stage 
of the local disease, is sometimes met. 

The lymph nodes in cases of syphilis are always affected by an overgrowth of 
connective tissue after the primary infection. In the third stage gummatous 
masses may develop in them. 

Next to changes produced in the organs of circulation syphilis manifests its 
gravest changes in the central nervous system. It has been shown that in late 
syphilis of the brain as in paresis the perivascular spaces, and the cortical and 
subcortical tissues are loaded with spirochete and this has completely changed 
our views as to the so-called late nervous lesions hitherto thought to be due to the 
fact that infection had once been present. The meninges may be the seat of 
gummata with or without the presence of chronic, indurative overgrowth of con- 
nective tissue. In the brain it causes gummata manifesting the symptoms of 
brain tumor; it also produces a syphilitic inflammation which is associated with 
the formation of a gelatinous tissue, this gives rise to serious degenerative changes 
in the arteries which interfere with the nutrition, and later by rupturing bring 
about cerebral hemorrhage. It also causes gumma of the cord and its membranes, 
which usually have their origin in the tissues of a bloodvessel or in the pia arachnoid. 
Rarely it affects the peripheral nerves, through pressure, as they emerge from the 
cerebrospinal sheaths. In the spinal cord it causes degenerative changes of cells 
and fibres and overgrowth of the sustentacular tissue. 

Paresis, meningo-encephalitis, locomotor ataxia, etc., will be discussed with dis- 
eases of the nervous system, although our present knowledge indicates that they 
might well be considered in this article. 

Symptoms. — The symptoms of acquired syphilis are best described as they 
appear in the three stages of the disease. 

First Stage. — In from twelve to twenty-one days after exposure and infection 
the patient develops at the site of original contact with the virus a small papule 
or pimple which has an area of indurated tissue about its base, the so-called primary 
lesion or hard chancre. Further examination of the patient will reveal the fact 
that the inguinal glands are slightly enlarged. 

This period of primary syphilis lasts from three to ten days or two weeks, and 
is followed by the development of the secondary stage. 

Second Stage. — In the secondary stage we find fever as an early symptom, 
which varies in its degree very greatly in different patients. In some instances 
it is so mild as to be overlooked; in others it may rise to a point as high as 104° 



SYPHILIS 309 

or even 105°. The more common febrile movement is one in which the temperature 
for some days stays in the neighborhood of 101°. When the fever intermits, 
being fairly high at one period and then breaking sharply, it may mislead the 
physician into a diagnosis of malarial infection or acute sepsis. I have seen several 
cases in which a diagnosis of typhoid fever, malarial fever, or tuberculosis was 
made when in reality the disease was early secondary syphilis. 

The skin eruptions of the secondary stage consist chiefly of the roseola, the 
development of which often marks the onset of the secondary stage. This roseolous 
rash may occur in limited areas or be widely distributed over the body and even 
involve the face. On one occasion a woman with a well-developed syphilitic roseola 
presented so scarlet a visage that, although she was veiled, she caused the other 
patients to leave my waiting-room in alarm, they thinking that she had scarlet 
fever. As a rule, however, the rash is not so marked on the face. 

In other cases, in place of roseola there develops a macular syphilide, character- 
ized by the appearance of reddish-brown or copper-like macules scattered over 
the trunk. 

As the secondary stage advances the eruption may be papular and finally pustular, 
and at this time it may closely resemble that of true variola. In still other cases 
a squamous or scaly eruption appears which differs from psoriasis in that it is not 
chiefly on the extensor surfaces as is ordinary psoriasis, and in addition it is fre- 
quently copper-colored. 

At the point of junction between the mucous membrane and the skin, as at 
the anus or at the angles of the mouth, " mucous patches," or ulcers, develop, and 
upon the skin in the neighborhood of these lesions warty growths of a flat character, 
the so-called syphilitic condylomata, appear. Mucous patches on the buccal 
mucous membrane and tongue also appear. 

There is nearly always some falling of the hair in secondary syphilis. Sometimes 
this falling is well distributed; in other cases it is in patches — syphilitic alopecia. 

A serious, oftentimes painful complication at this stage is syphilitic iritis. If 
the treatment is not active sight may be lost. 

A rapid development of anemia, which often becomes quite marked, not as to 
hemoglobin, but as to the number of the red cells present, is often observed. 

The secondary stage lasts from twelve to eighteen months, and is usually followed 
by a period during which the symptoms are modified or entirely disappear, the 
virulence of the disease seeming to have spent itself, but even if no syphilitic symp- 
toms are present a child begotten at this time will usually suffer from hereditary 
syphilis. 

Third Stage. — In the great majority of untreated cases the malady proceeds 
to the so-called tertiary stage. This is characterized by the presence of skin lesions, 
which are more severe than those of the secondary period, such as tuberculous and 
ulcerous formations of a subacute or chronic character. There is an overgrowth 
of connective tissue in different parts of the body, as in the secondary period, 
and multiple gummata are often present in numbers, developing in the skin, in 
the subcutaneous tissues, in the muscles, and in the internal viscera, particularly 
in the liver. When in the skin they often slough and produce ulcers, and in the 
internal organs they become filled with fibrous tissue and undergo contraction 
in the manner already described. 

Last, but by no means least, of the changes due to syphilis in its tertiary stage, 
we meet with lesions of the nervous system. These changes, as a rule, are late 
manifestations of the disease; occurring some years after the infection. Rarely 
they may appear as early as within the first six months, usually within the first 
ten years, sometimes as late as twenty years. (See Paresis and Ataxia.) 

Syphilis in certain cases may seem to possess great virulence and become destruc- 
tive in its course, almost from the onset. The chancre may rapidly ulcerate and 



310 DISEASES DUE TO A SPECIFIC INFECTION 

spread, the fever may be marked, and the anemia severe. The skin lesions become 
pustular, even in the secondary stage, and form deep ulcers, which, in turn, cause 
scars as they heal. Destructive changes rapidly develop in the bones and viscera. 
The patient may die within a few months of the infection. In these cases there is 
usually a lowered vital resistance which permits the disease to progress unopposed. 

In other cases the symptoms are remarkably mild. The chancre is so small 
that it is overlooked, the patient truthfully stating years afterward that he has 
never had a primary lesion. The rose rash may not occur, or be so faint and 
fleeting as not to attract notice, and the primary anemia may be entirely absent. 
Syphilis may end in complete recovery at the close of the secondary stage, but such 
a fortunate result is rare, unless active treatment has been instituted. 

It is a fact worthy of note that nervous lesions seem to occur more frequently 
in cases which have presented mild secondary symptoms than in those who have 
had severe secondary and tertiary lesions. 

Three intracranial conditions due to syphilis may produce violent headache, 
namely, arteritis, meningitis, and gumma. When arteritis is the cause, giddiness, 
weakness of groups of muscles, difficulty of speech, and, it may be, signs of general 
paresis develop. On the other hand, when the ocular muscles are affected and an 
optic neuritis is present, meningitis is the more likely condition, particularly if 
there is spasmodic contraction of certain cranial muscles and fever. Neuroretinitis 
is present in meningitis and in gumma, but is not commonly present in arteritis. 
(See Meningitis.) 

The symptoms of syphilis of the brain depend very largely upon the site of the 
lesion, for, as already stated in the section on the Morbid Anatomy of Syphilis, 
these lesions may be at the base, on the convexity, or in the membranes. By far 
the most common symptom of cerebral syphilis is headache, which is usually diffuse 
and constant, but if the meninges are involved, or a gumma is causing pressure, 
it may be exceedingly severe and characterized by what are known as "crashing 
pains." Patients with cerebral syphilis are often unduly somnolent. (See Diagnosis.) 

When gummatous growths form at the base of the brain the symptoms are 
those due to interference with the cranial nerves, such as squint, optic atrophy, 
and facial paralysis. When the convexity of the brain is affected the symptoms 
are those of localized or Jacksonian epilepsy, or of petit mat. Sometimes the 
epileptic seizure is general. Fournier laid down as a law that epilepsy beginning 
in adult years is, nine times out of ten, syphilitic. A third form of cerebral syphilis 
is that in which there are psychical disorders, such as melancholia or delusions of 
grandeur. (See Paresis.) 

Spinal syphilis manifests itself as the result of the presence of gummata or of 
connective-tissue changes in the cord. When the lesion is a gumma the symptoms 
are those of pressure on the cord. When connective-tissue changes occur the signs 
are those of spastic paralysis of the lower limbs, with markedly exaggerated reflexes, 
low muscle tension, and vesical disturbances. Often the disorder of the functions 
of the bladder is the first sign of spinal difficulty. The bladder may lose its expulsive 
power or incontinence may occur. As a late syphilitic affection locomotor ataxia 
is the most common nervous disease. (See Locomotor Ataxia.) 

Diagnosis. — The diagnosis of acquired syphilis is readily made if the patient 
presents the well-developed symptoms. In many cases, however, these are not 
manifested. The indurated base of the chancre is an invaluable sign if the chancre 
has not been cauterized, and the presence of enlargement of the lymph nodes in 
the groin and in the great chain of nodes in the neck is also a useful d' agnostic 
point. The presence of secondary syphilitic roseola, and fever with sore throat, 
and mucous patches, and above all the presence of the specific spirochete in these 
lesions are diagnostic. In some cases, however, the secondary symptoms never 
develop or are so mild as to be overlooked, yet well-marked tertiary signs develop 



SYPHILIS 311 

later. The employment of mercury or iodide of potassium, followed by the dis- 
appearance of the symptoms, is a therapeutic test, but such a result is not a path- 
ognomonic sign of syphilis. 

There are two tests for syphilitic infection which can be definitely relied upon 
if positive, namely, the Wassermann serum complement reaction test or Noguchi's 
modification of it, and the so-called luetin test for which we are also indebted to 
Noguchi. The Wassermann test should be made by an expert and if negative 
should be repeated at least once in a suspected case before it is finally accepted. 
This test is positive only after the infection has existed long enough to have resulted 
in general systemic infection. Within twenty-one days after infection it is present 
in 75 per cent, of cases and when secondary symptoms are well developed in about 
100 per cent. As time goes by it is found less frequently, so that in cases of several 
years' standing and which present no symptoms it may be positive in only 30 per 
cent. It is noteworthy that in late nervous syphilis the Wassermann test of the 
blood may be negative but that of the cerebrospinal fluid is positive. Such cerebro- 
spinal fluid contains a very great excess of small lymphocytes. Occasionally cases 
of suspected or suppressed syphilis which give a negative Wassermann reaction 
will on active treatment develop a positive reaction. Finally, all persons who 
have skin lesions and who give a positive Wassermann test are not necessarily 
suffering from the skin lesions of syphilis, for it may be that they have two diseases. 
A diagnosis of syphilis should not rest solely on a positive Wassermann test because 
an error in technique may give a positive reaction when it should be negative. 
A number of distressing incidents have followed such an error causing suicide, 
divorce or vows of life-long celibacy. Furthermore, a positive Wassermann reac- 
tion occurs in scarlet fever, w^hich in turn is sometimes taken with its roseolous 
rash and sore throat for syphilis, if it occurs in an adult who has been exposed. 
It also is positive in some cases of tuberculosis and of carcinoma and in yaws, 
trypanosomiasis and leprosy. In scarlet fever it disappears with convalescence, 
in syphilis it persists Finally it would appear that some healthy persons give a 
positive Wassermann reaction. Thus in 5946 non-syphilitics the test was positive 
in 1.1 per cent. 

The luetin test or reaction of Noguchi is positive in about 50 per cent, of late 
cases. It has the great advantage that it is present in late cases of syphilis when 
the Wassermann is negative, as in tertiary syphilis and in cases in which active 
treatment has prevented a positive Wassermann reaction. It fails to appear if 
syphilis is really cured. The test consists of injecting between the layers of the 
skin a drop of the suspension of the killed spirochetal in the medium in which they 
are grown, preserved by adding trikresol. If syphilis is present a small inflammatory 
nodule develops about the fifth day, but may be as early as the second or as late 
as the thirtieth day, at the point of injection. This nodule may slough but it does 
not occur in non-syphilitic cases, and begins to fade away after the second day. 
It is not accompanied by systemic symptoms. 

Prognosis. — The outlook in acquired syphilis as to severity of attack and ultimate 
recovery depends largely upon the state of the general health, and the promptness 
with which specific treatment is instituted. Much depends also upon the faithful- 
ness of the patient in carrying out the treatment for a sufficient length of time. 
In the great majority of cases active and skilful treatment permits a favorable 
prognosis as to absence of symptoms, and even as to the safety of future marriage. 
In the malignant cases, or those in which tertiary lesions have already formed, we 
can only hope to modify the progress of the malady, or perhaps arrest it without 
being able to remove all signs of its invasion. That a syphilitic may be told with 
perfect assurance that he is "curable or cured," in the sense that this may be 
said after an attack of pneumonia or typhoid fever, is questionable. He may 
have no late symptoms, and after a time, treated or not treated, he will be no 



312 DISEASES DUE TO A SPECIFIC INFECTION 

longer a disseminator of the malady, but it is yet to be proved that by any means 
now known is he completely and permanently rendered as free and wholesome as 
before he was infected. Gummatous growths may, however, be removed by treat- 
ment, even in the tertiary stage. 

Hereditary Syphilis. — The symptoms of hereditary syphilis may be present at 
birth, the skin being already the site of syphilitic eruptions, of which pemphigus 
neonatorum — that is, a bleb-like eruption about the wrists and ankles — is typical. 
The liver and spleen are usually enlarged, and the child may be wasted and poorly 
nourished. In other instances the child manifests no lesions at birth, but within 
its first six months of life develops syphilitic rhinitis, or, as it is called, "snuffles." 
This is accompanied or followed by cutaneous lesions, of which the most frequent 
is mucous patches about the anus and in the mouth. It may waste away from 
so-called syphilitic marasmus, developing a syphilitic rosary at its costocartilaginous 
junctures, as in rickets. The ends of the long bones are the sites of syphilitic 
epiphysitis. If the child lives to reach the period of second dentition its teeth may 
be notched — the so-called "Hutchinson" or "peg" teeth. This malformation 
does not appear in the milk teeth. In many cases of hereditary syphilis, in infancy 
the child looks like an old man, whereas in hereditary syphilis of early adult life 
the patient often looks very immature — "syphilitic infantilism." Children having 
hereditary syphilis are prone to suffer from syphilitic keratitis, from deafness, and 
from bone lesions which develop after several years of life. The periosteum is 
thickened and even nodular in its appearance, particularly on the tibia. 

Another lesion is deformity of the fingers, in which they become thickened at 
the base and taper rapidly to the tip, being somewhat pear-shaped or top-shaped — 
the so-called syphilitic dactylitis. 

Children suffering from hereditary syphilis give a positive Wassermann reaction 
nearly always. 

Treatment. — The treatment of syphilis is divisible into two parts, i. e., that by 
salvarsan or neosalvarsan and the older plan by mercury and iodides. But before 
any treatment is instituted it is of course essential that an absolutely correct 
diagnosis be made. If a smear from a suspected chancre can be submitted to 
one or two competent microscopists and they report the Spirocheta pallida present, 
there can be no doubt that salvarsan or neosalvarsan should be given at once to 
destroy the parasite in the chancre and anywhere else it may be in the body. 
When such a laboratory test is impossible some practitioners of experience have 
insisted that it is unwise to administer mercury to a patient suffering from a sus- 
picious primary lesion until, by the development of secondary symptoms, the 
diagnosis of syphilis is absolutely confirmed; since if we do not wait for these 
symptoms, the possibility exists that a patient who has not really acquired 
syphilis may be condemned to the belief that he has been inoculated, yet the 
malady is only suppressed, and this may cause him great mental suffering during 
the rest of his life. 

Another group of practitioners have strongly urged a view directly opposed 
to this, claiming that we have no right to permit the disease to become thoroughly 
engrafted upon the patient's system without instituting measures for its relief, 
or at least for the diminution of the severity of the infection. The leaders in 
this line of thought have advocated the excision of the chancre in the belief that 
by so doing the primary focus of infection was removed. It must be remembered, 
however, that the primary lesion does not develop until two or three weeks after 
the actual inoculation, and, therefore, although it appears at the site of inoculation, 
there is good reason to believe that it is not a source from which still further infection 
takes place, but rather a localized manifestation that inoculation has been accom- 
plished. Nearly always there can be found in the adjacent lymphatics evidence 
that they are affected as early as the chancre appears. The question as to whether 



SYPHILIS 313 

the chancre should be excised must, therefore, be left to the judgment of the individ- 
ual physician, with the statement that it is possible, but not probable, for the 
excision to have some influence for good. 

It is with those who believe in the immediate administration of antisyphilitic 
treatment as soon as the chancre is developed that I agree. It does not seem 
to me rational to permit the disease to run on uncontrolled until he who runs may 
read that infection has taken place. While it is true that the chancre at times 
is not sufficiently characteristic to enable us to make a positive diagnosis that it 
is true syphilis, we are justified in such a case in considering that it is such and 
proceeding at once to the relief of the patient. 

The production of salvarsan and neosalvarsan has provided us with a specific 
treatment of syphilis, but not a certain cure by the use of one large dose, as Ehrlich 
at first claimed, because very large doses are not always safe and because the 
spirochete is often in tissues which are not permeable to the drug when it is placed 
in the blood, for example, in the brain and spinal cord, and from these and other 
sequestered places the organisms sally out and reinfect the disinfected tissues 
whereby relapses ensue. It is also to be recalled that these new agents do not 
directly kill the spirochete but produce some change in the body whereby they 
are killed. Spirochete placed in a test-tube with salvarsan are not destroyed. 

Salvarsan should be given as soon after a chancre is discovered as possible, in the 
hope that it will abort the disease. Given in the early stages salvarsan acts like 
magic upon the parasites in open lesions. A mucous patch teeming with the 
specific organism one day is sterile the next, which is not only valuable to the patient, 
but prevents the spread of the disease to others. It may be said that early second- 
ary manifestations indicate this drug above all others. When gummata are 
present it is probably no more useful than mercury, except in gummata of the skin. 
Upon cutaneous eruptions and enlarged glands it is not materially more active 
than mercury, unless the skin lesions are breaking down, when it is often surprisingly 
effective. 

Where late syphilis of the nervous system is present salvarsan has limited power, 
first, because destroyed tissue cannot be replaced and, second, because unless the 
specific substance, induced by the intravenous injection of salvarsan, in the blood 
serum is injected into the subarachnoid space the remedy gets to the micro- 
organisms in too small an amount to be of service. 

In well developed syphilis the best results seem to be obtained by giving salvarsan, 
or neosalvarsan, in ascending doses every week for eight weeks and then giving a 
course of mercury, returning later to the newer drug if any acute symptoms develop. 

Concerning the effect of salvarsan, or neosalvarsan, on the Wassermann reaction, 
it would seem that except when used very early it has no more effect in producing 
a negative reaction than properly used mercurials. Occasionally in a suspicious 
case giving a negative test a dose of salvarsan provokes a positive reaction. 

Salvarsan is much more efficacious when used intravenously than when given 
intramuscularly, but it never causes death when injected into a muscle and has 
caused death when given into a vein, although very rarely in thousands of 
cases. 

When given intravenously it should be injected as is normal salt solution, by 
means of a sharp needle pushed into a vein in the arm, immediately after it is 
prepared for use as follows: 

Place in a glass cylinder of 500 c.c. capacity, provided with a stopper and 50 
glass beads, 30 c.c. of normal salt solution and add 0.6 of salvarsan. Cork and 
shake thoroughly until dissolved and then add 1.14 c.c. of 15 per cent, solution 
sodium hydroxide. Dissolve the precipitate by shaking. Add enough salt solution 
to make 300 c.c. and if need be to keep in solution add a few drops more of the 
sodium hydroxide solution. 



314 DISEASES DUE TO A SPECIFIC INFECTION 

The preparation of the drug in oil can be obtained in hermetically sealed glass 
ampoules ready for intramuscular use. 

Before salvarsan is given intravenously the patient should miss a meal and be 
well purged. He should be in the recumbent posture when treated and remain 
so for some hours. 

Neosalvarsan is less efficacious than salvarsan even if given in doses one-third 
larger but is more easily prepared and less prone to produce disagreeable symptoms. 
It is entirely soluble in water and should be dissolved in 250 c.c. of freshly distilled 
(not hot) water immediately before it is used. The solution must not be shaken 
or heated and is best given intravenously, very slowly, under strict antiseptic 
precautions with the patient recumbent and remaining so for several hours after. 

The dose of neosalvarsan varies from 0.15 gm. to 1.5 gm., and it comes in 
ampoules each of which contains a single dose. The first dose for an adult is 
usually 0.9 gm., gradually increased until the fourth dose equals 1.5 gm. In 
urgent cases it may be given every other day. Women usually receive one-third 
less and children 0.15 gm. to 0.35 gm. Infants 0.05 gm. 

Salvarsan is contra-indicated in acute and chronic nephritis, in advanced cardio- 
vascular lesions, in lymphatism, and in those with an idiosyncrasy to arsenic. 

Often its use is followed by an increase in the inflammation and redness of the 
lesions for a time; the so-called Herxheimer reaction. Sometimes this reaction 
is sharper after the second than after the first dose. In nervous syphilis this 
reaction about vital nervous centres may temporarily exaggerate the symptoms 
and cause a dangerous exacerbation, and if the symptoms are meningeal, another 
dose in less than a week may cause death. Mercury should be used in such cases 
until every evidence of meningeal irritation or cerebral disturbance has long since 
passed away. 

When salvarsan cannot be used the treatment of the secondary stage of syphilis 
must consist in the administration of full doses of the protiodide of mercury, which 
should be given in the form of uncompressed tablet triturates in the dose of i of 
a grain three times a day, increased by one or two quarters each day, until the 
patient manifests distinct evidences of the full systemic effect of the drug, as 
evidenced by some looseness of the bowels or by the development of tenderness of 
the teeth and slight salivation. It is important when this drug is given that tablet 
triturates, and not compressed tablets, are employed, as the compressed tablets 
are often unabsorbed, because of their hardness, and frequently cause irritation 
of the stomach, whereas, the properly made tablet triturate rarely does. 

As soon as the patient manifests any of the symptoms, mentioned as indicative 
of the fact that he is using all of this drug which he can well bear, it is proper to 
diminish the dose one-half, and keep it at this point, provided that this dose seems 
competent to prevent the development of further syphilitic manifestations. If, 
however, this half-dose is not sufficient for this purpose, the drug must be given in 
ascending doses the second time, and if the syphilitic manifestations are at all 
malignant it may be necessary to continue it, even if opium or bismuth have to 
be given to control diarrhea. 

It is essential in the use of the protiodide of mercury in syphilis, first, that the 
stomach shall not be disordered, because it is of vital importance that the patient 
should be able to take full quantities of highly nutritious food, in order that by 
maintaining his vitality his own vital processes may aid him to combat the infection. 

It is also essential that great care be taken against the development of mercurial 
stomatitis. If this condition once develops, it is often difficult to cure it while 
the mercury is continued, and it frequently will prevent the patient from taking 
sufficient doses of the drug to favorably influence his syphilitic infection. If the 
patient is directed to take the greatest possible care as to cleanliness of his mouth, 
to use a tooth-brush and some antiseptic dentifrice after each meal, to keep particles 



SYPHILIS 315 

of food from between the teeth by the use of floss silk, and, finally, if he also be 
given a prescription calling for 10 grains of chlorate of potassium and 10 drops 
of tincture of myrrh in an ounce of elixir of calisaya, which is to be diluted one-half 
with water, and used as a mouth-wash night and morning, it will be found that he 
will be able to take much larger doses of mercury than if these measures are delayed 
until some evidences of mercurial sore mouth present themselves. 

Should the manifestations of syphilis be virulent, then it is necessary to give 
the drug to the patient not only in the form of the protiodide by the mouth, but 
to use blue ointment rubbed into the skin at least once a day, in the dose of about 
1 drachm, choosing a different spot each time for the rubbing, and exercising great 
care that the rubbing is continued long enough to actually cause the absorption 
of the mercury. Usually a hot Turkish bath or, if this is impossible, an ordinary 
hot-water bath should be taken before the mercurial ointment is used, in order 
that the skin may be rendered pliable and put in such a state that the mercury 
can be readily taken up by the tissues beneath it. The entrance of mercurial 
ointment into the body may also be aided by smearing it on a flannel binder and 
placing this about the patient's waist. 

In other instances, in addition to the internal and external use of mercury, or 
in place of one of them, hypodermic injections of mercury may be employed. For 
this purpose one of the best preparations is corrosive sublimate dissolved in normal 
salt solution and given in the dose of J of a grain, injected deeply, but gently, into 
the loose cellular tissues of the buttocks or back, or, better still, into the body of 
the greater muscles, such as the gluteus. Great care must be exercised that anti- 
sepsis is complete, since otherwise the irritant drug, although antiseptic in itself, 
may cause abscess. This injection should not be given oftener than every two or 
three days. In other instances gray oil may be used, prepared by rubbing 2 drachms 
of lanolin with a sufficient quantity of chloroform to form an emulsion, continuing 
the rubbing until most of the chloroform is evaporated, then adding metallic 
mercury to the extent of 4 drachms, and rubbing again until the mixture is complete. 
This strong gray ointment, diluted still further by the addition of equal parts of 
olive oil, may be injected in the dose of 1 or 2 minims every second or third day in 
the same manner as corrosive sublimate. 

Still another way of getting mercury into the body is by means of the sublimation 
of calomel. The patient, being stripped of all clothing, is wrapped in a blanket 
,and placed upon a chair with a wooden seat. Under this chair is place an alcohol 
lamp and over it a disk of metal upon a small iron stand, on which 20 grains of 
calomel is laid. Upon this stand is also placed a tincupful of water. The heat of 
the lamp vaporizes the water and sublimes the calomel, and the mercury, being 
desposited upon the skin of the patient, is absorbed. This method of treatment is 
useful for the relief not only of the systemic symptoms, but also for the syphilitic 
eruption of the skin. A similar plan of sublimation can be carried out with 
inhalations, the patient holding his face eighteen inches away from the pan and 
inhaling the fumes. If this is done mucous patches in the mouth are very frequently 
rapidly healed, but after each employment of sublimation and inhalation, the 
mouth should be well rinsed with water, in order that an excess of mercury may not 
remain there and produce stomatitis. In many cases the best results are produced 
by a plan of treatment in which both the iodide of potassium and protiodide of 
mercury are given together or alternately. 

The treatment of the tertiary stage of syphilis consists chiefly in the administration 
of iodide of potassium or iodide of sodium or iodide of strontium, in as full doses 
as the patient can well bear, but should evidences of gummatous growth in the 
brain present themselves the iodide is not sufficiently active in its action, and 
mercury should be given with it. 

The dose of the iodides varies greatly with the susceptibility of different individ- 



316 DISEASES DUE TO A SPECIFIC INFECTION 

uals. As a rule, tertiary syphilis is not benefited by giving less than 100 grains a 
day. I have had a patient under my care who would take 800 grains a day with 
great benefit, with no other disagreeable symptoms than the development of an 
intense acne. But we rarely meet with instances where these enormous doses 
must be taken. 

The proper way to administer the drug is to order a saturated solution of iodide 
of sodium dissolved in the strength of 1 grain to the minim of water, and direct 
that 10 minims of this be given in a dessertspoonful of the compound syrup of 
sarsaparilla three times a day an hour after meals, being increased each day from 
1 to 5 minims at a dose. If careful attention is paid to the diet and to the condition 
of the bowels, patients who would not be able to take large doses at first soon become 
fairly immune so far as untoward effects are concerned, and can take effective 
quantities within a brief period of time. 

Hereditary syphilis is to be treated by the use of neosalvarsan and the active 
employment of mercury. In babies suffering from syphilis, gray powder may be 
given in the dose of 2 grains two or three times a day, and mercurial ointment may 
be rubbed into the abdomen and on the inside of the thighs and smeared upon the 
abdominal binder of the child. This will prove a most advantageous plan of treat- 
ment. The change in the nutrition and appearance of the infant under these 
circumstances is little less than marvellous. 

The diet should be carefully regulated, and, if the digestion will stand it, cod- 
liver oil should be given internally. The employment of the mercurial ointment 
produces an active systemic influence without disordering digestion, and is, there- 
fore, particularly advantageous when hereditary syphilis is being treated in infants. 
(For the treatment of syphilis of the nervous system see Paresis and Locomotor 
Ataxia.) 

MALARIAL INFECTION. 

Definition. — By malarial infection we refer to a condition produced by the entrance 
into, and development in, the blood of specific micro-organisms known as the 
Plasmodium malaria?, the hematozoon of malarial fever, or, more correctly speaking, 
the Hemameba malaria?. 

The infection is manifested by four different types : First, the so-called intermit- 
tent type, in which the patient has recurring attacks which are characterized by a 
chill, a fever, and a sweat. These recurrences commonly take place daily, on 
alternate days, or on every third day, and are called quotidian, tertian, or quartan. 
Second, a type in which there is present continued fever with remissions in its 
course, the so-called remittent malarial fever. Third, a type in which the infection 
is of a malignant or pernicious form with profound toxemia. Fourth, that form 
in which more or less subacute, or chronic, and profound cachexia is present, 
associated with marked anemia and enlargement of the spleen, and often of the 
liver. The first is due to the tertian or quartan parasite, the second and third to 
the estivo-autumnal parasite, while the fourth form may be due to any one of the 
three parasites. 

History. — Malarial fever was recognized as a distinct disease as long ago as 
five hundred years before Christ, and Hippocrates divided it into the quotidian, 
tertian, and quartan types we recognize today. Empedocles (500 B.C.) recognized 
the relationship of the disease to stagnant water and stopped an epidemic by 
draining stagnant- pools; but it was not until 1880 that Laveran, a French army 
surgeon, first recognized the specific organism, and in 1886 Marchiafava and Celli 
described it more fully. In the same year Golgi showed that the malarial attack 
occurred simultaneously with the sporulation of the parasite, but not until 1898 
did Manson and Ross, of England, and Grassi and Bignami, of Italy, prove that 
the infection is spread from man to man by a certain species of mosquito known as 



MALARIAL INFECTION 317 

the Anopheles. In the United States excellent work has been done by a number 
of investigators, of whom the most noteworthy are Osier, Thayer, and Hewetson 
in Baltimore, James in New York, Craig of the United States Army, and Dock in 
Texas. 

Distribution. — Malarial infection is more widely diffused throughout the tropical 
and temperate zones than any other disease. It is, as a rule, prevalent and severe 
in direct proportion to the proximity to the equator and is rare in far northern 
latitudes. Certain parts of the world, which at one time suffered severely from 
the disease, are now free from it. Forty or fifty years ago, for example, the valleys 
of the Delaware and Schuylkill Rivers near Philadelphia suffered greatly, whereas 
at present cases of the disease are rarely met with in these localities. On the other 
hand, it is very prevalent on the shores of the Chesapeake Bay, which is not more 
than one hundred miles away. At present the disease appears in its mild forms 
in France, Germany, and England, and in the Middle Atlantic and Central United 
States, and in its severe forms in the Southern States, particularly in certain lower 
portions of the Mississippi Valley. The virulent forms are chiefly met with in 
Africa, in certain parts of India, and in the tropics, as in the West Indies and in the 
Philippines, and in the tropical parts of South America. On the Pacific coast 
of the United States the disease is rare. So far as season is concerned, it may be 
said that the greater proportion of cases occur in July, August, September, October, 
and November in semitropical or temperate regions. 

The frequency of malarial fever varies greatly and depends entirely upon the 
prevalence of the Anopheles, the sources for its infection, and the climate which 
permits of the growth of the mosquito. In the United States the greatest prevalence 
of this disease is in the States bordering the Gulf of Mexico and that tier lying 
immediately north of them. The death rate from malaria in this area is about 
30 per 1000 deaths from known causes. 

Etiology. — The Mosquito. — There is but one direct etiological factor in the 
dissemination of malarial fever in man, namely, that form of mosquito known as 
Anopheles. Many species of the genus Anopheles have been described, but only 
two have so far been found to be present as malaria-bearing hosts in the United 
States, namely, the Anopheles maculipennis, which is the most common, and the 
Anopheles crucians. In Europe the infection is always borne by the Anopheles 
claviger, sometimes called Anopheles maculipennis. Fortunately, the anopheles is 
not universally distributed, the culex being the genus which is most commonly met 
with, at least in the temperate zones, and this mosquito seems to be incapable 
of carrying the infection. The anopheles can be readily differentiated from the 
culex by the fact that when it rests upon a plane surface its body is held at right 
angles, or at an angle of forty-five degrees, whereas the body of the culex lies parallel 
to the plane. Again, the wings of the anopheles show very distinct mottling, as 
its names punctipennis or maculipennis indicate. Most of the culex species lay 
their eggs in rafts or bottle-shaped masses, which remain intact until the larvse are 
discharged. The eggs of the anopheles are laid in groups that are readily broken 
up and scattered. Any stagnant or semistagnant accumulation of water is a 
suitable breeding-ground. 

The indirect factors in the causation of malarial infection are, therefore, stagnant 
or semistagnant water in which this mosquito can breed, and the presence of a 
source from which it can obtain the parasite so that it can transmit it to a healthy 
individual; for even if the Anopheles be present, it cannot inoculate a human being 
with malarial fever unless it has first bitten a person whose blood contains the 
hemameba. No more interesting experiments proving these facts can be adduced 
than those made by Patrick Manson on his son, who had never had malarial infec- 
tion. Bignami and Bastianelli sent Manson in England relays of mosquitoes which 
in Italy had been fed upon the blood of patients suffering from pure benign tertian 



318 DISEASES DUE TO A SPECIFIC INFECTION 

malaria. These mosquitoes were allowed to bite the younger Manson, and as a 
result he developed the same form of malarial fever as that suffered by the Italian 
patients, and the same parasite was found in his blood. 

The Hemameba Malakle in Man. — The parasite itself passes through two 
cycles of existence, namely, one which is carried out in the body of man, and another 
in the body of the mosquito. It appears in three distinct forms, namely, as the 
tertian parasite, the quartan parasite, and the estivo-autumnal parasite. Each 
of these lives in the red cells of the blood and to some extent exists in the plasma 
as well. 

Marchiafava, Celli, Bignami, and Grassi, of Italy, have endeavored to show 
that several species of the estivo-autumnal parasite exist, but their views have 
not been generally accepted, and recently they have admitted that there are not 
sufficient grounds for advocating this proposition. Craig believes there is one 
distinct separable type — the quotidian. 

In certain cases the patient suffers from a mixed infection in which the tertian 
and estivo-autumnal parasite are both present at the same time. 

The young tertian parasite, Plasmodium vivax, is a small colorless and hyaline 
body which occupies a small space in the corpuscle. When in a state of quiescence 
it is round, but if the specimen under the microscope is fresh and the temperature 
suitable it manifests active ameboid movements. As the parasite grows, reddish- 
brown granules develop in its interior. These pigment granules move rapidly, 
and are often seen in the ameboid projections of the parasite, so that it may appear 
that several parasites are in one corpuscle. As the growth continues the infected 
red cell becomes more and more pallid and swells up or expands, the ameboid 
movements of the contained parasite diminish in activity, and the pigment granules 
arrange themselves about the periphery of the parasite. At this time the corpuscle 
is nothing more than a shell of its former self. Later the pigment granules accumu- 
late near the centre of the body, and as they do so the process of segmentation 
begins; radial lines divide the parasite into twelve to twenty segments arranged 
around the central mass of pigment. Each segment has a nucleus, and as soon 
as the process of segmentation is completed these segments break out of the corpus- 
cular shell and float freely in the blood plasma, where they speedily attack and 
enter fresh red cells. The evolution and segmentation require about forty-eight 
hours, and the chill and other acute manifestations of illness in the patient develop 
at the time of segmentation. In some instances the parasite becomes unusually 
large, the pigment bodies become stationary without aggregation in the centre, 
vacuoles develop in it, and the parasite seems to die. Some of the parasites do 
not undergo segmentation. These are the sexually differentiated forms (gameto- 
cytes) and contain actively moving (dancing) pigment granules. (See Plate V.) 

The following distinctions serve to separate the tertian from the estivo-autumnal 
parasite: The nuclear body and chromatin mass of the young tertian parasite are 
achromatic to methylene blue, whereas the nucleus of the estivo-autumnal parasite 
is densely stained by this agent (Ewing). The tertian ring is coarse and granular, 
whereas the estivo-autumnal ring is a perfect circle and more delicate. The tertian 
ring is usually pigmented before the chromatin becomes subdivided, while in the 
estivo-autumnal parasite the chromatin is subdivided before pigmentation appears. 
There are, however, exceptions to this rule. Lastly, the infected red blood cor- 
puscle is usually distended or swollen as soon as it is attacked by the tertian parasite, 
whereas it is shrunken in appearance when the estivo-autumnal parasite enters it. 

The quartan parasite, Plasmodium malaria — that is, the organism that causes 
an attack every third day — resembles the tertian organism just described, but 
differs from it in the following respects: In the early stages it occurs as a hyaline 
body which is smaller than the tertian parasite. It speedily develops a sharper 
outline, it is more refractive, and the ameboid movements are slower. The pigment 



DESCRIPTION OF PLATES V AND VI. 1 

The drawings were made with great care and skill by Mr. Max Broedel, with the 
assistance of the camera lucida, from specimens of fresh blood. A Winkel microscope, 
objective 1-14 (oil-immersion), ocular 4, was used. 

Figs. 4, 13,- 23, 24, and 42 of Plate V were drawn from fresh blood, without the camera 
lucida. 

PLATE V. 

The Parasite of Tertian Fever. 

1. — Normal red corpuscle. 

2, 3, 4. — Young hyaline forms. In 4 a corpuscle contains three distinct parasites. 

5, 21. — Beginning of pigmentation. The parasite was observed to form a true ring 
by the confluence of two pseudopodia. During observation the body burst from the cor- 
puscle, which became decolorized and disappeared from view. The parasite became, 
almost immediately, deformed and motionless, as shown in Fig. 21. 

6, 7, 8. — Partly developed pigmented forms. 
9.— Full-grown body. 

10-14. — Segmenting bodies. 

15. — Degenerative form simulating a segmenting body. 

16, 17. — Precocious segmentation. 

18, 19, 20. — Large swollen and fragmenting extracellular bodies. 

22.— Flagellate body. 

23, 24. — Degenerative forms showing vacuolation. 

The Parasite of Quartan Fever. 2 

25. — Normal red corpuscle. 
26. — Young hyaline form. 

27-34. — Gradual development of the intracorpuscular bodies. 

35. — Full-grown body. The substance of the red corpuscle is not visible in the fresh 
specimen. 

36-39. — Segmenting bodies. 

40. : — Large swollen extracellular form. 

41. — Flagellate body. 

42. — Degenerative form showing vacuolation. 

PLATE VI. 

The Parasite of Estivo-autumnal Fever (Plasmodium falciparum) . 

1, 2. — Small refractive ring-like bodies. 

3-6. — -Larger disk-like and ameboid forms. 

7. — Ring-like body with a few pigment granules in a brassy, shrunken corpuscle. 

8, 9, 10, 12. — Similar pigmented bodies. 

11. — Ameboid body with pigment. 

13. — Body with a central clump of pigment in a corpuscle showing a retraction of the 
hemoglobin-containing substance about the parasite. 

14-20. — Bodies with central pigment clumps or blocks. Presegmenting forms. 

21-24. — Larger bodies with central pigment blocks. Presegmenting bodies. Seen in 
the peripheral circulation during a severe paroxysm. 

25-28. — Segmenting bodies from the spleen. Figs. 25-27 represent one body where 
the entire process of segmentation was observed. The segments, eighteen in number, were 
accurately counted before separation, as in Fig. 27. The sudden separation of the seg- 
ments, occurring as though some retaining membrane were ruptured, was observed. 

29-37. — Crescents and ovoid bodies. Figs. 34 and 35 represent one body which was 
seen to extrude slowly, and later to withdraw, two rounded protrusions. 

38, 39. — Round bodies. 

40 . — Pseudogemmation, fragmentation . 

41. — Vacuolation of a crescent. 

42-44. — Flagellation. The figures represent one organism. The blood was taken 
from the ear at 4.15 p.m.; at 4.17 the body was as represented in Fig. 42. At 4.27 the 
ilagella appeared; at 4.33 two of the flagella had already broken away from the mother body. 

45-49. — Phagocytosis. Traced with the camera lucida. 



1 These plates are taken by permission from Thayer and Hewetson's classical report 
in the Johns Hopkins Hospital Reports, 1895, vol. v. Four figures — viz., Figs. 21, 22, 23, 
and 24 — have been added to Plate VI, and are also from the drawings of Mr. Max Broedel. 

2 The color of the pigment in these figures of the quartan parasite has too much of a 
reddish tint. 



PLATE V 
The Parasite of Tertian Fever. 







v 

^s?/ 




■te" 



Ah 






ak 



s. -V, 



3£; 









>* 
*$*** 



f 



,,?< "<£*- >-v 






Q 
















V 



The Parasite of Quartan Fever 





*. 



^••S 
W 




*& 

•*// 



r« 



v. • 



.**"». 



v : .. 1 






*S& 



4 *„ 



i J 



'O- 







PLATE 



The Parasite of Aestivo-Autumnal Fever. 










■*? 




Vt 



<® 



it, 

it 



m 



f\ 



o 



%J 



Jfe 







SI 









C.3 



••**-.^ 



H •:•/• 



MALARIAL INFECTION 319 

granules are larger and darker, less active, and lie near the edge of the parasite. 
Again, it is noteworthy that the red cell does not swell as do those containing the 
tertian parasite, but grows smaller, darker, more refractive and metallic looking. 
The quartan parasite reaches its growth in from sixty-four to seventy-two hours, 
and then appears as occupying nearly the entire red blood cell, or it seems to float 
free in the blood serum. As the time for the paroxysm approaches the pigment 
granules at the periphery flow toward the centre in radial lines, so that it becomes 
arranged in stellate form and the protoplasm divides into from six to twelve pear- 
shaped segments, each of which has a refractive centre. These segments escape 
and infect new cells. Some of the parasites do not, however, go on to this develop- 
ment, but fail to sporulate and become sexual bodies or gametocytes. 

The third form of parasite, the estivo-autumnal form, Plasmodium falciparum, is 
smaller than the tertian and quartan organisms, and presents a ringed appearance. 
It contains much less pigment and, moreover, it soon causes the corpuscle into 
which it enters to become shrivelled and brassy looking. After a time, possibly 
a week, the parasite increases in size, becomes refractive, crescentic, or round, 
or ovoid in form, and, in the centre, masses of dark pigment accumulate. It is 
these latter bodies which are indicative of infection by the estivo-autumnal type, 
and it is to be remembered that, as a rule, they are not constantly present in the 
peripheral circulation, but only in the blood of such internal organs as the liver, 
spleen, and in the bone-marrow. Because of their small size, slow development, 
and the difficulty of obtaining blood from deeply situated organs, they are less 
readily discovered than the two other types. It appears established that the 
crescentic and ovoid bodies do not undergo segmentation or sporulation, but corre- 
spond to the sexual bodies described above, the gametocytes. These crescentic 
and ovoid bodies do not continue their development in the human being, sporulation 
being the human cycle. The fertilization of the female by the male body occurs 
in the extracorporeal or intermediate cycle. (See Plate VI.) 

The three forms of malarial parasite as they appear in man have now been 
described. The mosquito cycle of its existence is as follows: 

The Hemameba Malaki^e in the Mosquito. — A mosquito of the genus Ano- 
pheles, when it sucks blood from an individual in whom the parasite has developed 
sexual forms, receives into its stomach bodies ready for the sexual process ; in other 
words, gametocytes. The male bodies, or microgametocytes, develop long, actively 
moving flagella, called microgametes, which break loose from the organism and 
penetrate and fertilize the larger female bodies or macrogametes, these bodies 
being simple macrogametocytes which have extruded from their nuclear substances. 
The impregnated female now penetrates the wall of the mosquito's stomach, within 
which further development occurs. Within forty-eight hours there may be seen 
encapsulated in the muscular wall of the mosquito's stomach small, round, refrac- 
tive, and granular bodies which have in them pigment granules much like those 
present in the parasite existing in the red blood corpuscles. At the end of a week 
the parasite has grown considerably, and it is found to be marked by radial striations 
forming sporoblasts. When this stage is completed the mother body, sometimes 
called the oocyst, bursts, and so sets free in the celomic cavity of the mosquito a 
multitude of sporozoids. These sporozoids gain access to the veneno-salivary 
glands of the mosquito, and thence to the veneno-salivary ducts, from which they 
are ejected into the human being bitten by that mosquito. No sooner are the 
sporozoids deposited in the blood of man than they speedily become parasites 
which attack blood cells. 

Blood cells are therefore attacked in two waj^s : by parasites formed during the 
asexual or human cycle, and by parasites produced in the sexual or mosquito cycle. 

Prevention. — The prevention of malarial fever consists in (a) protection from 
the bites of the anopheles by the use of mosquito bars, particularly at night; (b) in 



320 DISEASES DUE TO A SPECIFIC INFECTION 

the removal of all marshes by filling them in or draining them so that the breeding- 
place of the mosquito is destroyed; (c) in the destruction of the larvae of the mosquito 
by diffusing coal-oil over the surface of pools or ponds, and (d) by not permitting a 
patient who has the parasite in his blood to mingle with his fellows when the 
anopheles are present, for from him they derive their supply of infection. The 
latter measure can often only be carried out in private houses and barracks. Such 
patients should always sleep under a mosquito-proof canopy. Finally, it is 
well recognized that by the use of small doses of quinine taken daily (5 grains) it 
is often possible to prevent infection. (See Latent Malarial Infection at end of 
this article.) 

Pathology and Morbid Anatomy. — The changes produced in the body by the 
presence of the malarial parasite are much less pronounced if the tertian or quartan 
parasite is present than if the estivo-autumnal is the offending body. Indeed, 
in many cases the morbid changes are so slight that they are speedily overcome 
by the natural processes of repair, and hence rarely cause death. For this reason 
our knowledge of the acute changes produced in internal organs is very limited. 
These changes may, however, for the sake of study, be divided into two forms, the 
acute and chronic. In the acute type the parts of the body which suffer chiefly are 
the blood, the liver, the spleen, the kidneys, and the alimentary canal. 

The changes in the blood consist in a distinct decrease in the number of red cells 
which are destroyed primarily by the growth of the parasites, and possibly second- 
arily by poisons produced by them. That some such agent is active seems to be 
proved by the granular degeneration of the red cells which is present in severe 
cases, and in the polychromatophilia which is met with in cells into which the 
parasite has not entered. There is also a diminution in the color-index; that is, 
of the individual richness of the cells in hemoglobin. The white blood cells are 
usually increased in the proportion of mononuclear leukocytes. Pigmented leuko- 
cytes are also found, and, if the infection has been severe, large white cells (macro- 
phages) are to be seen heavily loaded with pigment. In some instances particles 
of pigment are seen floating in the blood serum, having been set free from red blood 
cells destroyed by the parasite. 

The liver, besides showing great congestion, may present areas of necrosis and 
the capillaries may be found filled with a multitude of the parasites in all degrees 
of growth. The capillaries of the liver may also contain many pigment particles. 

The kidneys are enlarged and congested. They may contain dotlets of deposited 
pigment, and their capillaries may be filled by leukocytes laden with pigment. 
The number of parasites found in the renal vessels, however, as compared to those 
found in the hepatic masses, is small. Rarely an acute diffuse nephritis may be 
manifest. 

The spleen is swollen, soft, and its pulp is very dark. Many of the red blood 
cells which it contains are inhabited by the parasites, and these are often in the 
stage of sporulation. So intense may be the swelling and congestion of the spleen 
that it may be ruptured by sudden stress. 

The mucous membrane of the stomach and bowels is engorged and its capillaries 
often contain the plasmodium. 

If the bone-marrow is examined it is found to be filled with segmenting parasites 
and with pigment. The crescentic parasites are also apt to be numerous in these 
areas. 

The chronic changes consist in profound anemia, manifested by a diminution 
in red cells and in hemoglobin and by the presence of nucleated red cells. The 
liver is deeply pigmented, often slaty in color, the granules being deposited in the 
endothelial lining of the capillaries and the so-called cells of Kupffer, that is, the 
perivascular cells. The hepatic epithelium is commonly granular and a certain 
degree of hepatic cirrhosis may also be present. 



MALARIAL INFECTION 321 

The spleen also becomes markedly increased in size, slate colored from the con- 
tained pigment and later, due to increase in fibrous tissues it becomes very firm, 
the "ague cake." 

The kidneys are also markedly pigmented, and may suffer from chronic diffuse 
nephritis. In certain cases of the cerebral type the parasites may be found in the 
vessels of the brain and a malarial neuritis has been described. As in the acute 
form, the bone-marrow is deeply pigmented and the normal marrow may be replaced 
by red marrow in which normoblasts and megaloblasts are present in the majority 
of cases. All these changes are the result of estivo-autumnal infection. 

Symptoms. — The symptoms of malarial infection may be divided into two classes: 
those due to the tertian or quartan parasites, which are much alike, and those due 
to the estivo-autumnal parasites, which are very different from those produced by 
the more benign forms. 

The Symptoms of Tertian and Quartan Infection. — The predominant 
symptoms of infection by these parasites are the development at regular intervals 
of a chill followed by a fever, and this in turn by a sweat. 

The stage of onset begins with a feeling of malaise, in which headache and a general 
sensation of wretchedness are present. Patients who have had previous attacks 
are often able to recognize the fact that they will have a paroxysm in a few hours. 

After the lapse of from one to five hours the chill develops and is often in the 
form of a severe rigor, in which the teeth actually chatter and the patient is entirely 
unable to control his muscular quivering. At this time the skin is cold, the face 
is pinched and often anxious in expression; but while the patient complains of 
being cold and presents all the external signs of a lowering of body temperature, 
his actual internal temperature is raised so that fever is really well developed while 
the so-called cold stage is still manifest. Thus, it is not uncommon for the rectal 
temperature to be as high as 105° while the patient is shivering and trying to "get 
warm." Associated with this part of the paroxysm the patient is usually nauseated 
and may actually vomit, so that to the depression of the chill is added the relaxation 
and semicollapse of excessive nausea. Headache of the congestive type is also 
severe. The urine is copious in quantity and light in color, and the pulse small, 
rapid, and of high tension. 

This stage of chill lasts from a few minutes to an hour or more, and is followed 
by the true febrile stage, in which the surface of the body becomes flushed and hot. 
In place of the cold, pinched expression the face now appears hot and flushed, the 
eyes may be brightened by the fever, and the pulse, which has hitherto been small 
and tense, becomes full and bounding. Headache, however, still persists, and 
active delirium may develop, but the actual temperature of the patient is rarely 
higher than during the stage of chill; indeed, it may be a little lower. The so-called 
febrile stage is not therefore any more febrile than the stage of apparent coldness, 
but the intense sensation of heat in the skin at this time when the physician touches 
the patient is noteworthy. This stage lasts from thirty minutes to several hours 
and comes to an abrupt ending by the development of the stage of sweat, in which 
the temperature drops to normal; the surface of the patient becomes bedewed with 
sweat, which may be so profuse that it is truly a "dripping sweat." The headache 
and general wretchedness now disappear and the patient drops to sleep exhausted 
by the violence of his attack, but otherwise not ill. 

The accompanying charts (Figs. 61 and 62) show the typical temperature 
changes. 

As in all diseases, so in this one, it must be recalled that all cases do not go through 
these stages in exactly the same manner. Some individuals suffer from a very 
moderate chill and an equally moderate fever and sweat. Some suffer the paroxysm 
for twelve hours and some for a much shorter space of time. 

There are three important physical signs which may be demonstrable in many 
21 



322 



DISEASES DUE TO A SPECIFIC INFECTION 



if not all these cases. The spleen is found on palpation and percussion to be dis- 
tinctly enlarged, extending below the level of the ribs; some bronchial rales are 
usually to be heard in the chest, and the lips are apt to be affected by herpes at the 
close or after an attack. 

Fig. 61 



108 










— 
















































107 


— 


























tf 












zz: 


zzz 




zzz 


zzz 


zzz 








105 


;<: 

zoo: 


~z 


:>: 


_:e 


z~ 


:s: 


iz- 


~ 


:s 


::z 


-r 


s: 


::z 


::z 


s: 


::z 


:z 


? 


-r 


— 


s: 


::z 


::z 


s: 


:rz 


ZTZ 


sz 


:;z 


~6j 


:q_: 
:■*: 


ICOZ 


~<N~ 


"■*: 


zco: 


s 


:or 

3£ 


T 


ri>r 


:<: 
3J 


:co: 


TcnjZ 


_Q-Z 


S 


I 


:< 






Q. - 
3C 


:co_ 


ZoT 




rco: 


_CM- 


or: 


oo: 


_jl05 


:co: 


-CNJ- 


oi04 
h103 
jjjlOB 

£101 


=3 


Z£Z 


rrz 


= 


E| 


zz: 


EE 




F 


- 


- 


ZE 


= 


~ 


- 


P 


EE 


= 


EE 


EE 








= 




1L 




= 


<100 
99 

NORMAL 

98 
97 


i 

EE 


= 


1 


= 


— 


F 




= 


1 


= 


= 


— 


— 


= 




= 






5= 


H 










zEE 


W\ 


=H 





























































Chart showing daily paroxysm due to double tertian infection. One set of parasites segmented 
at 8 p.m. and the second set at 4 p.m. Paroxysm stopped by quinine on fourth day. 



Fig. 62 



1U< 
















































































































































\m 














■S- 

.00- 


:S: 














:iz 


Zoi 


s 


"<<r 


-<: 


S- 


raj: 


.5 
or 

-:0_ 


:s: 


:*z 


:<: 


5: 


-2- 


->- 


zS_ 

Zc\|Z 


z<: 


?: 

z<: 

-:0Z 


-s" 


-s' : 


ol~ 


2 


:S: 


-S~ 


■x- 


zcl: 


:S: 


z<: 


-CL- 


s' : 




■<- 


|sE 




'az; 


:az 


Kb 




-M- 




■■&- 


LOO- 


*_L»_ 


--t~ 


00^ 


CG~ 


ii 


--t- 


-00- 


-— - 


— - 


— 




















































































-A- 






































!04 
































































































































































































































-ft 






























































































\ 
























-U 














103 










'\ 
























j- 
























j-\ 






































































L 














HXt 










L \ 






























































101 














































































1 
























/- 








































100 




































Hji 


— 








































































































99 






































































RMAL 

98 










zzz 


zzz 


szz 





















— i — 










— 


' 












IZZ. 




















































































































































































































































































97 

































































Chart showing paroxysms of tertian fever, the segmentation of the organism occurring at 

about 12 o'clock every other day. 

The severity of all the signs depends, of course, upon the resistance of the patient 
and the virulence of the malarial infection. 

There yet remains to be considered the periodicity of these attacks. They 
may occur daily, in which case they are called quotidian; or every other day, when 
they are called tertian; or every third day, when they are called quartan. The 
tertian type is due to the tertian parasite, which sporulates every forty-eight hours, 
so that the next paroxysm develops at the beginning of the third day; hence the 
term tertian, or third. When the attack occurs daily it is due to the fact that a 
double infection of the tertian parasite has taken place, so that a different set of 
organisms mature each day; in other words, it is a "double tertian infection." 
This form is more frequently seen in the United States than any other type. When 
the attack occurs at the end of every third day — that is, after the lapse of seventy- 
two hours, which is really therefore on the beginning of the fourth day of actual 
time — it is due to the quartan parasite. Sometimes, however, the infection with 
this parasite is a double one, the sporulation in each infection taking place sepa- 
rately, in which case the attacks occur in two successive days with a free day follow- 
ing. In still other cases a triple quartan infection may cause a daily or quotidian 
manifestation of the disease. A daily malarial attack may therefore be due to a 
double tertian or a triple quartan infection. 



MALARIAL INFECTION 323 

On the days free from paroxysm the patient is entirely free from chills, fever, 
or sweats, and except for some impairment of strength may be almost as well as 
ever. It is for this reason that the disease is called "intermittent fever." 

Diagnosis of Intermittent Fever. — The diagnosis of this type of malarial fever 
is easy in the majority of cases, but the physician should not hurry to this conclusion 
until he has carefully excluded several other states that cause a similar temperature 
curve. These states are tuberculosis of the lungs with chills, fever, and sweats; 
septicemia and ulcerative endocarditis with the same train of symptoms, and 
typhoid fever with chills of a sharp, distinct character. The number of poor 
human beings who are dosed ad nauseam with quinine for malaria when they have 
tuberculosis is appalling. The history of the case, the physical signs in the lungs, 
and the fact that the attacks of chills and fever do not cease if quinine is given, 
prove that malaria is not the cause of the illness. Careful examination of the 
patient ought to discover sepsis by the finding of a definite focus of pus, and in 
many cases ulcerative endocarditis can be discovered by the changes in the heart 
sounds. Typhoid fever can be discovered by the state of the tongue, that of the 
bowels, the rose rash, and the Widal test of the blood. Better than all for an 
absolute diagnosis is the discovery of the malarial parasite in the blood by the use 
of the microscope. Unfortunately, this is only possible to the expert. (For 
examination of the blood for the parasite see Pathology.) 

Prognosis of Intermittent Fever. — Intermittent malarial fever cannot be considered 
a self-limited disease. It is true that individuals affected by it recover without 
medication if they are otherwise healthy and have favorable surroundings, but it 
is notorious that they are very liable to subsequent outbreaks of the disease when 
for various reasons their vital resistance is impaired or the system is affected by 
change of climate. Thus it is by no means unusual for patients seemingly well 
of the infection to be attacked by paroxysms on going to a higher altitude. If 
quinine is used with skill, and further infection is avoided, complete recovery usually 
is reached if no complication arises. 

Treatment of Intermittent Fever. — In the treatment of intermittent malarial fever 
the fact is always to be borne in mind that in quinine we have a true specific for 
the disease in that this drug, even in exceedingly weak solution, is capable of causing 
death of the malarial parasite. So complete is the cure produced by the proper 
administration of this drug that no other form of remedial measure can be considered 
until after it has been given full opportunity to do its work. But, on the other 
hand, it must not be forgotten that quinine cannot destroy the malarial parasite 
until it (the quinine) has entered the blood, that it cannot enter the blood until 
it is absorbed, and that it is impossible for it to be absorbed if the gastroduodenal 
and hepatic circulation is so disturbed that catarrh of the stomach and bowels 
is present, making it impossible for the quinine to be taken up by the circulation. 
It is therefore essential, in almost every case of intermittent fever, that the bowels 
shall be thoroughly unloaded, preferably by full doses of calomel of which not 
less than 5 nor usually more than 20 grains are required, this in turn being followed 
by a saline purge. If, in addition to these measures, it is insisted upon by the 
physician that the patient shall rest in bed during the time that the quinine is 
being given, it is surprising how comparatively little quinine is needed to destroy 
the parasites; whereas, if these precautions are not taken, enormous doses may be 
given with no curative effect. 

Quinine may be administered at two periods in connection with the paroxysm 
of intermittent malarial fever. One method is to administer the drug several 
hours before an expected paroxysm, with the hope that it may prevent sporulation, 
or at least destroy the spores as soon as they escape. This plan is always to be 
resorted to when the physician is confident that an attack is threatened and that 
a sufficient time will elapse to make it possible for the quinine to be absorbed. The 



324 DISEASES DUE TO A SPECIFIC INFECTION 

other method consists in administering the drug in the sweating stage of a paroxysm, 
for the purpose of destroying the young parasites which have just escaped from the 
red blood corpuscles, in the hope that they may be destroyed before they can 
attack new cells. It is evident, therefore, that neither of these plans is contradic- 
tory, but they are to be resorted to according to the period at which the physician 
sees the patient. It should always be the endeavor of the physician to have the 
quinine in the blood an hour or two before an expected paroxysm, and this means 
that it should be given several hours before, when taken by the stomach. 

When the attack is quotidian quinine must be given daily, when it is tertian 
it must be given every other day, and when it is quartan a full dose of quinine 
should be given on the day of the expected attack and smaller doses on the off 
days. If it is a double quartan infection the quinine should be given on the two 
consecutive days and only a small dose on the third day. 

The quantity of quinine which is required varies of course with the severity 
of the infection and the rapidity of the absorption. Ten to 15 grains are usually 
sufficient in the milder types, but in the more severe types 30 to 60 grains are often 
required, although a larger quantity is usually needless if attention is given to 
the processes of absorption. The quinine should be given in powder in soft capsules 
easily dissolved. 

The dose of quinine should be generous since moderate doses may seemingly 
cure the patient by arresting sporulation without destroying the parasite in the 
spleen and bone-marrow where the parasite may become immune to quinine. (See 
Relapse and Latent Malarial Infection.) 

There is some evidence to prove that methylene blue has a destructive influence 
upon the malarial parasite. It may be given in the dose of 1 to 4 grains in capsules. 

So far as the attack itself is concerned, aside from the use of quinine, the physician 
may modify to some extent the effects of the paroxysm by the use of stimulants 
to support the circulation, and prevent congestion by using hot compresses or hot 
foot-baths. If the alimentary canal is overloaded with food or fecal matter, the 
stomach should be emptied by an emetic and the intestine by a purge or a large 
enema. Alcoholic stimulants, as a rule, are not advantageous. If the attack 
is exceedingly severe, a dose of morphine may be given hypodermically, or deodor- 
ized tincture of opium may be used. During the fever the patient may be relieved 
by a tepid sponging, but usually antipyretic measures are entirely unncessary, 
and coal-tar products ought never to be employed. The vomiting, if excessive, 
may be controlled by hourly doses of 1 grain of oxalate of cerium with 5 grains of 
bismuth, and by counter-irritation over the epigastrium. 

The Symptoms of Estivo-autumnal Infection or Remittent Fever. — From the stand- 
point of severity and danger to the individual attacked, this type of malarial infec- 
tion is by far the most important, although it is not as widely distributed, and 
therefore not as commonly met with as the tertian and quartan forms, except in 
certain localities which are usually tropical or semitropical. The term "estivo- 
autumnal fever," applied to it first by the Italian investigators, Marchiafava and 
Celli, indicates that it occurs most commonly in the summer and fall months. 

The symptoms of this type of infection differ markedly from the intermittent 
type of the disease in a number of particulars. Thus, it is not characterized by 
an intermittence of the fever and of the other signs of illness, but instead is typically 
remittent; that is to say, the fever and associated symptoms diminish in severity 
at times, but they do not entirely disappear. On the contrary, they persist in 
some cases to such a degree that the amount of remission is very slight indeed. 

As the g astro-intestinal disturbance due to this infection is very prone to be marked, 
and as the liver is usually much affected, this type of the disease is sometimes 
called "bilious remittent fever" or "bilious fever." Vomiting, which may be 
very persistent, and which may be markedly bilious, is a common symptom. 



MALARIAL INFECTION 325 

The remissions just spoken of may occur regularly, but in the majority of cases 
they are very irregular, both as to the time of their occurrence and to the degree 
of their individual severity. In some instances the chills and sweats are distinct; 
in others they are so ill-defined as to be scarcely noticeable. Further than this, 
the febrile movement, which is so sudden in onset and which ends so sharply by 
crisis in the intermittent form, is usually gradual in onset and equally deliberate 
in its fall in the remittent type. The temperature falls by lysis, not by crisis, in 
each paroxysm. This lack of sharply defined waves of temperature may deprive 
the physician of one of the most important means of recognizing that the illness 
is really due to the estivo-autumnal parasite, and may mislead him into the diag- 
nosis of typhoid fever, to which conclusion he is aided by the heavily coated tongue, 
the somewhat apathetic face, the enlarged spleen, the tympanitic belly, and the 
state of the bowels, which are lax in some instances and constipated in others, just 
as they are in typhoid fever. As many cases of typhoid fever have chills and sweats, 
the confusion is all the more readily made, particularly as a subacute bronchitis 
can often be discovered on ausculting the chest, just as it can be found in typhoid 
fever. 

The severity of the symptoms varies over a wide range. In some instances the 
patient is only moderately ill; in other cases he is manifestly suffering from a severe 
malady. Delirium may be marked, and the mental stupor may be very noticeable. 
The pulse varies from 90 to 110, as it does in typhoid fever. 

There still remains to be discussed that form of estivo-autumnal infection which 
is so violent in its course that the term "pernicious malarial fever" has been applied 
to it. Pernicious malarial fever is very rare, except in the tropics and in a 
few isolated places not far removed from these areas. It manifests itself in 
two forms. 

(a) The comatose form, in which a patient is seized with symptoms resembling 
intense cerebral congestion or apoplexy, or develops acute delirium followed by semi- 
consciousness or coma. The fever is usually very high and the skin intensely 
hot. The patient may die in twenty-four hours without regaining consciousness, 
but if he survive so long a remission in the symptoms sometimes appears and 
recovery takes place; or, instead, a second paroxysm comes on in which death is 
likely to occur. These cerebral symptoms are due in part to the profound systemic 
disturbance caused by the infection, but chiefly to the formation of thrombosis 
of the cerebral vessels by a host of the parasites. 

(b) The algid or cold form, in which the febrile movement is absent or very mild, 
and in its place signs of collapse and exhaustion appear, with great coldness of the 
surface of the body and a complaint of feeling cold on the part of the patient. With 
these symptoms of profound depression g astro-intestinal disturbances, which are 
choleraic in type, may develop. There may be violent vomiting and active serous 
diarrhea, the patient being at death's door by reason of the exhaustion. Here 
again the centralization of the symptoms about the intestines is due apparently 
to the accumulation of vast numbers of the parasites in the capillaries of the intes- 
tinal mucosa. These pernicious forms usually affect persons whose resistance 
has been impaired by earlier attacks of malarial infection, but occasionally develop 
in previously healthy persons with great suddenness as early as one week after 
exposure to infection. Children under ten years are more susceptible than adults, 
as are also the aged. 

Complications and Sequelae of Estivo-autumnal Infection. — The most serious com- 
plication of infection by the estivo-autumnal parasite is the development of bloody 
urine, which is of two forms, namely, a true hematuria with free blood cells in the 
urine, and a true hemoglobinuria in which only the coloring matter of the blood is 
present. The former is obviously the result of a solution of continuity in the 
renal vessels, and the latter is equally obviously due to a destruction of a large 



326 DISEASES DUE TO A SPECIFIC INFECTION 

number of red cells in the blood itself. This " black-water fever," as it is sometimes 
called, is practically unknown except where the estivo-autumnal parasite is found. 
It occurs chiefly in certain of the Southern United States and in Africa and in 
Greece. 

The symptoms associated with the development of the bloody urine are those 
which are often manifested by ordinary cases of severe remittent malarial fever. 
If the blood is examined before the urine becomes bloody, a large number of estivo- 
autumnal parasites are usually found. On the other hand, after the bloody urine 
has appeared, it is commonly stated that an examination of the blood does not 
reveal the malarial organism. 

The statement that quinine is capable of producing malarial hematuria is 
indorsed by so many practitioners of experience that it cannot be ignored, but 
I cannot help feeling that coincidence has been a large factor in the development 
of this view. 

As sequelae of malarial fever very marked anemia, with chronic enlargement of 
the spleen, sometimes called "ague cake," develops; the patient is exceedingly pallid, 
the abdomen may be distinctly enlarged because of the swelling and congestion of 
the liver and spleen, and there may be some swelling about the ankles. There is 
dyspnea on exertion. Hemorrhages in the retina may occur. Fever is usually 
not marked, unless there be attacks of malarial infection superimposed upon the 
chronic state. 

It is quite remarkable that in young children, who suffer from severe malarial 
anemia and cachexia with associated enlargement of the spleen, recovery will take 
place under the administration of suitable tonic doses of arsenic, the avoidance 
of fresh malarial infection, and resort to a bracing climate. Even the spleen, which 
seems so hard and enlarged that any diminution in its size may appear impossible, 
undergoes an extraordinary degree of shrinkage, so that in adult life any evidences 
of it having been chronically enlarged may have disappeared. Similar improve- 
ment sometimes takes place in adults, but slight enlargement of the spleen is often 
a persistent evidence of earlier malarial infection, even after the disease has been 
apparently absent for years. 

Among the rarer complications of malaria may be mentioned neuritis, 
pleurisy, ascites, intestinal hemorrhage, splenic abscess, and inflammation of the 
lymphatic glands. Cases of orchitis have been reported by French military 
surgeons, and a rapidly developing and very painful form has been observed 
in Sumatra, by Martin, who describes it as a fulminating inflammation of the 
testicles. 

Choux has collected 147 cases of rupture of the spleen due to malaria. He 
recognizes two forms: one which occurs in persons who have not suffered very 
long from malaria, and whose spleens are not greatly enlarged, and one which 
affects the subjects of chronic malaria whose spleens are enlarged and deformed 
by splenitis. In the later class rupture is usually caused by traumatism. Play- 
fair, during a residence of two and a half years in East Indies, observed twenty 
deaths from rupture of the spleen. 

Hemiplegia, either with or without aphasia, is the most common of localized 
cerebral complications. Paraplegia is less common, and monoplegia is of still 
rarer occurrence. Amaurosis, deafness, and perversions of taste and smell are 
occasionally observed. Symptoms of motor irritation, such as tremor and chorei- 
form movements, have also been reported as rare complications, and a case of post- 
hemiplegic malarial chorea has been described by Boinat and Salebert. Paralysis 
of the lower extremities, due to lesions in the cord, occurs, and is often accompanied 
by loss of control over the rectum and bladder. All of these disturbances may be 
transitory. Occasionally some of the paralyses are rapidly fatal. Multiple sclerosis 
is a relatively frequent nervous sequela, and tetany and paralysis agitans are among 



MALARIAL INFECTION 327 

the less frequent complications. Peripheral disturbances, such as hyperesthesia 
and anesthesia occur in a few cases, and supra-orbital, trigeminal, and intercostal 
neuralgia also complicate a small number of cases. 

I* Of functional nervous complications and sequela?, hysteria, neurasthenia, and 
insomnia may be mentioned. The various psychoses are of rare occurrence. Pas- 
manik in an analysis of 5412 cases of malaria found 106 cases of mental derange- 
ment. None of these patients affected were known to have an hereditary predis- 
position to insanity, and only 4.8 per cent, of the number were alcoholics. 

Diagnosis of Estivo-autumnal Fever. — Estivo-autumnal fever must be carefully 
differentiated from typhoid fever and from the so-called continued thermic fever 
of hot climates. Its differentiation from typhoid fever is possible and should 
always be achieved; yet during the recent Spanish- American war the number of 
cases reported as malarial fever which were typhoid fever and the number called 
typhoid fever which were malarial was very large. 

The presence of estivo-autumnal infection is determined by the fact that the 
patient is, or has been, living in a region in which this disease is prevalent or at 
least may occur. It practically never occurs, except in imported cases, north of 
the State of Delaware in the United States, or in any of the northern parts of 
Europe. Again, its presence is determined by the discovery of the estivo-autumnal 
parasite in the blood. This is not an easy test for the tyro, and the blood is not 
easy to obtain from the deeply seated organs in which the parasite is found. After 
the first week of the illness the absence of rose spots and the Widal reaction will 
determine the case not to be one of typhoid fever. Finally, good-sized doses of 
quinine will modify the fever of this type of malaria, but will not affect typhoid 
fever at all. 

Prognosis. — The prognosis in estivo-autumnal infection is more grave than in 
the tertian and quartan types. In the pernicious forms the mortality is about 
27.6 per cent, according to Deaderick, who bases these results on 18,529 cases 
collected from various writers. 

Treatment. — The treatment of remittent fever is much more difficult than that 
of the intermittent form. The disease is more dangerous and often more rapid 
in its course. Further than this, the fever is so much more prolonged that it is 
of itself deleterious, and, as the patient does not have periods of intermittence in 
which he can make a partial recovery, strength is much more rapidly lost. The 
estivo-autumnal parasite seems to be more resistant to the influence of quinine 
than either the tertian or quartan parasite, and, finally, it is much more difficult 
to cause the absorption of quinine in most cases of bilious remittent fever, both 
because vomiting is frequently a persistent symptom and also because absorption 
seems for the time being to be put aside. It is evident, therefore, that where vomit- 
ing is too persistent to permit of the administration of quinine by the stomach, it 
must be given hypodermically. The best way to administer it is intramuscularly 
in the form of the bihydrochloride of quinine, which is soluble in equal parts of water. 
The solution should not be concentrated but diluted, for concentrated solutions 
are prone to cause abscess. The injection is best given by means of an antitoxin 
syringe, and which may be injected in the following manner: Dissolve 15 giains 
of hydrochlorate of quinine in 15 minims of alcohol and 2 J drachms of distilled 
water. Strict asepsis is essential to avoid abscess. The more dilute the solution 
the less is the danger of abscess. Just before using, add a drop or two of dilute 
hydrochloric acid. The difficulty with the administration of quinine by the rectum 
in these cases is that absorption is too slow. But, nevertheless, the drug may be 
given in this manner dissolved in starch-water whenever it is advisable to get quinine 
into the blood by every possible avenue. 

Even when it is impossible to administer quinine by the stomach, it is usually 
advisable to move the bowels freely, and this may be accomplished by the use of 



328 DISEASES DUE TO A SPECIFIC INFECTION 

Seidlitz powder given in divided doses, or by the employment of citrate of mag- 
nesium. 

If the vomiting becomes so excessive as to be a dangerous symptom in itself, 
it may be controlled by hypodermic doses of morphine, or by 5 to 20 minims of 
spirit of chloroform given with the same amount of compound spirit of lavender 
or of cherry-laurel water. Counter-irritation may also be applied over the epigas- 
trium in the shape of a mustard plaster. Some cases are also benefited by the 
application of hot compresses over the liver. The value of large doses of calomel, 
amounting to 20 or even 30 or 40 grains, for their effect in overcoming hepatic 
torpor cannot be denied. All practitioners of experience in intensely malarial 
districts are agreed as to this point. 

Should hematuria or hemoglobinuria complicate a case, a careful consideration 
of the stage of the disease is essential. The value or harmfulness of quinine in 
malarial hematuria is still a "bone of contention" with many practitioners, some 
claiming that the quinine is capable of actually producing bloody urine, and others 
asserting equally positively that it is always needed. The writer has expressed 
the view on several occasions that some of these cases of bloody urine, complicating 
malarial fever, may be due to an associated parasite upon which quinine has little 
influence. Craig, of the Medical Corps of the United States Army, believes that 
all causes of so-called malarial hemoglobinuria are due to an associated parasite 
not identical with the Plasmodium malarice. In a certain number of cases it is 
probably true that the bloody urine is a sequel rather than an accompaniment 
of the development of the parasite in the blood. Under these circumstances, as 
enormous doses of quinine can have little influence upon the malarial parasite 
and also may irritate the kidneys, it is conceivable that the use of this drug at 
such a time is distinctly contra-indicated; whereas, if an examination of the blood 
reveals the presence of the estivo-autumnal parasite, then the quinine must be 
given, since the danger of producing hematuria by its administration is more than 
counter-balanced by the desirability of destroying the cause of the illness. In 
other words, to give quinine in some cases of malarial hematuria, when the specific 
parasite is not present, is like locking the door after the horse is stolen; while in 
others its administration is timely and appropriate. 

A number of important papers on this subject, notably those of Craig and Brem, 
have appeared since the last sentence was written some years ago. I can see no 
reason for changing this opinion, but many reasons for adhering to it. 

Many physicians of large experience strongly urge the use of hyposulphite of 
sodium in doses of from 15 to 60 grains every four hours for this complication. 

The use of normal salt solution by hypodermoclysis is often a valuable measure 
for relief. If the patient is moribund it should be given intravenously. 

Latent Malarial Infection and Relapse. — Latent malarial infection is probably 
much more common than physicians believe, although the laity have an exag- 
gerated view of its occurrence. Craig has reported the result of examining the 
blood of 47 men in one company of the United States Army, all of whom had 
been exposed to malarial infection in the Philippines, but all of whom were at least 
well enough to be on duty. Twenty-seven of them had the parasite in their blood, 
and 25 were infected by the estivo-autumnal parasite. This persistence of infection 
not only possesses ordinary interest, but shows that by the distribution of returning 
troops to various parts of the country this parasite may be disseminated in areas 
hitherto uninfected. Similar results have been recorded in India by Hehir 
and Adiel Aside from the ultimate cure of the individual it is important to 
control such sources of infection. All cases in which definite malarial parasites 
have been found should receive quinine for at least three months after all symptoms 
have ceased. Koch advises that 15 grains of quinine be given on the consecutive 
days, every seven days for this purpose. 



RELAPSING FEVER 329 

Relapse in malarial fever occurs under several conditions independent of a new 
infection. The parasites may be kept in abeyance by good health and moderate 
doses of quinine only to become active when the health is impaired or the quinine 
is stopped on a return to a non-malarial district. Sporulation is stopped but the 
parasite is not destroyed. Such cases reveal no parasites in the blood until the 
relapse occurs because they are hidden in the sperm and bone-marrow. These 
cases are therefore often very difficult to cure because of the hiding place of the 
parasite and because the small doses of quinine have been sufficient only to induce 
quinine immunity in the parasite. Such cases often can be cured only by hypo- 
dermic or intravenous use of large doses of quinine or by the use of salvarsan. As 
Craig points out, the development of a masked malarial infection may greatly 
mislead the surgeon, both before and after an operation. 



RELAPSING FEVER. 

Definition. — Relapsing fever, as its name indicates, is characterized by an attack 
of fever which lasts about six days, this in turn is followed by a period in which 
fever is absent, and this again by a recurrence of a period of fever. These alternat- 
ing periods may be repeated three or four times. Sometimes it is called Febris 
Recurrens, "Seven Days' Fever," and "Famine Fever." 

History. — The history of relapsing fever is, when compared to some other infec- 
tious diseases, fairly modern, for the first descriptions of it occurred in medical 
literature about 1729, although it was not until 1739 that Rutty gave a clear 
description of its course. After this for nearly a century no reports of its existence 
are to be found, but between 1842 and 1852 it appeared over a wide area, occurring 
in England, Ireland, Scotland, Germany, and finally in America, to which country 
it was brought by a shipload of immigrants who came from Liverpool and landed 
in Philadelphia in 1844. It became epidemic in the United States in the decade 
from 1861 to 1870, and it is interesting to note that as the American, Gerhard, first 
aided in the differentiation of typhoid fever from typhus in Philadelphia, so Pepper, 
Rhoads, and Parry, of the same city, have contributed to medical literature the 
best account of the disease as it has appeared in this country, having observed a 
larger number of cases than any other clinicians. 

Distribution. — Relapsing fever has occurred in almost all parts of the civilized 
world. 

Etiology. — It has been claimed that filthy surroundings and bad food are active 
in the development of relapsing fever, but they probably exercise a general influence 
by lowering vitality rather than by directly aiding infection. Sex, age, and nation- 
ality exercise no influence, and it is doubtful if any one season of the year increases 
the prevalence of the disease. The actual cause of relapsing fever, as already stated, 
is a spirillum sometimes called the spirillum of Obermeier, now known as Spirocheta 
recurrentis in the European type and Spirocheta novyi in the relapsing fever of 
America, which is constantly found in the blood of patients suffering from the 
disease during the stage of fever. It is absent from the blood in the intermissions, 
although small, glistening bodies, said to be spores, can be seen. The disease is 
contagious, that is, it requires contact with the patient or with his garments for 
the infection to be spread. Patients may be infected by insects, for example, by 
bed-bugs which have previously bitten patients suffering from relapsing fever. 
That the disease is ever conveyed by the air is doubtful. Relapses may be explained 
by the hiding of the spirochetal in tissues which cannot destroy them. Darling 
has shown that the so-called Relapsing Fever of Panama is sometimes distinct from 
the forms commonly found in the eastern hemisphere, although belonging to the 
same general class in that the specific organism is the S. duttonia or the S. carteri. 



330 



DISEASES DUE TO A SPECIFIC INFECTION 



Pathology and Morbid Anatomy. — The changes produced in the body by relapsing 
fever are not only not marked, but not at all characteristic. The spleen and liver 
are swollen and engorged, as in nearly all febrile infectious diseases, and the volun- 
tary muscles may undergo granular degeneration. Similar changes may be found 
also in the heart muscle. Sometimes multiple infarctions and hyperplasia of the 
bone-marrow are present and ecchymotic spots, which are found antemortem, are 
seen in the skin and subcutaneous tissues. All the organs may show this staining. 
Darling has shown that the body's mechanism of defense is phagocytosis carried 
on chiefly by the endothelial cells of the liver. 

tit; Symptoms. — As a rule about six or seven days after exposure to the disease the 
infected person is abruptly seized by a severe chill, or more rarely by headache and 

Fig. 63 



Day of 

Disease. 


1 


2 


3 


4 


5 


6 


7 


8 


9 


10 


11 


12 


13 


14 


15 


16 


17 


18 


19 


20 


21 


22 


23 


24 


25 


26 




M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 


M | E 


M 


E 


M j E 


M 


E 


M 


E 


M 


E 


M 


E 


M E 


M 


E 


M 


E 


M j E 


M 


E 


M | E 


M E 


M E 


M 


E 


M 


E 


M 


E 


M 


E 


M 


E 
































































i 






























































1 






I 




























































































1 
























































1 














































1 
































! 














1 






1 










107 - 
























. 


































1 


















































i 


1 f 










1 


1 












l/T 






1 














1 


































llf 


ifl 




1 




1 


1 












i/1 






1 














1 






1 
















| 












I /\ 


1/ 










1 


















i 














1 


1 


1 








0- 

106 - 












1 f\ 






r/T 












1 


1 


1 






1 












1 












1 


1 






















'/ ^ 






\ \ 




































|, 














1 


























I 




















( 










1 


\ft 










'fl 
















1 
























I 








1 








1 














1 


1 S 


























1 


1 
























\ 






;i 


/r 


r~ 






1 












1 


1 






/ I 


1 
















1 


1 




















\ 1 ' 






1 


\ F" 










1 














1 


1 






1 I 


II 






















I 






105- 














V 






1 


\/l 










1 














1 










/ 1 


































l/\ 






H»- 








\ /' 


11 










1 
























1 




















1 
















1/ \ 










— 


il 1 


Jli 1 








1 














1 








1 ' 






1 " 












1 




1 






104 - 

0- 
103- 

0- 
102- 

0- 
101 - 


100 - 1 

99" 

9 8°- 



97; 


96 








v / 












1 


1 






1 












1 








W 1 ' 
















I 






1 












V 1 


1 












1 


1 


























1 




















1 


1 




1 










/l 






1 












1 




































)2 




1 
























































"1 


— 























— 


— 


— 




— 


~ 


— 




— 






































f\ 












— 











| 
















— 


— 






























— 














— 


— 




— 






1 






































— 


— 


— 


































































— 








— 






































































































if 




| 
























































































-j- 
















1 






































































































J 














— 


1 


















- 


— 


— 


- 






— 




— 


~ 


— 


— 


— 












T 
















J 


















































1 












1 
























































































\ 
























































— 






















- 


- 


— 


— 










-1- 
































— j 


" 






— 









— 










































































































































































































j 


































































































- 


- 


— 












— 












1 














































— 


— 


— 


— 


— 


— 






— 


— 


— 


— 


























l 
















_ 


— 


— 


— 


-/- 


— 
















1 






































































1 














































— 


— 










1 ! 








— 






— 




























( 




















































































1 






























~~ 


— 


























-4— 










































j 
































































j 


















































1 








— 




— 


— 


— 


— 


-4 


— 


— 


— 


— 


— 






— 


— 




— 














. 




















































































| 
























. 












A 








































-V 


— 


A- 


— 


— 


— 




f- 


A 




— 


f- 


— 


— 


— 


— 


— 


— 


— 


— 


— 




— 


— 


— 


E 


— 


/- 




S 


L \ 




•- 


— 






























— 





— 


/ 


i 












— 


- 
















\ 






















] 




v 


— 


V 






— 














I 














\ 


































































/ 






\ 


1 






























^ 


1 






















































1 






f 


^ 


/ 






\ 
































A 














































- 


— 


- 


w 





7 


/_ 


^A 


K 


— 


— 


\ 






— 


— 


— 






— 


— 












/ 


/ 






















— 


- 


— 


— 


— 


— 















\ 1 


















1 


v 






































V- 




V 


































































































































y 








































































































































































— 














































































































— 










- 


















































































































































































l'ulse. 


•% 


s 


O 


c~, 


■z 


?i 


'.' 




s 


^ 


CO 


c 

T 1 


co 





- 








03 







O 


00 


Cl 


Cl 


c-j 




S 


Cl 





Cl 


s 


i 


1 


c~ 


Cl 





-r 


O 









'J 


Cl 


-r 


to 


-* 


O 


~ 


CO 


g 


s 


- 




X 


00 


Respiration 


2 


a 


r, 


3 


s 


?: |8 


O 





~v 





ift 


-# 




to 





CI 


M 


O 


ci 




-v 










Cl 


2 


Cl 


C>1 


CI 


Cl 

CO 


s 


Cl 

^0 








? 


S3 


-1- 


Cl 



ct 


§ 


C) 


CO 


- 


M 


Cl 


§ 


?: 


2 


?! 




Cl 


CO 


CO 


2 



Typical case of relapsing fever terminating in recovery. One relapse with slight postcritical rise in 

temperature. 



vomiting. The face becomes flushed, but the expression is not dull and apathetic 
as it is in typhus fever, unless the infection is very severe, when typhoid symptoms 
may soon develop. A moderate degree of jaundice also is present in many cases. 
No characteristic eruption appears on the skin, although small petechia? or ecchymo- 
tic spots may occur in severe cases. Many observers have recorded the presence 
of a disagreeable, musty odor about the patient. 

The febrile movement is the most notable manifestation of the disease. The 
fever begins to rise while the stage of chill is still young, and reaches 102° or 103° 
in the first twenty-four hours and 104° or 106° in the next twenty-four hours. 
During the febrile stage of about six days this level of temperature is fairly con- 
stantly maintained, although irregular remissions of 1° or 2° may occur. Sometimes 






TRYPANOSOMIASIS 331 

the fever reaches 108°. In some cases the primary febrile period lasts only two 
days. While the febrile movement just described is characteristic, its ending is 
more so, for a critical fall of temperature takes place with a suddenness and com- 
pleteness which is rarely met with in any other disease unless it be croupous pneu- 
monia (Fig. 63). Not rarely it falls 6° in three hours, although a fall of 1° an hour 
is more common. The rapid fall may carry the temperature a little below normal. 
After a few days of no fever the relapse takes place with the same sudden onset 
as occurred with the primary attack. It runs a course in all respects like the 
original seizure, but it more commonly ends by lysis than does the first paroxysm. 
The third and fourth attacks, if they occur, are usually milder than the first two. 
The duration of the period of intermission varies from one to ten days, although 
it is usually six days or a week, and the duration of the entire illness may vary 
from eighteen to ninety days, according to the number of relapses. 

The pulse during the early attacks is rapid, and it may be bounding, but if 
the patient be enfeebled by prolongation of the illness it may be small and compress- 
ible. Severe frontal and occipital headache is often experienced by the patient 
in the first attack, but delirium is rare except it be due to serious complications 
or to very high fever. 

Prognosis. — The prognosis as to ultimate recovery is quite good, the mortality 
of the disease usually being about 4 per cent. 

Treatment. — The introduction of salvarsan has provided us with a specific treat- 
ment for relapsing fever in that this drug destroys the spirillum. (See Syphilis.) 
Good nursing, careful feeding, and the use of stimulants, if the patient is feeble, 
are of course needful. The action of the bowels and kidneys, as in all infectious 
diseases, should be carefully attended to. No results from the use of hydrotherapy 
in relapsing fever have been published, so far as the writer is aware, but the course 
of the febrile movement scarcely indicates this plan of treatment. 

PSOROSPERMOSIS. 

This term is applied to an exceedingly rare condition in which psorosperms 
become parasites, growing in cells and producing nodules. These nodules may 
be large enough to be felt through the abdominal wall. The patient presents 
symptoms which are like typhoid fever in character. There is diarrhea, stupor, 
some fever, hepatic and splenic tenderness, and feeble circulation. Autopsy in 
such cases has shown the presence of masses closely resembling tubercles, which 
are scattered over the liver, the spleen, the peritoneum, and in the kidneys. 

Another form of infection by sporozoa has been described as occurring in the 
skin, but Stelwagon states that the condition called psorospermiasis by Darier 
is now known not to be due to this cause. On the other hand, Rixford and Gilchrist, 
in Baltimore, have recorded two cases in which tuberculosis of the skin was thought 
to be present for eight years. During this time the lymphatic glands were enlarged, 
other parts of the body became affected, and finally death ensued. Numerous 
nodules, looking like those of tuberculosis, were found scattered very widely through 
the body, and these were found to contain large numbers of sporozoa. 

TRYPANOSOMIASIS. 

Definition. — Two phases of one disease are recognized in man as due to infection 
by trypanosomata. These are, first, an ill-defined fever resulting from invasion 
of the circulation by the Trypanosoma gambiense, and second, African lethargy, 
or sleeping sickness, due to the presence of the same parasite in the cerebrospinal 
fluid. Other trypanosomes, as the ugandense and rhodesiense, have been described 
as separate species in the countries indicated by their names. It now appears 



332 DISEASES DUE TO A SPECIFIC INFECTION 

quite certain that the first, and probably the second, is in reality the gambiense. 
The statement that all the trypanosomes found in man are identical does not, 
however, at present appear warranted. 

The trypanosomata are flagellated protozoa, found in the blood of vertebrates. 
They were first discovered by Gruby in 1843 in frogs, and by Doflein in 1845 in 
rats and hamsters. Since that time they have been found in practically all verte- 
brates. These organisms were first supposed to be spirilli before their animal 
nature was understood. In the large majority of instances they are not pathogenic. 
As far as our present knowledge goes, the varieties represent distinct types, confined 
to the particular animal which they infect. At least six trypanosomata that are 
pathogenic occur in mammals. Thus, the Trypanosoma evansi and the Trypanosoma 
brucei are the causes of very fatal diseases, known as surra and nagana among 
horses, mules, camels, buffaloes, and wild animals. Trypanosoma equiperdum is 
the cause of an exceedingly fatal disease of horses in Algiers and the Mediterranean 
coast, called "dourine" transmitted only by coitus. Trypanosoma equinum is 
also the cause of a fatal disease of horses in South America. Trypanosoma theileri, 
the largest of the known trypanosomata, is the cause of a serious cattle disease in 
South Africa. The most widely distributed is Trypanosoma lewisi, the parasite 
infecting rats. This particular variety is very common in the rats of the United 
States, and has been found in practically every city where search has been made 
for it. 

A trypanosoma consists of a leech-shaped, granular body from 13m to 25^ long 
and from 2/z to 4/* wide. This body contains a nucleus and a rod-shaped centre 
known as the centrosome, or micronucleus. Along one edge of the parasite, begin- 
ning at the centrosome, is a delicate, fringe-like membrane known as the undulating 
membrane, upon the outer edge of which is a single flagellum extending from 7/jl 
to lhjji beyond the anterior end of the parasite. In freshly drawn peripheral blood 
these parasites are seen to be in most active motion, progression being in the direc- 
tion of the flagellum. In hanging-drop preparation they live several days, and 
as long as fifty days if the slide be kept cold and moist. McNeal and Novy have 
succeeded in cultivating Trypanosoma lewisi and Trypanosoma brucei on a culture 
medium of agar and defibrinated rabbit's blood. This is the first instance in which 
animal parasites have been obtained in pure culture. 

Human trypanosomiasis is disseminated or conveyed and inoculated by the bites 
of suctorial flies and perhaps bed-bugs. The view that one species of fly only 
can act as host for a particular trypanosome is generally held, but is by no means 
established. Among the known transmitters of trypanosomiasis, of which our 
knowledge appears accurate, are the tsetse fly or Glossina palpalis for those of 
trypanosoma fever and sleeping sickness, and the Glossina morsitans for nagana 
and possibly human trypanosomiasis. 

The transmission is direct, or purely mechanical, that is, it is a direct inoculation 
without the parasite first going through a cycle of development in the fly. These 
flies become infective about thirty-four days after they feed upon an infected 
animal or man and remain so for about seventy-five days or longer. The fly 
which bites an infected individual, if it bites a healthy person at once, also 
transmits the disease. This statement of Bruce contradicts seemingly his state- 
ment as to infectivity only after thirty-four days. 

Prevention. — It having been proved that trypanosomiasis is due to a parasite 
infecting human beings and that the disease is transmitted by insects, it follows 
that cases known to be infected should if possible be isolated and protected from 
flies. Healthy persons should also be protected from flies, not only by the use of 
nettings, but by living, if possible, where flies are not numerous; on hillsides as far 
as possible from materials that aid in the breeding of flies. Wild game and domestic 
animals undoubtedly harbor the parasite and the latter should be protected from 



TRYPANOSOMIASIS 333 

flies. Indeed it has been proposed to attempt the extermination of all game in 
those parts of the world where trypanosomiasis is prevalent. 

Human Trypanosomiasis (Trypanosoma Fever). — The first reported case of 
trypanosoma in man was made by Nepveu, and his paper contains a fair drawing 
of the parasite. Forde, in 1901, described the parasite in the case of a European 
from the Gambia River Colony suffering from an atypical fever. Since that time 
Manson, Dutton, Todd, and others have reported cases, nearly all of them from 
the Congo and Gambia River district. Manson's case occurred in a woman aged 
forty years. The temperature ranged from 97° in the morning to 100° in the 
evening. The pulse was always rapid and feeble. Erythema was a constant 
feature in the case, and was first observed when the fever began. Edema was also 
present, and was most pronounced on the back and face. There was marked 
enlargement of the spleen. 

In many cases the history of an inflamed and painful insect bite can be 
obtained. 

In Dutton's case there was the history of the patient being bitten by a rat. 

The parasites are found free in the peripheral blood and never in the corpuscles. 
They are not numerous, varying from one to twenty in a cover preparation. 
They may be absent for days at a time. In the case reported by Manson 
experimental inoculation on animals was negative, showing the distinct nature 
of the parasite. 

The blood condition is interesting. There is a moderate degree of anemia in 
all cases and a marked increase in the large mononuclear leukocytes, running as 
high as 22 per cent. The increase in these cells seems rather constantly associated 
with sporozoal infection, just as metazoal parasitism is accompanied by eosinophilia. 

The clinical phenomena in the reported cases are chiefly these: In some cases 
the parasites occur in the blood without the patient manifesting any conspicuous 
symptoms. In other cases there is an irregular fever which may be high, continu- 
ous, or remittent in type. It does not yield to quinine. After persisting from three 
days to two or three weeks, it is followed by an apyretic interval. During the 
course of the fever large erythematous patches occur all over the body, associated 
with irregularly distributed areas of cutaneous edema. The edema and erythema 
may or may not coincide. The edema is most marked on the face, especially on 
the lower eyelids. The pulse is rapid and running, a peculiarity also observed in 
sleeping sickness. 

There is a diminution of intelligence followed by tremors, increasing mental 
hebetude and unsteady gait. Finally comes the third stage of subnormal tempera- 
ture and profound lethargy. The mortality is 100 per cent, unless the disease 
is treated fairly early by salvarsan or by atoxyl or sodium cacodylate. 

African Lethargy (Sleeping Sickness). — Sleeping sickness is a chronic disease 
characterized by increasing lethargy, and, after an exceedingly chronic course, 
death occurs from coma or from inanition — "a patient sleeping himself to death." 

Sleeping sickness is at present confined to tropical Africa, principally along the 
west coast. The northern limit of its extension is the Senegal River; the southern 
limit is the Portuguese Colony. It is common in Senegambia, along the Gold 
Coast, and at Old Calabar. It has existed for a long time in the basin of the Congo 
River from Stanley Falls, in the heart of equatorial Africa, to the lower Congo. 
It has recently extended from Victoria Nyanza to the head-waters of the Nile. 
In the last few years the disease has assumed epidemic proportions in Uganda 
and many thousands of the natives have perished. In the days of the slave traffic 
sleeping sickness was frequently carried to the West Indies, Southern United States, 
Brazil, and the Bahamas, but it never succeeded in establishing a foothold in any 
of these places. 

The older views that sleeping sickness is due to poisoning, intoxication, and 



334 DISEASES DUE TO A SPECIFIC INFECTION 

filaria have been superseded by the demonstration of a trypanosoma in the cere- 
brospinal fluid by Castellani, and the confirmation of this observation by Bruce 
and other members of the English Sleeping Sickness Commission, who have success- 
fully propagated the disease in monkeys. The trypanosoma of sleeping sickness 
is indistinguishable from that of trypanosoma fever, and, like the latter, is also 
. found in the blood. Apparently the advent of sleeping sickness in a patient having 
trypanosoma fever is determined by colonization of the parasites in the cerebro- 
spinal fluid. The exact relation of the hypnococcus, described by Castellani and 
other members of the Spanish Commission, as the cause of the disease is not as 
yet perfectly clear; apparently it is only a terminal infection. 

Sleeping sickness attacks persons of all ages and of every race. 

Pathology. — Mott has shown that the lesion of sleeping sickness is an extensive 
meningo-encephalomyelitis. In the cord and brain extensive round-cell infiltration 
is found about the capillary vessels. The cerebrospinal fluid is deeper in color 
than normal owing to the presence of numbers of red blood cells. Besides these, 
numerous leukocytes and the specific trypanosoma are found. In the latter stages 
of the disease there is some ground for believing that there is a concomitant — in 
a terminal sense — streptococcus (hypnococcus) infection. 

Symptoms. — The incubation period is variable, but always long. The natives 
believe that the disease may develop as long as seven years after exposure. As a 
matter of fact numerous instances are on record where the disease has appeared in 
negroes several years after leaving the endemic area and settling in other countries. 
It would appear, from the meagre knowledge of the parasite now available, 
that it may be found in the peripheral blood without producing any symptoms. 
The causes that determine colonization of the parasites in the cerebrospinal system 
are unknown. 

The disease sometimes begins with marked psychical prodromata, including 
epileptiform seizures, melancholia, and even transitory mania. In the larger number 
of cases there is headache, vertigo, puffiness of the face, and slight fever. At this 
point the lethargy begins. The patient at first is somnolent or stupid, but he can 
easily be roused for nourishment or to attend to the calls of nature. When so 
awakened his gait is staggering and the moment he is released he sinks into a deep 
sleep. In the early stages there are no evidences of paralysis, tremor, or convulsion. 
The patellar reflexes are decreased, sometimes abolished. Gradually the lethargy 
deepens until finally the patient can only be aroused with the greatest difficulty, 
if at all, and immediately falls again into a deep sleep. Partly from the disease 
itself, but largely because the lethargy prevents regular nourishment, nutrition 
fails, emaciation becomes progressively more marked, and bed-sores develop. 
Toward the close paralyses of various muscle groups develop, convulsions occur, 
and fatal coma supervenes. 

Diagnosis. — The symptoms are fairly characteristic, but a positive recognition of 
the diseased rendered easy by puncture of a gland, in the juice of which the parasite 
may be found. Glandular enlargement all over the body but particularly in the 
posterior cervical group is a very constant symptom, and persons suffering from 
such a state in an area known to be infected by sleeping sickness should be suspected 
and the contents of glands examined. In other instances a diagnosis may be 
reached by lumbar puncture, centrifugalization of the cerebrospinal fluid, and 
demonstration of the parasites by a microscopic examination of the sediment. 

Prognosis. — The course of the disease is chronic. Cases may last from three to 
four years, but rarely more than eighteen months. The prognosis is bad. 

Treatment. — The treatment of trypanosomiasis consists chiefly in the use of 
salvarsan or neosalvarsan (See Syphilis) or an arsenical preparation, called "atoxyl" 
or meta-arsenic-anilid. This drug is given hypodermically in 10 per cent, strength 
in normal saline solution. The first dose is 2 grains and this is increased every 



KALA-AZAR 335 

second day by half a grain, until as much as 15 grains are given or until some signs 
of toxemia from its use are produced. The signs consist in pain in the belly, pectoral 
cramps, slowness of the pulse and cold extremities. Notwithstanding its name, 
atoxyl also causes serious changes in the optic nerve and may cause blindness. 
For this reason and because it is more active, salvarsan is always to be used by 
preference if obtainable. Purging in the early stages does good and in some cases 
temporarily arrests or delays the disease. Massive doses of arsenic are of some 
service and should be used when atoxyl or salvarsan are not available. 

KALA-AZAR. 

Definition. — Kala-azar or Tropical Splenomegaly, sometimes called Dum Dum 
Fever, is a chronic infectious disease, characterized by long-continued remittent 
fever, extreme emaciation, profound anemia, marked enlargement of the liver 
and a characteristic pigmentation of the skin. It is almost invariably fatal. 

Much uncertainty has existed as to the nature of kala-azar, and our present 
knowledge rests largely upon the investigation of Leishman, who in 1903, showed 
that it is due to a parasite, the exact nature of which is yet uncertain. Some 
consider it a form of Trypanosome, others place it in the genus Herptomonas. 
The Leishmani donovani occur as small round or oval bodies, 2/z to 4/* in diam- 
eter, with a spherical nucleus and a rod-shaped chromatin body at right angles 
to it. In cultures they have a flagellated stage. The bodies are numerous in 
the spleen, liver, and bone-marrow and are also found in other organs and intes- 
tinal ulcers. They are occasionally found in the leukocytes of the peripheral 
blood, especially in advanced stages of the disease. The parasites are best obtained 
by puncture of the spleen or liver, spreads of the fluid .being stained by Giemsa's 
or Irishman's stain. These bodies have been found in persons suffering from 
kala-azar in India, the Egyptian Soudan, Algiers, and elsewhere. 

. There are at least two other types of Leishmani, the infantum and the tropica. 
Microscopically all three are identical. The infantum causes a disease similar 
to kala-azar but only in children under six years and especially in infants of one to 
two years, hence is known as infantile kala-azar. It has been found in Tunis and in 
Italy. The tropica causes a granulomatous lesion known as Oriental sore or Aleppo 
or Delhi boil. Wright, of Boston, discovered the parasite in this type of lesion. 

Donovan asserts that careful examination of the peripheral blood will give 
results in 93 per cent, of cases. 

Manson believes that the intermediate host of this parasite in some scavenger-fly 
which derives the parasite from the intestinal or other discharges of the patient 
and then infects the human being by a bite. There may be a sexual multiplication 
in the fly, but in the human host the parasite multiplies by fission, and Manson 
thinks that this multiplication is asexual. Rogers states that the bed-bug (Cimex 
rotundatus) is the disseminator of the disease. 

Pathology and Morbid Anatomy. — The autopsy in a case of kala-azar shows enor- 
mous enlargement of the spleen, which is firm and friable. The liver is also greatly 
enlarged and toughened in texture. The bone-marrow and the organs just named 
are crowded with the parasites. Leishman bodies can also be found in the 
lymphatic glands, the suprarenal capsules, in the testicles, and in the inflam- 
matory exudates in the pleura and peritoneum. The direct cause of death seems 
to be an associated dysentery or pneumonia. 

Mortality. — In certain parts of India the death rate is very high. Thus Rogers 
reports one district in which 54,179 deaths due to this malady occurred in ten years. 

Symptoms. — The symptoms in onset resemble those of malarial fever, being 
characterized by daily chills and fever, followed by free sweating, these symptoms 
recurring about the same time every afternoon. After a period of ten days or 



336 DISEASES DUE TO A SPECIFIC INFECTION 

two weeks these symptoms diminish and a period of remission occurs, followed after 
another period of ten days or two weeks by a return of the paroxysm. This may 
last for weeks or months. Occasionally the remissions already spoken of fail to 
occur, and profound inanition develops after some months. In still other cases 
the febrile movements are exceedingly irregular and varied. Enlargement of the 
liver and spleen begin early. The patient complains of languor, dyspnea, and the 
general manifestations of profound anemia. The constant symptoms are fever, 
enlargement of the liver and spleen, the progressive emaciation, and grave anemia. 
Treatment. — This consists in the use of salvarsan, neosalvarsan or atoxyl. (See 
Syphilis and Trypanosomiasis.) 

TROPICAL SORE. 

Aleppo Boil, Bouton d'Orient, Oriental Sore, Bagdad Sore is a sore or ulcer on 
the skin or mucous membrane due to the presence of the same parasite as kala- 
azar (Leishmani donovani). The sore has been met with outside of the Tropics, 
as on the shores of the Mediterranean Sea and even in America and Brazil. The 
sore is usually on an exposed part of the body and is supposed to be induced by the 
bite of some insect. The parasite is found in the sore with great ease. The lesion 
has a natural but slow tendency to heal, leaving a bad scar. Healing may be 
hurried by curetting, excision or by the application of powdered permanganate of 
potash followed in some days by a 10 per cent, solution of methylene blue. 

NEMATODES. 

Ascariasis. — Ascaris lumbricoides, or round worms, are found in the small 
intestine of man more commonly than any other parasite. 

They are not segmented as are the cestodes, but occur as smooth worms, not 
unlike an ordinary earth-worm, except that they are provided with small papillae 
or hairs. The worm also possesses longitudinal stria? and transverse rings, a mouth, 
and an anus. They are not hermaphroditic, but occur in the form of the male and 
female worm. 

They are met with far more frequently in children than in adults. The female 
worm is of a light brown, or red, color, and is usually about 10 to 20 cm. long and 
0.5 cm. thick. The male is about one-half the size of the female. 

How these worms gain access to the body is not known, although it may be by 
ingestion. While they most commonly are found in the small intestine, they 
occasionally find their way from the intestine into the stomach, and cases are on 
record in which they have wandered into the esophagus and mouth, and even into 
the nose and bronchial tubes. Cases have also been reported in which the migra- 
tion of a worm into the gall duct has produced obstruction, and still other 
instances are recorded in which they tiave found their way through an ulcer, or 
through a perforation in the appendix vermiformis, into the peritoneal cavity. 
As a rule they are present in the intestines in numbers and do not occur singly. 
In rare cases coiled, mottled masses of lumbricoids have caused intestinal 
obstruction. 

A form of round worm, somewhat like that found in man, is found in the intestine 
of cats and dogs; but it is considerably smaller in size and does not infest man. 

Symptoms. — The symptoms of the presence of this worm do not differ materially 
from those produced by the tapeworm (which see). Occasionally, however, this 
worm seems to have the power of producing an irritant poison which not only causes 
intestinal irritation, but when absorbed may cause great nervous irritation and 
apparently be responsible for convulsions in young children. 



NEMATODES 337 

Treatment. — The treatment of a patient suffering from Ascaris lumbricoides 
is abstinence from food for twelve or eighteen hours and the administration of 
1 drachm of the fluid extract of spigelia, or 2 drachms of the more old-fashioned, 
but efficacious, fluid extract of spigelia and senna. In other cases, 5 to 15 minims 
of the oil of chenopodium in capsule or emulsion, or on sugar, may be administered. 
In still other cases from 1 to 2 grains of santonin may be given in tablets or troches. 
All of these drugs should be followed by castor oil or a saline purge in order to 
sweep out the worms while they are poisoned by the drug. 

Oxyuris Vermicularis. — Under the name Oxyuris vermicularis or thread-worm, 
sometimes called pin-worm, a very small nematode worm exists in the rectum of 
young children and is sometimes found in adults. Occasionally it infests the entire 
colon. The length of the female is about 10 mm., and of the male about 4 mm. 
This worm may be present in great numbers without producing any symptoms 
whatever. Some irritation about the anus may be the only disturbance produced 
by their presence. 

Seat- worms are to be removed by the injection into the bowel of soap and water, 
which, after it is passed, is to be followed by a pint of warm water which has been 
medicated by boiling in it from J to 1 ounce of quassia chips. 

Trichina Spiralis. — A patient infected by the parasite known as the Trichina 
spiralis is said to suffer from trichiniasis. This parasite was first described by 
Owen in 1835. It was found in the flesh of the hog by Leidy in 1847, and in a 
human being by Zenker in 1860; the patient, a young girl, being thought to be a 
sufferer from enteric fever until at autopsy the parasites were found free in the 
bowel and encapsulated in the muscles. 

Etiology. — In practically every case the infection of a human being comes from 
eating the flesh of an infected hog. It is scarcely necessary to state that infection 
does not occur if the pork has been well cooked. 

The frequency with which the disease occurs is not known, but it is not as rare 
as some have thought. Williams found it present 27 times in 505 unselected 
autopsies in Buffalo, New York. 

If the muscle of a man infected by this parasite is examined, tiny little white 
or gray dots will be found upon its surface and through its texture; later the parasites 
encapsulate and look like deposits of calcareous material of about the size of miliary 
tubercles. If such a calcareous deposit be opened it may be found to contain the 
embryo of the parasite, or if the worm be dead a granular detritus only is present. 

When uncooked meat containing this parasite is swallowed, the digestive juices 
dissolve the capsule of the parasite, and in this way the embryos are set free in the 
stomach. Here they rapidly develop and become sexually mature in about seven 
days. The female parasite gives off an immense number of embryos, so that it is 
estimated that one parasite may throw off from one to two thousand young. These 
parasites soon find their way through the wall of the intestine, enter the lymph 
spaces, and so reach the circulation, by which they pass to the muscles. Their 
favorite position for settlement is the striated muscles. They enter the muscular 
connective tissue and then the sarcolemma, where they coil themselves and cause 
a disintegration of the contractile substance. Here they become encapsulated 
in about six weeks, partly by the inflammatory exudate which is produced by 
their presence, and partly by the calcareous material which they seem to have the 
power of collecting. In these capsules the parasite remains alive for a very long 
period of time, possibly for twenty-five years. Occasionally, however, it dies, 
and the entire mass undergoes calcification. 

When one of the domestic animals swallows meat infected in this way, the same 
process takes place in the muscles as occurs in the muscles of man. In the muscles 
of the hog the parasite may escape notice, as it often lacks the calcified capsule. 

Moreover, an infected hog may be in excellent health, 
22 



338 DISEASES DUE TO A SPECIFIC INFECTION 

Pathology and Morbid Anatomy. — The lesions of trichiniasis consist in gastro- 
intestinal irritation, overgrowth of the lymph nodes in the abdominal cavity, occa- 
sionally bronchopneumonia with great swelling of the bronchial glands, still more 
rarely fatty degeneration of the liver, and constantly a parasitic myositis due to 
the embryos invading the muscles. Almost every muscle of the body may be 
found infected; but where the number of trichinae is not very great, the muscles 
of the neck, the intercostal muscles, and the diaphragm seem to be the parts in 
which the greatest aggregations occur. Furthermore, the greatest number of 
trichinae are usually found near the insertions of the muscles. 

Symptoms. — The symptoms consist in muscular soreness and pain, and disinclina- 
tion to move. A diagnosis of muscular rheumatism is often made because of these 
symptoms. Headache, puffiness of the skin about the eyes and nose, and moderate 
fever are also present. Not rarely the symptoms may closely resemble those of 
typhoid fever, with great prostration and emaciation. For some unknown reason 
a marked leukocytosis develops, which is peculiar in the fact that the eosinophile 
corpuscles are chiefly increased. From investigations made by Opie it would 
appear probable that this eosinophilia is of some value from both a diagnostic 
and prognostic stand-point. The eosinophiles are not greatly increased, if the 
infection by trichinae is excessive, and their greatest development seems to occur 
at about the time that the embryonal trichinae are passing from the intestine by 
way of the lymphatics and blood to the muscular tissues — that is, during the third 
week after the ingestion of the trichinatous meat. 

Diagnosis. — In a suspected case the diagnosis may be reached by taking a small 
piece of muscle and examining it with a microscope. The stools of the patient 
should be flattened to a thin layer between two sheets of glass resting upon a black 
background, and then examined by means of a hand magnifying glass, when the 
parasite may be found as small, short, glistening, thread-like bodies. 

Prognosis. — The prognosis depends largely upon the severity of the infection. 
In the worst outbreaks the mortality may be as high as 70 per cent. Many cases 
recover by the end of a fortnight. Others remain ill for weeks or months before 
recovery takes place. 

Treatment. — There is no treatment which can be directed to the removal of the 
parasite after it has entered the muscles. The only thing the physician can do is 
to give a nutritious diet, and relieve pain or other symptoms by symptomatic 
remedies. If the discovery is made that the patient has swallowed trichinatous 
pork within a few hours, then 5 grains of thymol followed by a dose of sulphate 
of magnesium should be ordered, to kill the parasite and sweep it out of the 
intestines before it can migrate into the tissues. 

Uncinariasis (Ankylostomiasis). — Definition. — Uncinariasis is an infection by 
different varieties of worm of the uncinaria species; it occurs not only in man, but 
in many of the lower animals. The parasite is often called the Ankylostomum 
duodenale, or hook-worm. The chief symptoms are severe anemia, abdominal 
pains, asthenia without emaciation, and edema. The parasite was described as 
uncinaria by Froelich in 1789; Dubini, in 1843, gave it the name ankylostoma. 

The condition is also known as " brickmakers' anemia/' "Egyptian chlorosis," 
"miners' anemia," "miners' cachexia," "miners' disease," "Porto Rican anemia," 
"St. Gothard's tunnel disease," "tunnel disease," "tunnel anemia," "tropical 
chlorosis," and "hook-worm disease," besides a host of local names. It is one of 
the most ancient diseases known to man, for it was described by the Egyptians 
3500 years ago. 

Frequency. — Uncinariasis occurs in all the tropical and practically all the sub- 
tropical world. According to Thornton it is the greatest enemy of the human 
race in the tropics; greater even than plague or cholera. In portions of India 75 
per cent, of the population are said to be affected. In Egypt this worm is found 



NEMATODES 339 

at nearly every postmortem. It has been the most disabling of all diseases in the 
Egyptian army, as well as the greatest cause for the rejection of recruits. In 
Ceylon its ravages are said to be more serious than those of cholera. Harris has 
found it in Georgia and Florida, and believes it is the common cause of the severe 
anemias of the Southern United States that have hitherto been regarded as malarial. 
Stiles has also made very valuable studies of its characters and recurrence in the 
Southern United States. In Assam it is almost universal, 299 cases having been 
found in 300 postmortems. According to Alden, 22.5 per cent, of the total death 
rate of Porto Rico was ascribed to tropical anemia due to uncinaria, and Igaravidez, 
King and Ashford found that 90 per cent, of the peasants were infected, 300,000 
persons having less than 50 per cent, hemoglobin. In more temperate regions it 
has been found in nearly all our States as far north as New York. In the Cornwall 
and Westphalian mines the disability caused by this parasite has become so great 
as to threaten the existence of these industries. 

Etiology. — The uncinaria is a nematode worm of the family Strongylidce. It is 
very widely distributed in the animal world, in distinct species. In man two 
species are recognized, viz., Uncinaria duodenale (Dubini) and Necator americanus 
(Stiles), commonly spoken of as the old-world and the new-world uncinaria, or 
hook-worm. The two sexes are distinct; the male worm is from 8 to 10 mm. long 
and the female slightly longer, 10 to 18 mm. They are grayish-white in color, 
cylindrical in shape, with a contracted head, and in the female a broad caudal 
bursa. When male and female worms are present, as they usually are in the propor- 
tion of one male to three females, the female produces an enormous number of ova. 
When deposited in favorable surroundings these ova develop into embryos in 
twenty-four hours. The embryo grows rapidly, passing through two ecdyses in 
about five days. The second ecdysis is the termination of the extra-corporeal 
phase, and the embryo is now infective for man. When taken into its appropriate 
host the worm goes through three more ecdyses, making five in all; the fourth mark- 
ing the formation of a provisional buccal armature; the fifth, the appearance of the 
definite armature. It then reaches an adult or mature form in from five to six weeks. 

In by far the larger proportion of cases the infection takes place through 
the skin during or after the second ecdysis of the worm. Even exposure to infected 
mud for a few minutes may be followed by itching, redness, swelling and the develop- 
ment of papules which become vesicles and sometimes pustules. This state is 
called "ground itch." Very rarely the infection depends upon the ingestion of 
infected water or food and the accidental ingestion of infected earth from soiled 
hands. There is no doubt that geophagy in infected areas is a common manner 
of taking the disease; but it is also true that this habit does not show itself, in many 
cases, until the disease is fully developed. In these cases it seems clear that the 
earthy matter is eaten in obedience to an instinctive craving, and that it brings 
relief by mechanically loosening a number of the parasites. 

Prophylaxis. — Prophylaxis of uncinariasis demands the exclusion of all infected 
persons from earth- workings. Where large bands of laborers are collected in 
districts in which the disease is prevalent, in mines, in tunnels, and in excavations 
of all kinds, systematic examination of all cases of anemia should be made. Defeca- 
tion in the workings or tunnels should be rigorously prohibited. Water-tight 
latrines should be provided, and the contents rendered harmless by a cheap disin- 
fectant. In the Arlberg tunnels the pail system was used with good effect. 
Personal prophylaxis should include careful washing of the hands before eating, 
and the wearing of sound shoes when working in suspected soils. 

Pathology and Morbid Anatomy. — Postmortem the subcutaneous fat, the pannic- 
ulus adiposus, and the mesenteric fat are fairly well preserved. The parasites 
are found in the jejunum, still attached to the bowel wall if the section is early, or 
free in the intestinal contents if the section is delayed. They vary in number 



340 



DISEASES DUE TO A SPECIFIC INFECTION 



Fig. 64 



from 100 to 600 or more. "The jejunum is covered with old and recent pinhead, 
bloody extravasations. The bowel is thickened in spots, and there may be small 

cavities in the bowel wall filled with blood and con- 
taining the heads of one or two parasites. The liver 
and kidneys commonly show some degree of fatty 
degeneration. The cause of the anemia is probably 
twofold — the mechanical abstraction of a consider- 
able amount of blood by the parasites, and a hemo- 
lytic effect from a toxin elaborated by the worm. 
That hemolysis occurs is indicated by increased 
iron in the liver, the occurrence of hematoidin in 
the liver and kidneys, as well as free iron in the 
stools. The spleen is shrunken. 

The blood shows the ordinary changes similar to 
those observed in pernicious anemia. In early cases 
the color-index may be low, the loss of hemoglobin 
being more rapid at first than the red-cell loss. The 
actual hemoglobin is often remarkably low, reaching 
8 per cent., 15 per cent, being commonly found. 
As the case advances, however, the hemoglobin 
index rises and may be plus. Megaloblasts are not 
seen in as large numbers as in other pernicious ane- 
mias. There is no marked leukocytosis; there is, 
however, a fairly constant relative increase in the 
eosinophiles, ranging from 3 to 30 per cent., and 
Ashford and King of the United States Army have 
shown that a rise in the number of eosinophiles is of 
favorable omen. A low eosinophile count in severe 
cases is an evil sign. 

The feces contain the ova. They also contain 
considerable blood, in which differential staining 
will demonstrate a great many eosinophiles, showing 
that there is not only a general increase in these 
cells in the circulation, but that there is an active 
determination of them to the intestinal lesions. 
Charcot-Leyden crystals are constantly present. 

Symptoms. — The symptoms vary with the number 
of parasites in the intestines and with the general 
condition of the patient. Recent observations seem 

to make it clear that the new- 
world hook-worm is not nearly 
so fatal as the old-world hook- 
worm. If there be but a few 
worms, the general symptoms 
produced are very mild. If, on 
the other hand, the worms run 
up into the hundreds or thou- 
sands, the blood destruction is 
extensive. In conditions of great 
., , , A , , , , , , , , . , deterioration, in the half-starved 

Male oi Ankylostoma duodctiale: a, head; b, esophagus; „, • i i • 

c, gut ; d, anal glands ; e, cervical glands ; /, skin ; g, muscular Or lll-llOlirished, 111 acute Or chronic 

layer; h, excretory pore; i, tri-Iobed bursa; k, ribs of bursa; I, dysentery, the presence of Only a 

seminal duct; m, vesicula seminalis; n, ductus ejaculatorius; e f +1^™ nflr r,oit P o mflV an + nc . 

o, its groove; p, penis; g, penile sheath. Magnification, lew Ot tJiese parasites may act as 

20. (After Schuithess, from ziegier.) a very dangerous complication. 




NEMATODES 



341 



In well-developed cases the symptoms are those of pernicious anemia. The 
principal phenomena are dyspeptic symptoms with colicky pains in the early stages, 
followed by progressive anemia with little or no emaciation, and with terminal 
edema. The pain in uncinariasis is colicky in character, is one of the earliest symp- 
toms, and is fairly constant throughout, the disease. In cases in which only a few 
parasites are present, it may amount only to uneasiness; when there are many, it 
may be severe. Like all abdominal pains due to intestinal parasites it is relieved 
by food for the time being. The appetite is very variable; it may be voracious 
or it may be diminished, and curious perversions of taste, such as earth-eating, 
may develop. 

Fig. 65 




I i i ' i [ i i jSE 



TZC 



I 



10. fo 



' ! ' ' Ej S g 



I I I I I I I III 



I ! I 



C.h 



Ova and embryo of Uncinaria americana: a, unicellular ovum; 6, c, d, e, ova showing various stages 
of segmentation; /, g, ova containing larval uncinarise; h, peculiarly shaped ovum; i, larval worm just 
emerged from shell; j, larva extended after emergence. (Stiles.) 



Following the development of the colic, anemia appears and rapidly becomes 
profound. There is very little wasting, the subcutaneous fat being fairly well 
preserved. The shin is a lemon-white color; the conjunctivae and lips are exsan- 
guinated; the scleras pearly or muddy-white. All the subjective phenomena of 
profound anemia become marked. There is lassitude, breathlessness on the slightest 
exertion, vertigo, and occasionally dimness of vision from retinal hemorrhages. 
Crises of fever occur that may last for days or weeks. Auscultation over the precor- 
dial area reveals soft hemic bruits, propagated to a remarkable distance into the 
great vessels. The face and ankles become puffy, and there may be a slight general 
edema. Harris has reported a case of uncinariasis with symptoms resembling 
pellagra. When the disease attacks children before the age of puberty, bodily 
and mental growths are stunted. The pubic hair, the axillary hair, and the hair 
on the face is scanty or absent, the limbs are thin and undeveloped, and the children 
are markedly pot-bellied. Stiles describes a fish-like, staring expression of the 
eyes in these cases. 

Diagnosis. — The diagnosis is easy, once the attention is directed to the intestinal 
parasites. The occupation of the patient, if it be one that predicates working 
in earth, is very suggestive. The anemia is very commonly diagnosticated as 
malarial. There really is no diagnostic difficulty between malarial anemia and 
the parasitic anemia. This very common error has been made because, in the 
intensely malarial regions, the existence of this parasite has not been generally 



342 



DISEASES DUE TO A SPECIFIC INFECTION 



known. The disease has also been mistaken for beriberi, but there is a complete 
absence of paralytic symptoms in uncinariasis. 

A diagnostic sign is the occurrence of triangular black or bluish patches on the 
dorsum of the tongue, looking as though a pen had been wiped on it. This 
appearance is quite striking. It is very constant, and appears early, even before 
the advent of pronounced anemia, and persists to the end of the disease. 

The diagnosis is definitely made by the demonstration of the ova or parasites 
in the feces. Search should be made in as fresh specimens as possible, to avoid 
confusion in case embryos have occurred and quitted the ova. A small amount 
of the material is placed on a large glass slide diluted with distilled water, and 
pressed down with a thick cover. The ova of uncinaria are very striking bodies. 
They are clear, transparent, light gray in color; they have a delicate, transparent 
capsule, containing in its centre from one to six gray yolk segments with granular 
nuclei. In shape, they are regularly oval, with an average length of 60 microns and 
an average width of 35 microns. Leichtenstern has found as many as 4,216,930 ova 
in a single stool. Care must be taken not to mistake the egg of the Ascaris lumbri- 
coides for the egg of the uncinaria. The former have a thick, gelatinous, often 
mammillated covering, and unsegmented protoplasm. So, too, the egg of the 
Oxyuris wrmicularis, which is a thin, symmetrical shell, one side of which is almost 
straight and which contains an embryo, may be mistaken for the ova of the uncin- 
aria. The egg of the whip-worm, Trichocephalus dispar, possesses a smooth, 
thick shell, apparently perforated at each end, with unsegmented protoplasm. 



Fig. 66 




trlO 



2 3 

bOSES OF THYMOL 



Boycott's chart showing results of treatment with thymol in ankylostomiasis. 



Stiles has well described a rapid and effective test, where microscopic evidence 
cannot be obtained. The stool is placed on ordinary white blotting-paper, and 
allowed to stand for one hour. A rusty-red discoloration or stain develops along 
the edge of moisture, resembling somewhat that due to the presence of blood, and 
indicates the probable presence of uncinaria. Stiles directs that if uncinariasis is 
suspected, and it is not practicable either to make a microscopic examination or to 
delay matters until a specimen can be sent away for examination, still another 
method of diagnosis is possible. Give a small dose of thymol, followed by Rochelle 
salts, and collect all of the stools passed. Wash the stools thoroughly several times 



NEMATODES 343 

in a bucket, and examine the sediment for worms about half an inch long, about 
as thick as a hairpin or hatpin, and with one end curved back to form a hook. 

Treatment. — In the treatment of uncinariasis there are two drugs of value: male 
fern and thymol. Of the two the more effective is thymol or its derivative, thymol 
urethane (thymol carbonic ether). Thymol should be given in capsule, or in 
emulsion with acacia, in the dose of 30 grains repeated in two hours to a strong adult. 
In these doses the drug occasionally causes vertigo, excitement, and smoky urine. 
For one or two days prior to the administration of the remedy patients should be 
put on liquid diet and given a brisk saline purge the night before. It is best to 
restrict the quantity of food. In administering thymol, it is essential that none of 
the solvents of the drug be given either with it or immediately after. Several 
cases of poisoning have occurred when alcohol or alcoholic drinks have been given 
with, or closely after, a dose of thymol. Similarly, ether, chloroform, glycerin, and 
most oils act as solvents, and may cause severe toxic symptoms owing to the absorp- 
tion of the drug in bulk. In order to prevent poisoning, therefore, thymol should 
be followed by a saline purge, and castor oil should not be used. Weekly examina- 
tions of the stools should be made, and as long as ova or Charcot-Leyden crystals 
are found the use of this remedy must be repeated. Sometimes thymol is vomited, 
and in rare cases proves inactive. In these the male fern should be adminis- 
tered the the usual way, or beta-naphtol, 30 grains at a dose, or eucalyptus oil 
employed. After the expulsion of the worm, the therapeutic indications are the 
same as for advanced anemia from any other cause. Ashford showed that by the 
use of thymol in Porto Rico 90 per cent, of 300,000 infected persons were cured 
at a cost of 60 cents apiece (Fig. 66). 

Filariasis (Filaria Sanguinis Hominis). — Definition and History. — The group of 
Filar ice includes a number of species. The human parasite was first discovered by 
Demarquai in 1863 in a chylocele and demonstrated in the peripheral circulation 
by Lewis in 1872. The principal varieties affecting man are the following: Filaria 
nocturna, Filaria diurna, Filaria perstans, Filaria demarquaii, Filaria ozzardi, 
Filaria magalhaesi, and Filaria loa. Of this group the Filaria nocturna and the 
Filaria loa are the only ones known to cause definite pathological conditions. 

The geographical distribution of the Filaria nocturna is very extensive. It is 
found in all tropical and in most subtropical countries. Its southerly limit of 
observation is Brisbane. In the United States it has been found in Alabama, 
Louisiana, South Carolina, Pennsylvania, Illinois, and New York. In the Samoan 
Islands from 10 per cent, to 50 per cent, of the inhabitants are said to be infected, 
and in the Friendly Islands 32 per cent. In Porto Rico the native troops showed 
12 per cent., and small communities may have as high as 70 per cent, of the total 
population infected. 

Filaria Nocturna. — This parasite has two corporeal and one extracorporeal 
phase. First, the parent worm, whose normal habitat is the lymphatic system; 
second, the embryo found in the circulating blood, and third, the intermediary 
stage in the body of the mosquito, which has been definitely shown to be the inter- 
mediary host for this parasite. When examined in a drop of peripheral blood the 
embryonic form is found as a minute transparent worm, one-eightieth of an inch 
in length and about the diameter of a red blood corpuscle. It has a transparent 
sheath, or sac, somewhat longer than the body of the embryo, and is usually present 
in very great numbers. 

The most striking cahracteristic of this filaria is the periodicity of its appearance. 
They are found only at night in the peripheral circulation, hence the name Filaria 
nocturna. In the daytime they entirely disappear and retire to the larger vessels, 
particularly the vessels of the lungs. The periodicity may be reversed by causing 
the patient to sleep in the daytime, when, after a few days, the embryos are found 
in the peripheral blood during the day and are absent at night. 



344 DISEASES DUE TO A SPECIFIC INFECTION 

The microscopic demonstration of the worm is easy. The blood should be 
drawn near midnight, when the parasites are most numerous. A large drop of 
blood should be taken and a thick, coarse spread made. The slides are dried in 
air without covers, or, if it is desired to study the parasite in motion, the blood drop 
is covered with a cover-slip and ringed with vaselin. In such a preparation the 
filaria retains its motility for days. The worms are quite large; an inch objective 
will be ample for the search and demonstration. 

As already stated the mosquito is the intermediary host. When a mosquito 
sucks the blood of a patient containing filarise the parasites escape from their 
sheath while the blood is still in the stomach of the insect. Thence they pass to 
the thoracic muscles. In this location, in from six to seven days, the metamorphosis 
from embryo to the young of the adult form takes place. The minute filarise 
migrate to the proboscis and are found lying in pairs in the labia, whence they are 
undoubtedly carried into the circulation of the first warm-blooded animal bitten 
by the insect. The possibility of the filarise being passed into water when the mos- 
quito lays her eggs, and being carried thence into the stomach in drinking water, 
is also to be remembered. Female mosquitoes, both of the culex and anopheles 
species, are capable of acting as the intermediary host. 

The adult form of the parasite, commonly known as the Filaria bancrofti, is a 
long, delicate, nematode worm. It is from three to four inches in length and the 
thickness of a coarse hair or bristle. The sexes are distinct. The habitat of the 
parent worm is the lymphatic system, commonly the thoracic duct, although any 
portion of the peripheral lymphatics may be invaded. There may be only one 
worm of each sex or there may be many. 

The Filaria diurna presents minor differences in structure and occurrence from 
the Filaria nocturna. The chief difference is that it is found in the peripheral 
circulation only in the daytime. It is supposed that the Filaria diurna is the 
embryonic form of the Filaria loa. Nothing is known of its pathological significance. 

The .Filaria perstans is common in certain districts of West Africa, where it 
occurs in as much as 50 per cent, of the population. This parasite is found in the 
peripheral circulation at all times, day and night; hence its name. The pathological 
significance of this filaria is unknown. It was for a time supposed to be the cause 
of sleeping sickness, and was also found very commonly in association with craw- 
craw, an itching, pustular affection of the skin. 

Pathology and Morbid Anatomy. — Filariasis causes no symptoms in the large 
majority of cases. The embryos are innocuous. When symptoms develop they 
are due to the parent worm or an immature product of the parent worm. The 
lesions produced are divided into two broad classes, namely, those which are due 
to lymphatic varix from stasis, and those due to edema from lymphatic obstruction. 
The parent worms, when present in numbers, may mechanically plug the thoracic 
duct or one of the larger lymphatic trunks. They may also initiate a lymphangitis, 
with thickening and occlusion of the lymphatics. Under either circumstance, 
stasis and retrograde movement of the lymph current are inaugurated and eventu- 
ally a compensatory lymph circulation is established. The result is engorgement 
of some portion of the lymphatic system and the development of a peculiar group 
of phenomena: lymph scrotum, lymphatic groin glands, varices of the pelvic or 
lumbar lymphatic trunks or of the lymphatics of the bladder, ureter, or kidney. 
As these varicosities grow, they become more extensive, and rupture. If the 
rupture be in the genito-urinary tracts, chyluria develops; if into the tunica vagi- 
nalis, a chylocele; if into the abdominal cavity, chylous ascites. These are the 
lesions due to lymph stasis and lymphatic varices. 

In the second group the lymph stasis is associated with lymphangitis followed 
by obstruction, resulting in the formation of the peculiar solid edema and the huge 
hypertrophies of the affected tissues known as elephantiasis. 



NEMATODES 345 

The majority of cases of elephantiasis are clearly due to filarial disease. The 
geographical distribution of elephantiasis and filariasis are identical; elephantiasis 
is most common in the areas most severely affected by filaria. Lymphatic varix 
and lymph scrotum are not only found in the same districts as elephantiasis, but 
very commonly terminate in elephantiasis. The disease is also seen in cases of 
operative removal of lymphatic varices. In a large number of these cases the 
embryo filarial cannot be demonstrated in the peripheral circulation. This is due 
to the fact that the parent female worm lies in the centre of the inflamed tissue and 
because the embryos cannot pass through the occluded portion of the lymphatic 
circulation. Manson's theory as to the direct causation of elephantiasis is that 
the parent female worm migrates to one of the peripheral trunks. While in this 
position she receives an injury which is followed by premature parturition and the 
expulsion of ova instead of embryos. These ova are Hve times the diameter of the 
embryos, so that although the embryos pass freely through the finer lymphatic 
radicles the ova block up the smaller lymph channels, forming minute emboli. 

Following this stage of embolism, lymphangitis with inflammatory thickening 
occurs. When the inflammatory process subsides the deposit is in small part 
absorbed, but when the inflammation recurs an additional deposit is added to the 
remnant of the first. This occurs with the commonly observed clinical history 
of elephantiasis, which advances by crises of inflammation and a general symptom- 
complex known as elephantoid fever. 

As already stated, filariasis may occur without any symptoms being present 
until the lesions just described develop. 

Symptoms. — Elephantiasis. — The most common location of elephantiasis is in 
the legs; next in the scrotum of the male and the labia of the female. It occurs 
in the breast, in the arms, and as interstitial or pedunculated masses in other parts 
of the body. These tumors occasionally grow to enormous dimensions. A scrotal 
tumor of 50 pounds is not at all uncommon, and one has been reported weighing 
224 pounds. These large tumors develop as described with elephantoid fever. 
With each crisis of fever and lymphangitis there is not only an increase in the size 
of the area already affected, but an extension into new territory. 

Elephantoid fever is the systemic expression of the lymphangitis originating in 
filarial varices or in tissues already the seat of elephantiasis. The attacks recur 
at varying intervals of weeks or months. Exciting causes may be slight traumatism 
such as friction of the clothing over the occluded lymph channels. The attack 
begins with rigor and high fever, with all the usual manifestations of febrile disturb- 
ance, as anorexia, nausea, and, in severe cases, delirium. The skin over the inflamed 
lymphatic area is hot, tense, and red, with a marked degree of inflammatory thicken- 
ing. After persisting a few days, the attack ends in a critical sweat. The inflamma- 
tory thickening remains. The attack may be so intense as to result in the formation 
of abscess. When this takes place in superficial lesions, the condition is readily 
recognized and the treatment is obvious. When it occurs in the deeper varices, 
as in the pelvis or loin, there will be deep-seated pain, tenderness, and rapidly 
developing sepsis. 

Hematochyluria is usually paroxysmal and is due to the leakage of chyle into 
some portion of the genito-urinary tract. The common location of the leak is 
in the lymphatics surrounding the pelvis of the kidneys or the lymphatics of the 
bladder. The appearance of chyle in the urine is intermittent and is not accom- 
panied by any increase of symptoms. The urine is opaque and varies in color 
from a milky-white to a deep red in proportion to the amount of blood that may 
be mixed with the chyle. Chylous urine coagulates on standing into a soft, jelly- 
like clot. In a few hours the clot contracts and forms a firm, white ball floating 
in a milky fluid. Microscopically, the urine contains fat, blood cells in varying 
amount, and occasionally embryo filaria. Chyluria may persist for many years 



346 DISEASES DUE TO A SPECIFIC INFECTION 

without great deterioration of health. The only symptoms may be a dull pain in 
the loins or pelvis. Osier reports a case of intermittent chyluria which persisted 
for eighteen years without any special discomfort. When chyle escapes in large 
quantities, clots are occasionally formed in the bladder and may cause urinary 
retention. Medical treatment is of no avail in this condition, but the patient 
should be put at rest on dry diet, with as great restriction as possible in the fatty 
elements of his food. Under this regimen the amount of chyle may be notably 
diminished. 

Varicose groin glands is a varicose condition of the superficial and deep inguinal 
lymphatics, and it is usually bilateral. It gives rise to doughy, soft, painless 
swellings in both groins. They cause little trouble until lymphangitis develops, 
when they may become very painful. They have been mistaken for the buboes 
of plague, and are commonly mistaken for hernia. 

Lymph Scrotum. — In this condition the filarial varix is situated in the lymphatics 
of the scrotum and is usually bilateral. It may be associated with the enlargement 
of the groin glands, and, like that state, it is prone to accessions of lymphangitis. 
When the deeper lymphatics are involved, the lymphangitis may extend to the 
testicle, forming what is known as filarial orchitis. 

Treatment. — The treatment of these conditions is surgical. When the tumors 
become so large as to be a burden to the patient, or when the inflammatory symp- 
toms cause great pain, their removal should be undertaken. The removal of an 
enormous scrotum or the amputation of a gigantic limb may be done to rid the 
patient of a drag that has, by its sheer weight, anchored him to his bed or chair 
for years. These growths may be removed with comparatively little risk. All 
surgical treatment in filarial disease must be regarded as palliative unless the parent 
female worm is included in the excised tissues, when the cure will be a definite one. 

As far as any plan of treatment aimed at the destruction of this parasite, adult 
or embryo, is concerned, there is no remedy of even the slightest value. During 
the attacks of filarial or elephantoid fever the affected part should be elevated, 
cooling lotions should be applied, and the patient freely purged. After the acute 
symptoms subside elastic bandages should be tried, and frequently give great relief. 

In countries where filarial diseases are common segregation is impracticable, 
but the danger of dissemination would be greatly lessened if patients harboring 
the parasites would so live as to avoid mosquitoes; such precautions might be 
advisable for sporadic cases in countries wherein filariasis is only occasionally 
introduced. 

Guinea-worm Disease (Dracontiasis). — Definition. — Guinea worm is sometimes 
called Dracunculus medinensis, or Medina worm. 

Distribution. — This parasite is distributed throughout the tropics. It was known 
in medicine long before the Christian era, and there is some reason for believing 
that the Biblical mention of the serpents affecting the Israelites near the Red Sea 
were these parasites. Though very widely distributed, the infection occurs in 
sharply defined areas. It exists on the west coast of Africa, particularly on the 
Gold Coast, in Abyssinia, Southern Egypt, and the Soudan. In Asia it occurs 
along the Caspian Sea, the Gulf of Persia, and in some sections of British India. 
It was common enough in the West Indies and Tropical America during the days 
of the slave trade; but seems to have established a permanent hold only in a few 
South American Islands and in isolated spots in Brazil. In the United States this 
parasite is encountered from time to time in imported cases, although at least three 
cases have been recorded in persons who had never lived in or visited tropical 
regions. Thus, Van Harlingen reports it as occurring in a case of a man who had 
never lived outside of Philadelphia; Jarvis, in the case of a man who lived at Fortress 
Monroe, Va., for thirty years; and Walker, in a case from Georgia. 

The Dracunculus medinensis is a nematode worm. We have definite knowledge 



NEMATODES 347 

of the female only. The adult female worm is cylindrical in form, from 60 to 
80 cm. in average length and about 2 mm. in thickness. The head of the worm is 
blunt, with a triangular mouth and eight papillae. The tail is tapered and recurvated 
ventrally. The vascular tube and alimentary canal extend as straight canals the 
length of the worm, ending as blind pouches. 

Charles found in the mesentery of a cadaver two female guinea worms in con- 
jugation with two smaller worms. These worms were about 4 cm. long and attached 
to the females, which were quite small, about 14 cm. from the head end. It is 
assumed that these were males. In the adult female the uterus occupies almost 
the entire body and is filled with myriads of tightly-coiled embryos averaging 0.6 
mm. in length. 

Fedschenko and Manson have shown that the intermediate host of the guinea 
worm is a minute water flea (Cyclops quadricornis) . The recently escaped embryos 
penetrate the cyclops, in which they pass through one stage of larval development 
lasting about six weeks. 

It is assumed that infection occurs through swallowing the cyclops itself or the 
larva in drinking water. While this intermediate stage in cyclops is the usual 
history, Plehn has shown, experimentally, in monkeys, that direct infection by the 
embryos may also take place. 

Negroes and the laboring classes are more frequently attacked than others, 
and usually, in each small area, the infected well or spring may be identified. The 
greater number of cases occur at the close of the heavy rains, probably because these 
conditions are then more favorable to the development of cyclops. 

The worm is taken into the body through the stomach. The males and females 
probably pass through the intestine to the mesentery, where conjugation takes 
place.. The male dies and becomes calcified or absorbed and the female migrates 
in the connective tissue of the host. In these migrations she usually tends toward 
the lower extremity and appears in the foot or the leg, although she may appear 
in the subcutaneous tissues of the trunk, arm, or even the head. When the sub- 
cutaneous tissue is reached complete development takes place, and when the 
embryos are ready for expulsion a small boil or vesicle forms, which bursts and 
leaves a small sinus leading down to the head of the worm. The period of incuba- 
tion from the ingestion of the embryo to the appearance of the adult embryo- 
bearing female in the subcutaneous tissue is about one year. The migrations of 
the worm are not attended by pain or any other symptoms. 

Symptoms. — At the time of development of the vesicle or boil there may be some 
slight febrile disturbance, and there is slight pain from the local irritation and 
inflammation. The rupture of the vesicle leaves a flattened, shallow ulcer, at the 
bottom of which is a small opening. At this opening the head of the worm may 
appear. If the ulcer be douched or sprayed with cold water a small quantity of a 
milky fluid exudes from the orifice, or the uterus of the worm may be protruded as a 
delicate tube which is seen to fill up and suddenly empty itself of a few drops of 
milky fluid which, examined microscopically, contains myriads of embryos. Usu- 
ally when parturition is completed, or nearly so, the worm spontaneously leaves 
her host. In a case reported by Francis, in which five worms were observed in 
the feet, one complete worm containing its embryos and measuring twenty-six 
inches was passed in about half an hour. Usually a much longer period is required 
(fifteen or twenty days) before the worm emerges. Exceptionally, parturition 
being completed, the worm dies, becomes encysted, and can be felt as a firm, 
fibrous cord under the skin. 

Treatment. — The older method, and the popular one with the natives, is to 
grasp the presenting head of the worm, fix it to a smooth stick, and gradually wind 
her out by twisting out a few inches every day. By this method the worm may 
easily be torn and a swarm of embryos liberated in the subcutaneous tissues. In 



348 DISEASES DUE TO A SPECIFIC INFECTION 

the case reported by Francis, a temperature, with morning and evening variation 
between 98.8° and 104.5° lasting several days, occurred after rupture and retraction 
of a worm. These accidents have occasioned severe infections, resulting in death. 
Manson advises douching with cold water, application of a cold pack or cold baths 
to hasten expulsion of the embryos and the spontaneous emergence of the worm. 
Massage and electricity have been used with success. The best methods of treat- 
ment we owe to the suggestion of Emily. He advises injection of 0.1 per cent, 
solution of mercuric chloride into the head of the worm or into the swelling. This 
solution causes death of the worm, which may then be easily extracted. Similarly, 
Aoulkes advises injection of alcohol, and Tufnel, pure carbolic acid. 

Prophylaxis consists in careful filtration or sterilization of drinking water. 

Strongyloides Intestinalis. — Definition. — Strongyloides stercoralis is a nematode 
worm infecting the intestinal canal. When present in large numbers it causes a 
chronic diarrhea, with anemia and emaciation. 

Distribution. — This parasite is widely distributed throughout the tropical and 
subtropical countries. It is extremely common in Cochin China, where it is 
supposed to be the cause of the severe diarrhea of that country known as Cochin- 
China diarrhea. Powell has found it in India, in 15 out of 20 cases of anemia. 
It has been observed in Martinique, Sicily, Egypt, India, Porto Rico, and the 
Philippine Islands. In Italy, Germany, Brazil, and California it has been fre- 
quently observed in association with uncinaria. It was first reported in the United 
States by Thayer, and is now known to be fairly common in all our Southern 
States. 

Much confusion has arisen over the various nematode worms resembling this 
parasite. These are now believed by the majority of observers to represent mor- 
phological variations of the same worm. The following classification is given by 
M. L. Price: 

1. The rhabditiform embryo, formerly known as Anguillula stercoralis, found 
in the fresh stools, is a slender, active nematode worm, 0.3 mm. long and 0.04 mm 
broad. 

2. Filariform embryo found in the stools after standing one or two days, and sup- 
posed to develop from the rhabditiform embryos. The embryo is twice as long 
as the preceding form, and is also actively motile. 

3. The sexually differentiated form, Rhabditis stercoralis, which may be developed 
from the preceding in five days. The male is a fine nematode worm 0.7 mm. in 
length, the female 1 mm. in length, which, when cultivated extracorporeally, 
produces filariform embryos. Finally there is: 

4. The parthenogenetic mother-worm, Anguillula intestinalis, found in the 
intestinal canal at autopsy. A slender worm, 2 mm. in length, easily recognized 
by the string of five or six eggs in the centre of the body. Infection probably 
takes place by the ingestion of the filariform embryo in water or on uncooked 
vegetables. Leichtenstern has experimentally shown the incubation period to 
be seventeen days. 

Later researches have disproved much of the pathological importance previously 
attached to this parasite. It is a mistake, however, to say that the worm has no 
clinical significance. The principal symptom is a continuous diarrhea, without 
pain or temperature disturbance. Secondarily, intestinal indigestion develops 
and nutrition is very much lowered. As a consequence, there is anemia and toasting. 
Blood examination shows an ordinary anemia and, in marked contrast with other 
verminous anemias, shows neither leukocytosis nor eosinophilia. 

Treatment. — Thymol, given fasting, in the same manner as for uncinariasis, 
is the best remedy for expulsion of strongyloides. If, for any reason, thymol 
should fail or if it should be rejected, or the patient show any intolerance to the 
drug, male fern should be used in large doses. 



NEMATODES 



349 



Trichocephalus Dispar. — The Trichocephalus dispar, sometimes called a "whip- 
worm," is occasionally found in the intestinal canal of man. The male and female 
worms are about equal in size. The male is usually coiled in a spiral form, but 
the female is nearly straight. The posterior portion of the body is thicker than 



Fig. 67 




A, Egg of Cochiu-China diarrhea worm (Strongyloides stercoralis) found in stools. B, Rhabditiform 
embryo of same, from the stools. C, Filariform larva of same derived, by direct transfoimation, from a 
rhabditiform embryo. The figures were drawn from life, as seen under Leitz, objective 7, ocular 3. 
Bulletin of the United States Marine Hospital Service, No. 10, 1903. (After Thayer.) 



the anterior part, and by the slim anterior filament the parasite embeds itself 
in the mucous membrane of the intestine. This parasite is not common in the 
United States, but is frequently observed in France and Southern Italy. Its 
chief area of development is in the cecum, and more than one worm is usually 



350 DISEASES DUE TO A SPECIFIC INFECTION 

present. Sometimes very large numbers are found. It is supposed to possess 
no pathological significance and to be incapable of producing serious symptoms, 
but some writers have claimed that it may cause diarrhea and anemia of a serious 
character. 

CESTODES OR TAPEWORMS. 

Tapeworms are very frequently found in the intestinal canal of man. As their 
name indicates, they are flat, broad, white parasites, which consist of segments, 
each of which is rectangular in shape, but somewhat elongated. Each of these 
segments represents a single individual. From the head the segments just named 
develop. The technical name for the head and neck is the "scolex," and for the 
segment "proglottis." By means of the head the worm is attached to the mucous 
membrane of the intestine, but there is no mouth in the sense that an opening 
exists which communicates with an intestinal canal. Each segment of the worm 
is hermaphroditic; that is to say, each segment contains male and female organs 
of reproduction. 

There are several varieties of tapeworms. The most frequently found are the 
Tenia mediocanellata, sometimes called the Tenia saginata, or unarmed tapeworm, 
or beef -worm, the Tenia solium (pork-worm), and the Tenia echinococcus. Less 
common forms are the Dibothriocephalus latus, or Russian tapeworm, derived 
from eating infected fish; the Tenia nana, the Tenia confusa, and the "double- 
pored dog tapeworm," Dipylidium caninum. The Tenia nana is sometimes 
called the Hymenolepis nana, or dwarf tapeworm. 

The Tenia solium usually gains its entrance into the intestinal canal of man 
by the ingestion of imperfectly cooked pork, the Tenia mediocanellata by the eating 
of uncooked beef, and the Tenia echinococcus by the ingestion of food which has 
been fouled by the excrement of the dog. 

All tapeworms pass through three stages of existence. The segments of the 
worm give off eggs which are discharged from the intestinal canal of the host, 
enter the alimentary canal of some animal, and are hatched out as parasites which 
pass through the wall of the intestine, gain a place of rest in the muscles or other 
tissues, and there form cysts. When these muscular tissues are eaten, the parasite 
in the cyst once more enters the alimentary canal', becomes attached to its mucous 
membrane, and from it is developed the adult worm. 

The Tenia solium may be several yards in length. At one time it was thought 
to be solitary; hence its name. It not infrequently happens, however, that more 
than one worm is present. The head, which is very small, scarcely larger than a 
pinhead, has a proboscis, or rostellum, about which is arranged a double row of 
horny hooklets. The hooklets in the anterior row are larger than those in the 
posterior row. Below these are four sucking disks at the sides of the head. By 
these means the worm attaches itself to the bowel. The segments of the worm 
are about 10 to 12 mm. in length and from 5 to 6 mm. wide, but they vary con- 
siderably in size; those nearest the neck of the worm being shorter and narrower 
than those which develop several feet away from the neck. When the egg of the 
Tenia solium is hatched out so that a scolex (or head) is set free, and this parasite 
becomes encysted in the muscles of a pig, the pork is said to be "measly." When 
it finds a resting place in the muscles or the brain, or other parts of the human 
being, it is known as the Cysticercus cellulosa. These cysts vary in size from that 
of a small pea to that of a bantam's egg, and are separated from the surrounding 
tissues by a formation of connective tissue which acts as a capsule. 

The Tenia mediocanellata possesses a head which differs materially from the 
head of the Tenia solium. There is no rostellum or hooklets, but there are four 
sucking disks, which are much nearer the point of the head than they are in the 
Tenia solium. This worm further differs from the Tenia solium in addition in 



CESTODES OR TAPEWORMS 351 

that its segments are generally broader and shorter, and the entire worm is usually 
much longer. 

This worm may reach the length of about 25 or 30 feet, and it is not very rare 
for from 15 to 20 feet of a worm to be passed intact. When the scolex of this 
worm is found in the muscles of cattle it is called the Cysticercus mediocanellata. 

In Germany, where imperfectly cooked pork is largely eaten, the Tenia solium 
is most frequently met with, but in this country, where the people eat largely of 
beef, the Tenia mediocanellata is much more common. 

The Tenia echinococcus is very rarely met with in the United States. It is, 
however, exceedingly common in Australia. This worm possesses a double row 
of hooklets and four sucking disks. It is rare for more than three or four segments 
to be attached to any one head, but as the parasite is often present in numbers 
many disconnected segments may be discharged. Like the other forms of tape- 
worm, the segments increase in size as the distance from the head is increased. 
This worm does not inhabit the intestine of man, but produces its evil influence by 
reason of the entrance of its eggs into his alimentary canal, from which place they 
wander into other parts of the body, forming what are known as hydatid cysts. 
In other words, the infection of human beings by the Tenia mediocanellata and the 
Tenia solium is quite different from the infection of human beings by the Tenia 
echinococcus, for in the first cases the patient swallows the parasite when it has 
reached the second stage of its existence and is prepared to develop its segments; 
whereas, in the case of the Tenia echinococcus the patient takes food which has in 
some way become contaminated by the fecal discharges of the dog, which fecal 
discharges contain the eggs of the parasite, and from these eggs are developed 
cysts. A patient infected by the Tenia echinococcus therefore suffers from the 
cystic stage of development of the worm. 

The hydatid cysts formed in this manner most frequently infest the liver, but 
almost any portion of the body may be affected. Such cysts, in the liver in particu- 
lar, are always surrounded by a layer of connective tissue which is thrown out in 
an endeavor to circumscribe the invading parasite. The wall of hydatid cysts, 
therefore, is formed of two layers; the outside layer is lamellated and is sometimes 
called the cuticula. The inner wall of the cyst often contains muscular fibres and 
bloodvessels, and is called the parenchymatous layer. Not rarely the primary 
cysts give rise to secondary cysts called daughter-cysts, and these daughter-cysts 
may develop in themselves cysts which are called granddaughter-cysts. 

On the inner surface of these cysts the scolices, or heads, of the worm are formed. 
At the posterior end of the scolex is a stem, or pedicle, by which it is attached to 
the wall of the brood capsule. In some instances the scolex may be found free 
inside of this capsule. In most cases, after the cyst has existed for a long period 
of time, the scolices die, the fluid is absorbed, and a granular mass remains. This 
granular mass may contain the hooklets, or the hooklets may be found free in 
the contents of the capsules, or in the primary cyst itself. Occasionally, a hydatid 
cyst is found which is sterile, that is, in which neither sub-cysts nor scolices are 
developed. 

In addition to the scolices, the cysts contain a clear, limpid fluid which sometimes 
becomes turbid after the cyst has existed for a considerable period of time, the 
turbidity being due to disintegration of the lining layer of the cysts and the forma- 
tion of crystals of cholesterin, and to the presence of lime-salts. Occasionally 
the cyst shrinks, its contents become inspissated or thickened, and the entire mass, 
including the connective tissue which has been formed around the cyst, may become 
calcified. Sometimes, too, the daughter-cysts instead of growing inside grow 
outside. Indeed, this variation is more commonly seen in man than it is in animals 
that are affected by this parasite. This is called the echinococcus exogena. 

Under the name of echinococcus multilocularis a variety of echinococcus cyst 



352 DISEASES DUE TO A SPECIFIC INFECTION 

is found in the liver, which is characterized by a somewhat irregular distribution 
of groups of small cysts walled off by connective tissue, as are the larger cysts 
already described. These cysts are often sterile; that is to say, they do not contain 
scolices or hooklets. It is probable that this formation is due to a somewhat 
different parasite from the ordinary Tenia echinococcus. 

The Bothriocephalus lotus, or Dibothriocephalus lotus, is the largest of all human 
tapeworms, and has very broad, square segments. The head is egg-shaped, but 
possesses no disks or hooklets. On the contrary, its head is marked by long grooves 
by which it attaches itself to the intestine. Its neck is longer and more slender 
than that of other tapeworms. Two species have been described, the Bothrioceph- 
alus cordatus and the Bothriocephalus cristatus. Infection by this parasite occurs 
most frequently by the eating of imperfectly cooked fish, probably because the 
eggs develop to some extent in water and are swallowed by various fish, in whose 
flesh the cysts are formed just as the other scolices already described form in the 
flesh of the hog or ox. 

Tenia nana, or dwarf tapeworm, Hymenolepis, is only from one-fifth to two 
inches in length. It has four suckers and a single row of hooklets on its head. 
Stiles states that it may be present singly or by thousands, and is probably more 
frequent than is generally thought. Its intermediate host is usually the rat, from 
the stools of which food is infected. In the rat the cyst stage may occur in the 
intestinal wall and is called a cercocystis. Like other tapeworms, the embryos 
burrow into the wall of the intestine, but do not remain there, falling back into the 
lumen of the bowel to reach adult development with eggs in about fifteen days. 
The only teniafuge which has proved effective for the removal of this worm is 
aspidium. 

The Tenia cucumerina is slightly larger than the Tenia nana, and its head 
possesses four rows of hooklets. It is not infrequently found in the ileum of dogs 
and cats, but rarely affects man. Its scolices inhabit the dog-louse and by means 
of this parasite, or by the carrying of the embryos to the mouth by the hands after 
handling a dog or cat, infection of a human being may take place. 

Symptoms. — The symptoms produced by the presence of tapeworms in the 
alimentary canal are not pathognomonic. Not infrequently the worms exist 
for a long period of time without their host having any knowledge of their presence, 
and the infection is only discovered by the chance observation of one or more 
segments in a stool. The patient may suffer from symptoms of g astro-intestinal 
catarrh produced by the irritation caused by the worm, and sometimes an inordinate 
appetite is present, but this is by no means as constant a symptom of tapeworm 
as most persons imagine. Not infrequently, the host of a tapeworm suffers from 
anorexia rather than from excessive hunger. In children there may be a good 
deal of nervous irritation and peevishness. 

In some instances, however, the presence of a tapeworm produces a very much 
more serious train of symptoms, which consist in an intense anemia that may be 
so severe as to give rise to the suspicion that pernicious anemia is present. The 
Bothriocephalus lotus is said to be more prone to produce grave anemia than any 
other of the tapeworms. 

Treatment. — The treatment of a patient infected by tapeworm consists in the 
abstinence of all food for eighteen hours prior to the administration of one of the 
following drugs, which are known to possess the power of so paralyzing or killing 
the worm that it lets go its hold, and then is readily passed from the bowel under 
the influence of a purge. One-half to one drachm of the oleoresin of aspidium may. 
be given in capsule or emulsion to an adult, and followed in four or five hours by a 
saline purgative, such as citrate or sulphate of magnesium or Rochelle salts. In 
other instances pelletierine given in the dose of 3 to 5 grains may be used under the 
same conditions. It is commonly given in syrupy solution, and this syrupy 



TREMATODES 353 

solution is put up in a small container which holds one dose. If it is desired pelle- 
tierine may be followed by castor oil in place of the other purgatives named, but 
castor oil must not be used after aspidium is given, as it aids in the absorption of 
the drug into the body and so tends to poison the individual. A less agreeable 
method of destroying the worm is to administer a confection made of pepo, or 
pumpkin seeds which have been deprived of their hard coverings by the process of 
bruising. Several drachms of these seeds are, without doubt, very efficacious. 
The patient should always be instructed to pass the stool through a sieve and not 
to seek so much for the segments of the worm as for the small head. The mere 
passage of a large number of feet or segments does not indicate in any way that the 
patient is permanently relieved unless the head, from which other segments will 
grow if it remains in the bowel, is also passed. 

TREMATODES. 

Definition. — A large number of worms belonging to the Trematodes live as 
parasites in the body of man or of the lower animals. When the body is so infested 
the condition is said to be one of Distomatosis, this term arising from the fact that 
the word Distoma is oftentimes applied to these parasites. 

Up to the present time no less than thirteen species of Trematodes or Flukes 
have been described as occurring in human beings. Eleven of these belong to the 
family of the Fasciolidce, one to the family Paramphiscus, and one to the family 
Schistosomidce. 

When the human being is attacked the parasite is usually found in the genito- 
urinary tract, where it causes what is known as Bilharzia Disease or Endemic 
Hematuria. Less commonly it infests the lung and the condition is then called 
Distomatosis of the Lung, Endemic or Parasitic Hemoptysis or Lung Fluke; and 
it is also met with in the liver, forming the so-called Liver Fluke or Distomatosis 
of the Liver. The fluke found in the genito-urinary tract is the Schistosoma hemato- 
bium, that met with in the lung is the Paragonimus westermanni, sometimes called 
the Distoma ringeri or Distoma pulmonale, and that discovered in the liver the 
Fasciola hepatica or instead Dicrococlium lanceatum, Opisthorchis sinensis, the 
Opistorchis felineus, and the Opisthorchis noverca. 

Bilharzia Disease. — Bilharzia disease, or endemic hematuria, is due to the 
development in the body of the Schistosoma hematobium, and is characterized by 
hematuria and the formation of payillomatous tumors in the genito-urinary tract. 

Etiology. — The male worm is about 4 to 15 mm. in length and 0.6 mm. in breadth. 
The female averages 15 to 20 mm. in length and 0.28 mm. in breadth. The male 
has flattened sides, rolled up on both edges so as to form a deep groove, the gyneco- 
phoric canal, in which the female lies during conjugation (Fig. 68). 

History and Distribution. — Endemic hematuria has been observed in Egypt 
for centuries. At the present day it is said to be present in fully one-half of the 
population. According to Looss it is equally frequent in Uganda. It is practically 
limited to the African continent, although cases have been reported from Cyprus 
and Sicily, and Manson reports a case from the West Indies. It occurs frequently 
in British India, but always as an imported infection. A few cases have been 
reported in the United States and by Holcomb in the West Indies. The parasitic 
nature of the disease was discovered in 1851 by Bilharz. 

The ova of these worms are found in very great numbers in the urine. They are 
oval, and have a marked terminal spine and contain a ciliated embryo. It is 
supposed that the spine is the organ by means of which the embryo bores through 
the peripheral tissues. Ova with lateral implantation of the spine are frequently 
observed. Looss supposes these are examples of faulty development, and that 
the faulty position of the spine, limiting the mobility of the ovum, is the reason 
23 



354 



DISEASES DUE TO A SPECIFIC INFECTION 



many more of this form are found in section than free. In urine or in water the 
embryos very soon escape from the ovum and move about very actively by means 
of their cilia. In undiluted urine they die when it cools. In water they remain 
active for a long time. 

The embryos are probably taken into the stomach in drinking-water, penetrate 
the gastric or intestinal wall, and they develop into mature worms. Looss surmises 
and brings some evidence to show that, like the uncinaria, this parasite may also 
penetrate the skin. 

Fig. 68 




Male bilharzia worm carrying the female, showing the papillae on his skin. The small figure is a 
cross-section showing relative position of the sexes. (Looss.) 



Pathology. — The affected bladder is covered with a bloody, tenacious, mucous 
layer; the submucosa is greatly thickened; the muscular and serous coats, as a rule 
are unchanged. In older cases papillomata are found, varying in size from a small 
pea to large tumors filling the entire bladder. Microscopically the changes consist 
in marked degeneration of the epithelial layers, going on to complete destruction 
of the mucosa. The pseudomembranous covering then consists of ova, leukocytes, 
and urinary salts. In the submucosa enormous masses of ova are found, many 
of them calcified. The papillomatous tumors spring from this layer, and are very 
similar in their histological structure to nasal polypi. Similar changes occur in 
the rectum, urethra, ureter, seminal vesicles, prostate, and uterus. Secondarily 
these lesions produce stricture, urinary fistulse, pyelitis, prostatitis, and urethritis. 

The papillomatous tumors show some tendency to undergo malignant change, 
but by far the commoner complication of the disease is stone formation. In old 
cases a beginning deposit of lime-salts is found in the mucus covering the bladder 
wall, as small calculi embedded in the folds and loculi. In other cases large, free 
calculi are found with clumped masses of calcified ova as their nucleus. 

Tumors and masses of ova are sometimes found in the pelvis of the kidney, 
rarely in its parenchyma. 

Symptoms. — The symptoms vary with the intensity of the infection, the number 
of adult worms, and the location and extent of the lesions already described. The 
only constant symptom is hematuria. The amount of blood present in the urine 
may be so small as only to be evident on microscopic examination, or so large as 
to form clots of appreciable size in the bladder. As a rule, the blood is passed at 
the end of urination. The microscopic examination, in doubtful cases, should 
therefore be directed to the last few drops of urine expelled. In the large majority 



TREMATODES 355 

of cases hematuria will be the only symptom. In the severe infections, however, 
cystitis usually develops and becomes very troublesome. Following the develop- 
ment of inflammation the ordinary symptoms of tumor or stone develop. In severe 
cases, with diminished resistance, suppuration of these lesions occurs, with formation 
of extensive fistulous tracts. When the lesions are confined to or are most marked 
in the bowel, the early symptoms may resemble acute dysentery and, in older cases, 
chronic dysentery, with pain, tenesmus, and bloody and mucous stools. When 
tumors occur in the bowel they are readily recognized, although when situated 
low in the rectum they have been mistaken for hemorrhoids. 

The urine contains red blood cells, leukocytes, principally eosinophiles and poly- 
nuclear cells, besides large numbers of ova. With these the ordinary evidences 
of an extensive chronic cystitis are also found. The number of ova present varies 
very widely and bears no relation to the amount of blood in the urine. When they 
are very few in number they may only be found in the last few drops of urine passed. 

The blood changes, in severe cases, are marked. There is a pronounced fall 
in the number of red cells and a still greater reduction of hemoglobin. With this 
there is a moderate degree of leukocytosis, the increase consisting almost entirely 
of eosinophile cells, which are present in proportion varying from 9 per cent, to as 
high as 52 per cent. 

Diagnosis. — The blood condition pointing to a toxic or parasitic anemia, with 
the demonstration of the ova in the urine, make the diagnosis of Bilharzia disease. 

Prognosis depends on several factors, namely, the extent of the infection, the 
number of adult worms present, and, more important still, the conditions favoring 
reinfection. When all opportunity for reinfection is avoided, as by removal from 
the endemic area, after a time the adult worms die, and eventually all the ova are 
evacuated. This process may be a very long one. In some observed cases it 
has extended up to eight years. The prognosis also depends on the character and 
extent of the surgical complications and sequelae. 

Treatment. — There is no treatment that will influence either the worm or the 
ova in the slightest degree. All the anthelmintics have been tried and found 
useless. Similarly, local application of antiseptics and protoplasmic poisons to 
the bladder have failed. In most cases the hematuria does not require treatment. 
When it becomes severe, rest in bed should be enjoined. Cystitis should be treated 
on general lines by local medication, as well as the internal administration of uro- 
tropin, salol, benzoic acid, and remedies of this group. The complications of the 
disease, such as stricture, extensive tumors of the bladder and rectum, accessible 
ulcerations of the vagina or cervix, and prostatic involvement, call for appropriate 
surgical measures. In a general way, all the conditions which predispose to or 
aggravate cystitis should be avoided. These are exposure, chill, violent muscular 
effort, alcoholic debauches, spices, and highly seasoned food. With a view to 
obtaining an eventual cure, patients should if possible be removed from the endemic 
area. When this is not possible, proper means should be taken to ensure a good 
water supply. In this manner the constant reinfection of the patient is avoided. 
Similarly, in view of the possibility of infection through the skin, sound shoes 
should be insisted on and work in alluvial oozes should be avoided. 

Distomatosis of the Lung (Lung Flukes; Endemic or Parasitic Hemoptysis). — 
The lung fluke (Paragonimus westermanni) is widely distributed in Japan, Formosa, 
Corea, and North China. It has been carried by Oriental emigrants to many other 
countries. Isolated cases have been reported from the United States and Mexico. 

The parasite is a small, fleshy, trematode worm or fluke. It is 8 to 20 mm. 
long and 6 mm. in its transverse diameter. It is usually found in the lungs, but 
has been observed in other organs, notably the liver and brain. The worms dis- 
charge a vast number of ova. These ova are dark brown, oval, 0.08 mm. long 
by 0.05 mm. wide, possess a small operculum, and contain a ciliated embryo. 



356 DISEASES DUE TO A SPECIFIC INFECTION 

They are found in great numbers in the sputum. Infection probably takes place 
through contaminated water, although nothing is known of the extracorporeal 
phases of the parasites. By far the larger percentage of cases is observed in young 
males. Alcoholism is supposed to predispose to the disease. 

Pathology. — Patches are scattered all over the lungs, but particularly in the 
periphery, resembling hemorrhagic infarcts. On section these patches are found 
to be infiltrated and honeycombed with small tunnels and cavities, each of which 
contains one or more distoma and masses of eggs. Occasionally large cavities 
are formed by coalescence of the smaller lesions. 

In cases in which the parasite invades the brain, analogous conditions are found, 
but they are almost entirely limited to the cortical areas. 

Symptoms. — The commonest symptom is chronic morning cough, with a rusty, 
prune-juice, or bloody sputum. The amount of blood in the sputum may be so 
small as to be only demonstrable by the microscope, or there may be periodical 
and severe hemorrhages from the lungs. The rusty color of the sputum is due 
not only to the blood and the bloody pigments contained in it, but also to the large 
numbers of dark brown ova. The sputum also contains eosinophile cells, Charcot- 
Leyden crystals, and elastic fibres. The course of the disease is essentially chronic. 
Cases last from ten to twenty years without much discomfort and without much 
deterioration in the general health, excepting where marked secondary anemia 
results from repeated and severe hemorrhages. 

Prognosis. — The prognosis is good, excepting in the rare instances in which 
hemorrhage is sufficiently severe to cause a fatal ending. When the parasite 
attacks the brain, epileptic symptoms have been observed and the prognosis is 
grave. 

Treatment. — A large number of drugs have been administered to patients suffering 
from this condition, both by the mouth and by inhalation, in the hope that benefit 
might accrue. It is evident that the nature of the lesions renders any therapeutic 
measure of little value. 

Distomatosis of the Liver (Liver Flukes). — Liver flukes occur endemically in 
certain sections of Japan. For instance, Baelz estimates that 20 per cent, of the 
inhabitants of Okayama Province are infected with the liver fluke. Inouye found 
in various sections from 19 per cent, to 71.9 per cent, of the population infected. 
Infection has been carried all over the world by Oriental emigrants. In the United 
States an entirely analogous affection is seen in cats and cattle and several cases 
have been met with in man. 

The parasite commonly invades the biliary tract or the pancreatic duct, and is 
also found in the duodenum, the stomach, and spleen. The obstruction of the 
biliary ducts by the parasites causes dilatation and chronic catarrh. There is also 
overgrowth of the hepatic connective tissue, with atrophy of the parenchyma. 
Small but constant hemorrhage from the biliary passages may cause a grave 
anemia. 

Postmortem the parasites are found in great numbers in the walls of the gall- 
bladder and biliary ducts, or free in the ducts. They lie in small, cyst-like cavities 
connecting with the gallbladder or ducts. 

Symptoms. — The symptoms depend on the number of worms. The first symptom 
is rapid enlargement of the liver, with voracious appetite. The liver may reach 
to the umbilicus, it is tender on palpation, and there are recurring attacks of jaun- 
dice. Sooner or later diarrhea begins, and with it marked failure of nutrition. 
The patient becomes weak, emaciated, and anemic. The diarrhea in marked cases 
is severe, and the movements contain much blood, besides the ova of the parasites. 
Later, dropsy of the legs and belly develop, and the patient dies exhausted. The 
course of the disease is very chronic, and likewise depends on the number of 
parasites. Recovery never takes place. 



MYIASIS 357 

Treatment. — There is no treatment save the use of stimulants and good food. 

With the idea of prophylaxis Inouye advises against drinking or swimming in 
canal water or eating raw fish or mussels. He states that in one region notably 
infected with the disease the mortality from distomatosis has been reduced to zero 
by following these simple precautions. 



PARASITIC INFUSORIA. 

The parasitic infusoria which are found in man are protozoa of the sub-class 
flagellata. They are rarely met with. The Plagiomonas urinaria has been found 
in the urine of a man who suffered from chronic suppuration. The Trichomonas 
vaginalis is found in acid vaginal mucus, and the Trichomonas hominis has been 
found in the bowels and stools. They all possess but little clinical interest. 



CHIGGER (SAND FLEA). 

The chigger, or sand flea (Pulex penetrans), is distributed widely over tropical and 
many parts of subtropical America and the West Indies. It is supposed to have been 
carried in 1872 from South America to Africa. At present it is widely distributed 
on both African coasts and in certain sections of India. It is a very common pest in 
the Philippine Islands, where it is known as "tungau." The chigger is a minute, 
reddish-brown flea, and attacks man and animals. When impregnated the female 
attaches herself to the skin surfaces and burrows under the skin, head first. Ovula- 
tion takes place in the cutaneous tissue and the female increases to the size of a 
small pea. If unmolested the ova, when mature, are expelled through the point 
of entrance, through which also the female is ultimately extruded. The chiggers 
may vary in number from one to several hundred. They usually lodge in the feet 
and legs, but the hands, arms, genitals, and face may also be invaded. The bite 
of the insect causes little pain, and the female is usually detected when she com- 
mences to enlarge beneath the skin. There is then intolerable itching, with for- 
mation of small papules, with red, inflamed heads, and a black spot on the summit. 
The papules become pustular, discharge, form small ulcers, and eventually heal, 
leaving small, pitted scars. When the lesions are numerous, particularly when 
neglected in the unclean and the physically deteriorated, extensive infections and 
sloughing wounds may occur. Rarely tetanus and phagedenic areas develop. 

Treatment. — Treatment consists in complete enucleation with a needle or the 
point of a fine scalpel. Chloroform, turpentine, infusion of tobacco, mercurial 
ointment, and the essential oils allay the itching and kill the parasites. The 
essential oils, particularly the oil of eucalyptus, act not only as a cure, but also as 
a preventive against the bites of the insects. 



MYIASIS. 

Infection of Larvae of the Diptera. — Screw-worm (Lucilia Macellaria), the 
larva of the common blue-bottle flesh fly, a very common fly in the United States, 
West Indies, and South America, causes infection in man through the female 
laying her eggs on wounds in the skin and in the noses or ears of people sleeping 
in the open. During the campaign at Santiago de Cuba, in 1898, numerous cases 
of infection by this larva were seen in wounds and abrasions about the feet of the 
men and horses. In the tropics they have also been seen attacking the vagina of 
recently delivered women. The eggs deposited in these locations hatch out in a 



358 DISEASES DUE TO A SPECIFIC INFECTION 

few hours into the larvae, known as the screw-worm on account of the circles of 
minute spines running around the body of the worm very much as does the thread 
of a screw. The larvae are about three-quarters of an inch in length. They are 
extremely active, and burrow widely, causing extensive destruction of all the tissues. 
On account of the circles of spines they are extremely difficult to extract from their 
burrows in firm tissue. Screw-worm infections of the nose are very painful and 
exceedingly fatal. The larvae bore into the frontal and ethmoidal sinuses, and 
eventually may even enter the brain. There is intolerable pain at the bridge of 
the nose, with a bloody, fetid discharge from the nostrils. A very large percentage 
of the cases die from extension of the infection into the sinuses or meninges. When 
the larvae develop in the ear they penetrate the tympanic cavity, causing severe 
otitis media and even fatal meningitis. Numbers of such cases have been reported 
by army surgeons from the Rio Grande border. 

Treatment. — Treatment consists in the injection of strong parasiticides, such as 
carbolic acid and chloroform. Better still, chloroform is taken up on a small 
probe tipped with absorbent cotton, and, with a good light, the nose or ear is 
explored and each worm as it lies embedded in the tissues is touched with the 
chloroform-saturated cotton. This kills them immediately and they may then be 
readily extracted with small forceps. In superficial wounds the destruction of the 
larvae is much more simple. 

Intestinal Myiasis. — The larvae of diptera are very frequently found in the 
alimentary canal of man. They usually gain entrance by being swallowed on 
fly-blown food. No less than nineteen different species have been identified in 
human evacuations. As a rule no symptoms are produced, and the first the patient 
knows of the existence of the larvae is to find perhaps a copious mass of them in 
the stools. In tropical climates the passage of larvae is very much more frequent 
than in temperate countries, for obvious reasons connected with the difficulty 
of preserving food supplies. The appearance of the larvae is usually viewed with 
the greatest alarm by the patients, but, as a rule, they are entirely harmless. Occa- 
sionally they produce some symptoms of gastro-intestinal disturbance, such as 
vomiting, diarrhea, and abdominal pains. Free purgation is indicated whenever 
larvae are seen in the stools, to ensure evacuation of those remaining. For this 
purpose calomel is the best drug, as it exercises not only an evacuant but a toxic 
effect on the larvae. 

Dermatobia Cyaniventris. — This common American fly deposits its eggs on the 
skin of man and cattle. The larvae penetrate the cutaneous structure, producing 
large pustular lesions (locally known as ver macaque). Besides this fly there are 
great numbers of diptera whose larvae attack the skin of man. In all of them the 
lesions are similar to that above described. In America these are principally 
the Musca vomitoria the ordinary blue-bottle fly, and the bot-fly of the ox and sheep. 



TUMBU-FLY DISEASE. 

This is a condition met with in Sierra Leone and elsewhere on the west coast of 
Africa. The larvae of the Tumbu-Fly, or Cordylobia anthropophagia, burrow 
under the skin and produce sore and tender spots, the opening in the skin being 
maintained for breathing and excrementitious purposes. The maggot is about 
half an inch long and can be squeezed out of its burrow. The infection may be 
multiple or single. 



DISEASES OF THE RESPIRATORY SYSTEM. 



DISEASES OF THE NOSE. 

ACUTE CORYZA. 

Definition. — Acute coryza is an inflammation of the nasal mucous membrane, 
characterized in its early stages by hyperemia, redness, and swelling, and followed 
by free secretion of mucus and serum. 

Etiology. — Without any doubt acute coryza is an infectious malady, although it 
usually follows exposure to cold or wet. The exposure produces a condition 
favorable to the growth of the micro-organisms which cause the disease. No single 
organism has been isolated, and in some cases several are probably active at once. 
Coryza is a conspicuous symptom of certain forms of influenza and may be produced 
by a number of micro-organisms, among which the pneumococcus should be men- 
tioned. Hajek claims to have isolated an organism called the Diplococcus coryza?, 
which he believes is responsible for the malady. The Micrococcus catarrhalis, the 
pneumococcus and the bacillus of influenza are the most frequent causes. 

The disease can be transmitted from one person to another, probably by droplets 
of infected discharge, the susceptibility of an individual depending upon both a 
local and general lowering of vital resistance. The breathing of vitiated air, as 
in badly ventilated theatres and steam cars, and of dust-laden atmospheres, as in 
certain industries, is a frequent predisposing cause. The possibility of a diphtheritic 
origin in certain cases should not be overlooked. Damp cold, even if of moderate 
degree, is more provocative of the disease than dry cold. 

Pathology and Morbid Anatomy. — The pathology of acute coryza is that of an 
ordinary catarrhal inflammatory process affecting a mucous membrane. The 
bloodvessels of the submucosa become hyperemic, and from them an extravasation 
of white blood cells and red corpuscles takes place, accompanied by a transudation 
of serum, which increases the swelling, and finally escapes upon the surface of the 
mucous membrane, to be thrown off with the desquamated epithelium. The mu- 
cous glands secrete an excess of mucus laden with dead epithelial cells and leukocytes 
or pus corpuscles. As recovery takes place, the inflammatory exudate in the 
submucosa is absorbed, the dead epithelial cells are replaced by young cells, and 
in this manner the process of repair is completed. 

Symptoms. — The symptoms of acute coryza consist in primary chilliness and some 
restlessness and in a sensation of dryness of the nasal mucous membrane of the part 
affected. This is accompanied by a loss of the sense of smell and by a dull frontal 
headache, probably due to congestion in the frontal sinus. There is frequently 
severe sneezing, due to the irritation of the nasal nerves by the inflammation and 
to the tickling of the serum over the angry mucous membrane. The voice sounds 
as if the nose was "stopped up." As the disease progresses, large amounts of 
mucopurulent material are discharged from the nostrils and find their way back 
into the nasopharynx. The constitutional symptoms are often quite severe, and 
consist in chilliness and flushes of heat, followed by relaxation of the capillaries 
of the skin and more or less perspiration. Aching in the head, in the muscles, and 

(359) 



360 DISEASES OF THE NOSE 

the small of the back are prominent symptoms, indicating that the local nasal process 
is not the only part disordered, but that other parts are indirectly affected. With- 
out doubt, the two chief causes of these symptoms are the loss of large amounts 
of liquids by the nose, something like 1J to 2 pints a day in some cases, and the 
absorption of toxic materials due to the infection. 

Diagnosis. — The acute rhinitis due to an oncoming attack of measles, or that due 
to an attack of hay fever, are the two states that most closely resemble true coryza. 
In infants the possibility of the attack being due to syphilis, "syphilitic snuffles," 
must be considered. 

Treatment. — The treatment of acute coryza consists, if the patient is seen in 
the stage of onset, of the use of a saline purgative to deplete the system and unload 
the bowels, and in the internal use of full doses, 20 to 30 grains every hour for five 
doses, of bicarbonate of sodium in water or instead 10 grains of aspirin with 1 grain 
of camphor every four hours. In other cases the well-known combination called 
"rhinitis tablets" may be given. These consist of — 

1$ — Quininae sulphatis gr. j. 

Camphorse . gr. |. 

Ext. belladonna? gr. T V — M 

Sig. — One or two every thirty minutes till six are taken. 

The nasal mucous membrane should be washed by a gentle spray of normal 
salt solution, followed by a spray of — 

1$ — Cocainse hydrochloridi gr. iv. 

Chloretoni . . . gr. ij. 

Aquae destillat q. s. ad fgj. — M 

Sig. — Apply as a spray. 

Followed by a spray of — 

1^ — Antipyrini gr. x. 

Cocainae hydrochloridi gr- j. 

Aquae camphorae f 5iij- 

Aquae destillat . q. s. ad f 5j. — M. 

This, in turn, should be followed by a spray of menthol in the proportion of 
6 grains to the ounce of liquid albolene. 

In many instances a hot foot-bath and a dose of 5 to 10 grains of Dover's powder 
may be used to abort an attack. 

After the disease is well on its way, it is bound to run its course. We can only 
give relief by using a type of nasal treatment like that just suggested and in cleansing 
the nasal chambers of mucus. 

When the attack has run its course the consequent debility is best controlled 
by the use of fresh air, arsenic, ammonium benzoate, and bitter tonics. 

CHRONIC NASAL CATARRH. 

Definition. — Chronic nasal catarrh, as its name implies, is a chronic inflammatory 
state of the nasal mucous membranes, frequently due to repeated attacks of the 
acute variety, or' occasionally coming on more insidiously. When it is well de- 
veloped the tissues of the nasal chambers are relaxed and somewhat edematous, 
the secretion is abnormal in character and in quantity, and this pathological con- 
dition is often subject to acute exacerbations due to exposure to the usual causes 
of coryza. 

Etiology. — The causes of chronic nasal catarrh are, as just stated, repeated 
attacks of acute coryza and continued exposure to the action of irritating dust 
or of cold, moist air, laden with infectious materials. The condition may be of 



ATROPHIC NASAL CATARRH 361 

syphilitic origin or arise from depleted vitality from constitutional disorders, such 
as Bright's disease. Foreign bodies should be searched for, particularly if the 
patient is a child, and nasal growths may be found as a cause, although, as a 
rule, the catarrh causes the formation of growths. 

Pathology. — ^n examination of the nasal mucous membrane in cases of this 
disease shows that the bloodvessels are distended and have lost their normal 
elasticity, this favors congestion when other parts are chilled. Exudation into 
the connective tissues takes place, and so this structure becomes thickened and 
enlarged. At this stage the condition is sometimes called hypertrophic rhinitis. 

Repeated or protracted irritation induces hyperplasia of the connective tissue 
of the submucosa, continued epithelial exfoliation, glandular atrophy, and sclerotic 
changes in all the layers of the mucous membrane. In the earlier stages these 
changes are those already mentioned when discussing acute coryza; later cell 
proliferation and leukocytic accumulation in the nasopharyngeal submucosa 
greatly thicken the membrane, particularly over the turbinates and the septum 
(hypertrophic rhinitis), while organization (fibroid change) increases the fibrous 
tissue in the areas involved, followed by contraction with atrophy of erectile, 
glandular, and even nerve tissues (atrophic rhinitis) . This lessens secretion, which 
tends to inspissate, form scabs, and decompose, causing the fetid emanations to 
which the name "ozena" has been given. 

Extension to one or more of the facial sinuses, necrosis of bone, or involvement 
of the Eustachian orifice or tube are possibilities constantly to be remembered. 

Symptoms. — The symptoms of this stage of the disease consist in a constant 
secretion in excess of nasal mucus, which passes in large part into the postnasal 
and nasopharyngeal spaces. This secretion may be thin and liquid or thick and 
mucopurulent, and is apt to vary in quantity with exposure to cold or dust. The 
secretion is so thick that it readily becomes inspissated and partly blocks the nasal 
passages, and, furthermore, becomes loaded with bacteria, so that it may be some- 
what fetid, 

Treatment. — The treatment consists in maintaining nasal cleanliness by an 
ordinary nasal douche-cup, to be used night and morning, employing in it normal 
salt solution or Dobell's solution warmed to the temperature of the body. The 
physician should also cleanse the parts, when the patient visits him, by a mild 
alkaline wash, and when no acute exacerbation is present the hypertrophied mucous 
membrane over the middle turbinate should be cocainized and then lightly touched 
with a small electrocautery, a piece of oiled cotton being placed between the spot 
cauterized and the nasal septum, to prevent adhesions from forming during the 
period of acute swelling which follows the operation. Care should be taken to 
keep the parts clean for several days to prevent infection, if the patient is primarily 
anemic or debilitated. This treatment should not be resorted to before the general 
health is improved by tonics. 



ATROPHIC NASAL CATARRH. 

Definition. — In this condition the nasal mucous membrane and the underlying 
tissue undergo atrophy and contraction, with the result that the bloodvessels of 
the part are occluded or destroyed. 

Etiology. — Atrophic nasal catarrh follows the chronic type of ordinary nasal 
catarrh as a late condition. At times it seems to be due to some congenital defect 
in the shape of the nasal chambers, and in some cases it begins to develop as the 
result of one of the acute infectious diseases. 

Pathology. — The chief change is an atrophy of the cells of the nasal mucoue 
membrane and an overgrowth of the submucous connective tissue, which is prone 



362 DISEASES OF THE NOSE 

to undergo contractile changes. This cuts off blood supply and increases the 
atrophic process. 

Symptoms. — These consist in the formation of scabs, or crusts of thickened, 
tenacious mucus, which are usually infected by many pathogenic germs. Some 
ulceration of the nasal septum may appear, and the patient may complain of a 
constant feeling of dryness and irritation, or occlusion of the nasal passages. 

The nasopharyngeal mucous membrane is often dry and shiny in appearance. 
When the condition is far advanced a state of fetid ozena develops, in which the 
breath of the patient becomes fetid beyond the power of words to describe it. 
Nothing equals it, except the breath in a case of pulmonary gangrene. 

The sense of smell is practically destroyed by the process, and the patient is often 
ignorant of how disagreeable his breath has become. 

Prognosis. — The outlook for a cure of this condition is unfavorable. The bad 
odor can usually be relieved. 

Treatment. — The patient should be told to use a nasal douche-cup with warm 
Dobell's solution twice a day. Kyle recommends 1 drop of ordinary coal oil 
dropped into each nostril after this. The physician should see the patient every 
few days, cleanse the nasal chambers, and a 1 : 500 solution of formaldehyde may 
be used on an applicator. Excellent results have followed the use of a 5 per 
cent, ointment of scarlet red. 

HAY FEVER. 

Definition. — Hay fever is an inflammation of the nasal mucous membrane which 
occurs periodically and usually at a time of the year when certain plants are in a 
given stage of growth. Associated with the localized inflammation, there is 
often present an asthmatic condition, in which a sense of oppression is well de- 
veloped. In other instances true asthmatic attacks ensue. Hay fever is often 
called "autumnal catarrh/' "rose cold," "ragweed fever," or "periodic rhinitis." 

Distribution. — The prevalence of hay fever depends largely upon the presence 
in the air of the pollen of certain plants, and in those parts of the country where 
these plants do not grow the disease is unknown. It is more rare in England than 
in America, but much more common in these countries than elsewhere, being com- 
paratively rare in France and Germany. Negroes and Indians are apparently 
immune, and the lower classes very frequently escape, the disease being chiefly 
a malady of the so-called upper classes. The disease is comparatively rare after 
the fortieth year and affects males oftener than it affects females. 

Etiology. — There are two chief factors in the development of hay fever, namely, 
an idiosyncratic state of the patient and the presence of an exciting cause in the 
atmosphere. Much discussion has taken place as to what the condition is that 
renders the patient peculiarly liable to this affection. In some cases it seems to be 
a neurosis of the nasal cavities or a local disease; in others it is probably a type of 
anaphylaxis. In every case, however, there is a condition of nasal hyperesthesia 
which renders the nasal mucous membrane extremely sensitive to irritants. Many 
sufferers from hay fever present irregularities in the nasal chambers which may aid 
in predisposing them to attacks of the malady. 

The second cause of hay fever in the great majority of cases is the presence in 
the air of pollen from some plant, chiefly "ragweed." Pollen is not the only cause, 
however, for typical attacks occur in certain persons at seasons of the year when 
no pollen is present, the condition being induced by some irritating dust or vapor 
which in no way influences the ordinary individual. 

Pathology and Morbid Anatomy. — In the state of the nasal mucous membrane 
there is nothing peculiar to hay fever, which presents on examination the evidences 
of an acute catarrhal inflammation with swelling and hyperemia of the parts 
involved. 



HAY FEVER 363 

Symptoms. — The symptoms of "hay cold" are usually sudden in onset and often 
appear on a certain day which the patient can foretell, and nearly always at a 
definite period in the year, for the reason already given. An acute rhinitis develops 
with irritation of the nasal mucous membrane, and the running of salty fluid from 
the nostrils irritates the nares and the upper lip. The conjunctival mucous mem- 
brane is irritated and inflamed, and the eyes are tearful, partly because of this 
condition and partly because the tear ducts to the nose are stopped by the swelling 
of the mucous membrane. Photophobia and neuralgic pains in the head are often 
present and add greatly to the patient's misery. Frontal headache is constant 
and severe, and tinnitus and fulness of the head are also annoying symptoms. Some 
deafness may be present. Associated with these symptoms the patient often has 
marked systemic depression and wretchedness with great mental depression. 

On examining the mucous membrane of the nose there is found undue pallor, 
in long-standing cases, which is not to be expected when inflammation is present. 
If a probe is touched to the mucous membrane patches of hyperesthesia are dis- 
covered, as evidenced by sudden severe sneezing and other signs of acute irri- 
tation. 

The attack is prone to persist as long as the patient remains exposed to the cause, 
and upon his removal from exposure may cease almost as speedily as it came on. 
In cases in which a reflex asthma due to the nasal irritation ensues the patient may 
become a chronic asthmatic, even if the hay cold disappears. 

Prognosis. — The outlook for cure in the affection is not good unless the patient 
can go away to a resort where the cause does not exist, for a certain length of time 
each year. So far as life is concerned it never endangers it, but if the disease 
produces vital depression it undoubtedly increases the susceptibility to other 
diseases. The patient can be comforted by the statement that the attacks stop 
or diminish in many cases after forty years of age. 

Treatment. — A competent rhinologist should always be asked to correct all 
nasal irregularities during the period of quiescence, and the physician should 
correct any faulty nutritional state by the use of ordinary exercise, a good diet, 
and the use of the salicylates, or bitter tonics with arsenic to improve the state of 
the mucous membranes in general. Not infrequently good results follow the 
use of 30 grains of phosphate of sodium in a cup of hot water before breakfast, 
given to stimulate the gastroduodenohepatic glands. In other cases salicylate 
of sodium in 10-grain doses or salol may be used. These measures and the resort 
to a region free of the exciting cause in the autumn months are the prophylactic 
measures. A sea voyage usually confers complete immunity if taken at the 
proper time of year, and sometimes residence at some mountain resort does like- 
wise, particularly if the altitude is very great. 

In the way of local treatment for the attack the swollen mucous membranes 
may be constricted by the application of a solution of adrenalin chloride 1 : 5000, 
and after this is done the parts may be washed with a mild alkaline spray like 
Dobell's solution or normal salt solution which has been warmed. After this is 
done the cocaine solution and the antipyrin solution recommended for acute coryza 
may be employed and finally the parts coated by the use of the spray of menthol 
and camphor named in that article. 

Within the last few years several attempts to produce immunity to hay fever 
by the use of preparations of golden rod and ragweed have been attempted, the 
patients taking them for some time before the time of an attack in the hope that 
they would not suffer from the disease. This plan has not so far proved very 
successful. 

Dunbar, of Hamburg, claims to have isolated a toxin from the pollen of certain 
plants, and by giving it to horses produced an antitoxic serum which, he states, 
will protect a susceptible person. This is not used hypodermically, but is dried, 



364 DISEASES OF THE LARYNX 

mixed with sugar of milk, and then finely triturated. A small part of this powder 
is to be snuffed up the nose. When it is desired to use the remedy in the eyes 
the fluid serum is employed. It succeeds in some cases and fails in others. 

EPISTAXIS. 

Etiology. — Nosebleed is due to many different causes, chiefly traumatic. The 
condition only concerns us, from the medical stand-point, when it develops as a 
result of lesions in the nasal cavities or in the course of the infectious diseases, 
or in cases of heart disease in which there is cephalic congestion. Occasionally 
it occurs in very plethoric persons after severe exercise, and in them it may be a 
beneficial condition. 

Severe nasal hemorrhage usually arises from an ulcer on the nasal septum, from 
cardiac disease, the commonest lesion being mitral disease, and in typhoid fever 
as one of the prodromes. Occasionally it is a desperately persistent state in hemo- 
philia, and even more rarely it seems to be of the nature of vicarious menstrua- 
tion. Sometimes it is a manifestation of blood dyscrasia, as in leukemia. (See 
Hemophilia.) 

Treatment. — The treatment consists in plugging the nostrils with cotton, if 
necessary saturating the cotton with adrenalin chloride 1 : 2000, and in compressing 
the artery on the upper lip near the nose by pushing it against the jaw-bone. Inter- 
nal measures are usually unnecessary and useless. Horse or human serum may 
be injected hypodermically in some cases. 



DISEASES OF THE LARYNX. 

ACUTE CATARRHAL LARYNGITIS. 

Definition. — Acute laryngitis, or acute catarrh of the larynx, is an inflammation 
of the mucous membrane lining the larynx, as a result of which there is more or 
less loss of voice, or aphonia, and perhaps a sense of constriction or respiratory 
oppression. 

Etiology. — This condition arises as a result of any factor which directly causes 
irritation of the laryngeal mucous membrane, such as the inhalation of irritant 
vapors or dust. In some cases the inhalation of cool and damp air produces like 
effects, particularly if the voice has been used much before the exposure. Indirectly 
it arises as the result of getting the body chilled in a cold wind after exercise, and 
in still other cases it seems to be, at least in part, due to some disorder of metabolism 
whereby gouty conditions ensue, and these in turn cause laryngeal inflammation 
by some indirect effect when the voice is much used. Another cause, particularly 
in the case of children, is "mouth-breathing," which permits the air unmoistened 
by the nasal chambers to pass over the laryngeal surface. In still other instances 
it arises as a complication of one of the acute infectious diseases, as influenza and 
of hay fever. The possible diphtheritic origin of acute laryngitis, especially in 
children, should never be overlooked. 

Pathology. — The inflammation of the laryngeal mucous membrane is precisely 
like that of mucous membranes elsewhere, except for the fact that glandular tissue 
is quite scarce in these parts, and so there is but little mucus secreted even if a 
considerable amount of inflammatory exudate takes place in the tissues beneath 
the mucous membrane. The desquamation of epithelial cells and the presence 
of dead leukocytes cause the secretion to be white and tenacious, and the conges- 



ACUTE CATARRHAL LARYNGITIS 365 

tion of the bloodvessels gives rise to a sense of tightness in the laryngeal box which 
is distressing. As the congestion decreases the process of regeneration in the 
epithelial cells and submucous tissues takes place, secretion becomes more profuse, 
and perfect recovery ensues. 

Symptoms. — The patient finds it difficult to develop the full resonance of his 
voice and often single words in a sentence, or all the words, are spoken somewhat 
huskily owing to failure to move the vocal bands as readily as in health. There 
is a sense of tightness in the larynx and even aching pain may be present. In 
some cases hoarseness is the only symptom, but in others the loss of voice is com- 
plete. Speech at this time is often so painful that the patient endeavors to avoid 
conversation. 

An examination of the laryngeal mucous membrane at this time will reveal 
marked redness and hyperemia and even small punctiform hemorrhages may be 
seen, particularly if the patient has repeatedly and violently endeavored to clear 
his throat by hawking or coughing. The ventricular bands are swollen, and this 
may be the chief cause of the loss of voice, for it often happens that the vocal cords 
escape the inflammatory process. In other cases the edges of the glottic opening, 
the epiglottis, and the mucous membrane over the arytenoids are inflamed. 

As the process proceeds secretion is begun and small particles of mucus are 
occasionally coughed up. This is particularly apt to occur after severe coughing 
in the morning in order to dislodge inspissated mucus. The masses expectorated 
are often distinctly purulent, and discolored with soot if the patient lives in a city. 
Secretion gradually becomes more profuse. Pain disappears and the voice, which 
has been whispering, becomes hoarse and coarse in character, certain words which 
require effort being sounded with difficulty. Finally the voice recovers its normal 
tone and the attack is over. 

Diagnosis. — Care should be taken that sudden attacks of hoarseness are not 
considered as due to simple catarrhal laryngitis, until the possibility of diphtheria 
is excluded by a thorough examination of the throat and larynx. This is particu- 
larly important in children. In adults the possibility of aneurysm, tuberculosis, 
papilloma, and syphilis should not be forgotten. 

Prognosis. — The prognosis is always good as to recovery if the exciting cause 
is removed. 

Treatment. — The treatment of acute laryngitis consists primarily in removing 
the cause. If irritant dusts are present the patient must not be exposed to them, 
and if the outside atmosphere is raw and cold he must be kept in-doors until recov- 
ery takes place. When a gouty diathesis underlies the condition the salicylates 
should be freely used in the form of salicin, 5 grains three or four times a day, and 
the vegetable salts of potassium, such as the citrate, be given freely. About the 
neck may be fastened a capsicum draft, or, if this is not to be had, a folded hand- 
kerchief should be wrung in cold water and laid upon the larynx, being immediately 
covered by a cloth or piece of flannel, which is bound around the neck. The cold 
compress is promptly changed to a warm compress by the heat of the body, and 
this acts favorably upon the local inflammation beneath. The air of the room in 
which the patient is to sleep or rest during the day should be kept well moistened 
by steam disengaged by a bronchitis kettle or by adding pieces of unslaked lime 
to a tub of water. Into the water in the bronchitis kettle may be placed a few 
grains of menthol if it is desirable to exercise a very sedative effect, and the patient 
should be forbidden to go into any cold rooms or hallways. A hot mustard foot- 
bath and a hot lemonade with a drachm of sweet spirit of nitre at bedtime to produce 
sweating is also useful, or a dose of Dover's powder may be ordered if the patient 
is an adult. Kyle recommends the use of tablets of T ^ grain of pilocarpin every 
hour for four doses, or if it is important to attempt to abort the disease he suggests 
the use of 5 to 10 drops of dilute nitric acid in water every hour for three doses, 



366 DISEASES OF THE LARYNX 

and then every two hours for two doses. This* often gives temporary relief if it 
does no permanent good. 

For the hoarseness and thick secretion of the stage of convalescence benzoate 
of soda or of ammonia, in 10-grain doses three times a day, are useful, or 10 grains 
of ammonium chloride may be given thrice a day in licorice and water. In still 
other cases terpin hydrate in the dose of a teaspoonful of the elixir every three 
hours may be used. 

CHRONIC CATARRHAL LARYNGITIS. 

Symptoms. — Chronic catarrh of the larynx is characterized by chronic hoarseness, 
by constant clearing of the throat in an endeavor to speak clearly, and finally, 
in severe cases, by ulceration of the laryngeal mucous membrane. Not rarely 
after a period of rest the patient finds that after the first few words his voice forsakes 
him, or, instead, he may find that if speaking is difficult at the beginning it become 
more easy as exercise limbers up the infiltrated muscles and engorged mucous 
membrane. 

Pathology. — Pathologically the condition is characterized by chronic engorge- 
ment of the minute bloodvessels, thickening of the mucous membrane, and even 
infiltration of the submucous tissues and the laryngeal muscles. If this process 
persists for any length of time sufficient infiltration may be present to become 
unabsorbable and thus cause permanent alteration in the character of the voice. 
Not rarely there is thickening and swelling of the pharyngeal tissues as well, and 
the tonsils are the seat of chronic lymphoid changes. Spots of ulceration may 
develop between the arytenoid cartilages. 

Diagnosis. — As stated in the article on Tuberculosis, hoarseness which is persistent 
should always be carefully investigated, as it often is due to tuberculosis or syphilis, 
or even papilloma. When it is due to aneurysm the laryngoscope will usually 
reveal one cord paralyzed, and when due to syphilis the history of the patient and 
the benfit produced by specific treatment must be noted. In persons of advanced 
years the possibility of malignant growth must be considered. 

Treatment. — The treatment consists in the maintenance of cleanliness and free 
secretion in the upper respiratory tract by the use of alkaline sprays and nasal 
douches. To the larynx itself a spray of alumnol (3 per cent, solution) may be 
applied every second day. The use of tobacco and alcohol should be forbidden 
and the liver and kidneys kept active by mild alkaline purges and diuretics. Tonics 
to the general system, such as phosphorus, arsenic, and sometimes iron, particularly 
the syrup of the iodide are useful. 

EDEMATOUS LARYNGITIS. 

Definition. — Edema of the larynx occurs as an acute affection, occasionally 
of such a severe degree that it endangers life. It is essentially an acute cellulitis 
of the laryngeal tissues, and when it involves the upper part of the larynx in par- 
ticular it is called edema of the glottis. 

Etiology. — Edema of the larynx is far more frequently due to injury than to 
any other cause, and in many instances is produced by the inhalation of irritant 
vapors or fumes. The only cases I have seen have been due to the patient attempt- 
ing to swallow ammonia water undiluted, which both by actual contact of the 
fluid with the pharynx and of the fumes with the larynx has caused serious respira- 
tory distress. Another traumatic cause is fracture of the larynx, as by throttling 
or other injury. Of the non-traumatic causes we find that acute inflammations 
in other parts may be provocative of this state, as, for example, tonsillar abscess 
with inflammation of the adjacent tissue gradually extending to the larynx. Some- 



EDEMATOUS LARYNGITIS 367 

times it ensues as a result of grave lesions in the cartilages of the larynx, as in the 
chondritis arising in typhoid fever, or even in scarlet fever in association with the 
development of the "collar of brawn." Infection by the staphylococcus or strepto- 
coccus of the perilaryngeal tissues, the floor of the mouth or pharynx (as in Ludwig's 
angina) may extend to the epiglottis and larynx. While often an infection, it 
may arise in the course of some affection characterized by widespread edema, as 
Bright's disease or chronic heart disease, and so appear to have a dropsical origin. 

Pathology. — The condition of edema of the larynx, as its name implies, depends 
upon the extravasation of fluid into the submucous tissues, producing an edema 
or hydrops of the part, which is nearly always of an inflammatory origin. 
This swelling may involve all the laryngeal structures equally and even extend 
well along the trachea. In mild cases the parts affected are not, however, seriously 
disorganized, and the swelling may disappear as rapidly as it came on, leaving 
behind it little trace of its existence. In fatal cases the swelling is usually found 
at autopsy to have largely disappeared, although the parts may be red and inflamed 
and somewhat relaxed. In such cases the microscope commonly shows a serous, 
or serofibrinous, suffusion of the affected tissues, the exudate containing a varying 
number of leukocytes. In other cases the submucous and even the perilaryngeal 
tissues may be infiltrated by pus, diffuse suppurative interstitial laryngitis, a most 
fatal disease. 

Symptoms. — With the onset of this condition several characteristic symptoms 
at once develop, namely, impairment of the voice, stridulous or labored breathing, 
manifestly due to laryngeal obstruction, and increasing cyanosis. The patient 
is uncomfortable if lying down, and is more easy when sitting up and leaning 
forward. The tissues adjacent to the larynx may be swollen and the patient, if 
unable to speak, points appealingly to his larynx. 

In some instances a state of chronic edema, due to heart or renal disease, may 
ensue, which is rarely so severe or as pressing for relief as is the acute malady. 

Diagnosis. — Difficult laryngeal breathing may be due to a laryngeal crisis in 
locomotor ataxia or to the lodgment of a foreign body in the larynx. These con- 
ditions should be excluded before the physician decides that edema is the cause 
of the illness. Aneurysm of the aorta may produce severe laryngeal symptoms 
by pressure on the laryngeal nerves, and in children retropharyngeal abscess may, 
by rupture or pressure, produce somewhat similar symptoms. 

Prognosis. — In the absence of virulent symptoms the prognosis is usually favorable 
even if the symptoms are severe, provided that when they appear the physician 
is ready to give relief by intubation or tracheotomy. If the edema is due to the 
inhalation of irritating vapors and the lower respiratory tract is involved in the 
inflammatory process, the prognosis is, of course, very grave. 

Treatment. — The treatment consists in the administration of an active saline 
purge to deplete the vascular system, and the setting free of steam from a bronchitis 
kettle in the air of the room in which the patient lives. To the water in the kettle 
may be added a few grains of menthol for its soothing influence on the laryngeal 
mucous membrane. A 10 per cent, solution of alumnol may be sprayed into the 
larynx for its astringent effect. When the edema arises as a complication of renal 
or cardiac disease and is part of a general tendency to anasarca, so active a purge 
as elaterium or colocynth is indicated to remove fluid from the body, and a hot 
pack may be used to cause sweating if the heart is strong enough to stand it. The 
use of pilocarpine for this purpose is unwise, because it is so prone to cause pul- 
monary edema. When the laryngeal obstruction becomes marked it may be 
necessary for the physician to quickly perform intubation or tracheotomy, but 
while he should be prepared to do so at any moment it is scarcely necessary to 
add that tracheotomy should be done only as a last resort. 



368 DISEASES OF THE LARYNX 



SPASMODIC LARYNGITIS. 



Definition. — Spasmodic laryngitis, sometimes called "spasmodic croup," or 
" false croup" in distinction from diphtheria or true croup, is a condition of acute 
laryngeal catarrh involving the mucous membrane in the region of the glottis, 
and resulting in swelling of those parts, so that the ingress and egress of air is 
difficult. The spasm of the laryngeal muscles, while it aids in producing the symp- 
toms, is really of secondary importance as compared to this swelling. 

Etiology. — In the past it was customary to consider spasmodic croup a disease 
in itself. We now know that it is a symptom depending upon several causes, 
some of which are external, some internal. Appearing as it does almost always in 
children between one and six years, but sometimes persisting in its occurrence up 
to puberty, it depends chiefly upon rickets or malnutrition, the presence of postnasal 
adenoids, which make the child a mouth-breather, or to some defect in the nose, 
which causes the same condition. In some instances errors in diet before retiring 
to bed seem to precipitate an attack. Of the external causes which, however, 
are only active in those who have a tendency to attacks of this affection, may be 
mentioned furnace-heated air, which is so dry and dusty that if the child is a mouth 
breather the larynx becomes rapidly dry and irritated. An acute coryza may also 
bring on an attack in that it causes mouth-breathing. 

Treatment. — The treatment is evident from what has just been said. It may 
be divided into two parts, that for the relief of the attack and that for the cure 
of the underlying causes. 

When any sign of croup is manifested the nurse should place 1 or 2 grains of 
menthol in the bowl of a dry spoon and heat it over a gas jet or lamp. This sets 
free in the air of the room the menthol vapor and soothes the laryngeal mucous 
membrane. If the attack is well developed the nurse should, in addition, disengage 
from a bronchitis kettle steam laden with menthol, or with oil of pine and oil of 
eucalyptus, in the proportion of 15 drops of each in the water in the kettle or on 
the sponge usually placed in its neck or spout. Internally a dose of 5 to 10 grains 
of bromide of sodium may be given in syrup, and over the larynx should be placed 
a compress wrung in hot or cold water. 

For the prevention of future attacks the child should be relieved of adenoids 
or enlarged tonsils, should receive proper diet and tonics if rachitic, and should 
sleep in a bronchitis tent if the larynx is irritable. A sponge loaded with cold 
water may be sopped upon the skin over the larynx every morning to improve its 
vascular tone. 

TUBERCULOUS LARYNGITIS. 

Definition.— As its name implies, tuberculous laryngitis is due to the presence 
of the Bacillus tuberculosis in the laryngeal tissues and the consequent development 
therein of miliary or larger tubercles. (See Tuberculosis.) 

Etiology. — In the vast majority of cases of laryngeal tuberculosis the infection 
is secondary to pulmonary disease, and is due to infection of the larynx by the 
sputum which the patient coughs up, or by direct extension from below upward. 
In rare instances it is undoubtedly a primary affection. I have had such a case 
under my care while writing this article. As in tuberculous infection in other parts 
there must be, in addition to the presence of the bacillus, a susceptibility to infection, 
or one acquired by general or local lowering of vitality. This disease occurs most 
commonly in males between twenty and thirty years of age. 

Pathology.— Here, as elsewhere in the body, the development of tubercles takes 
place by leukocytic migration and the proliferation of cells, and is accompanied 
by the closing of bloodvessels and the necrosis of the masses formed, followed by 
breaking down and escape of the cheesy material, and the production of ulcers 



TUBERCULOUS LARYNGITIS 369 

in the laryngeal mucous membrane. As the process of infiltration proceeds the 
perichondrium is attacked and necrosis takes place in the laryngeal cartilages. 

In many other parts of the body the system makes efforts at repair, so that, 
even if the disease ultimately wins the battle, evidences of an active defense can 
be recognized; but in the larynx it very commonly happens that no such reparative 
or protective process occurs, and this is one of the reasons why the malady is so 
rarely cured. In some cases the infectious process takes on some of the aspects 
of a tumor, a tuberculoma, manifesting a tendency to infiltration and induration, 
with but little inclination to ulceration. 

Symptoms. — There are few maladies which present such a distressing picture 
of suffering as does laryngeal tuberculosis. The loss of voice, which permits speech 
only with great effort, cuts off the patient from pleasant intercourse with friends 
and from expressing any but his most urgent needs, and then only with great pain 
and effort. The thickening of adjacent tissues nearly always makes swallowing 
most difficult and painful, and for this reason urgent thirst must be satisfied with 
but one swallow of water. The same dysphagia makes the use of solid food impos- 
sible and the taking of liquid nourishment almost so, yet the patient cannot combat 
the malady unless well nourished. Because of these factors and the constant pain 
and loss of sleep, the loss of weight in laryngeal tuberculosis is often extraordinary, 
almost equalling that seen in some cases of malignant growth elsewhere. 

In the earlier stages the loss of voice and constant discomfort in the larynx may 
be the only symptoms. Cough is present in all cases to some extent, and is often 
exceedingly painful. After all the muscles about these parts have had their action 
inco-ordinated by direct infiltration or disordered nerve supply, particles of food 
get into the larynx and cause spasm and pain which is insufferable. 

A careful examination of the chest wall will reveal in most cases some tuberculous 
focus. 

If the laryngoscope is used in the early stages, an acute hyperemia may be found, 
but in the chronic type the appearance will be that of marked local anemia. A 
tuberculous lesion may be found in the epiglottis, whence it gradually passes 
downward, or the disease may begin below the cords and work its way upward. 
These tuberculous areas are composed of small nodules or swellings which are 
hyperemic in the acute cases and anemic in the chronic cases. As these nodules 
grow they may, by their mere mechanical presence, cause obstruction to free 
respiration. The infiltration of the epiglottis becomes marked, and the mucous 
membrane may become dotted by a multitude of small, yellow tubercles which are 
easily recognized. These break down and, having done so, form small ulcers which 
coalesce and form larger areas of ulceration. Comparatively rarely the vocal 
cords develop tiny vegetations. 

Diagnosis. — The discovery of a pulmonary tuberculous process in the presence 
of hoarseness, which is persistent and does not clear up under the ordinary 
treatment for acute or chronic laryngitis, raises a suspicion of the tuberculous 
character of this malady at once. In syphilitic laryngitis the history of the patient, 
the reddened areola about the ulcers, and the presence of signs of syphilis elsewhere 
will aid the diagnosis. From carcinoma of the larynx we can separate tuberculous 
laryngitis by the fact that the former disease occurs as a single new growth in a 
person who is usually past the period of life in which tuberculosis is prevalent. 

Prognosis. — The prognosis is most unfavorable even in cases seen in the early 
stages, because the ability to carry on repair in these tissues is so poor and because 
experience has taught us that these cases rarely recover. 

Treatment. — The treatment in laryngeal tuberculosis can be carried out only 

by a skilled and dexterous laryngologist. Even in his hands it may cause much 

distress and pain. In the hands of the tyro clumsy handling is probably worse 

than useless. For the palliation of the condition and of the suffering the parts 

24 



370 DISEASES OF THE BRONCHI 

may be sprayed with peroxide of hydrogen followed by a mild alkaline solution, 
and these in turn by a spray containing menthol 5 grains, oil of sandal-wood 5 
minims, and liquid albolene 1 ounce. General tonic treatment such as is used in 
all cases of tuberculosis, with careful feeding, is essential. As a rule, the patient 
should avoid high altitudes, particularly if they are windy, as the drying of the 
mucous membrane increases discomfort in the larynx. 



SYPHILITIC LARYNGITIS. 

Etiology. — Syphilis of the larynx appears during the secondary and tertiary 
stages of the disease. In the secondary stage it may amount to nothing more 
severe than hyperemia or erythema, such as is usually met with in ordinary acute 
catarrhal laryngitis, but in other instances mucous patches develop, which are 
most numerous about the aryepiglottic folds, the region of the vocal cords, the 
arytenoid cartilages, and on the edges of the epiglottis. If active treatment is 
instituted they usually readily yield, but they may become distinct ulcers. When 
these heal there may be sufficient thickening of the parts to cause permanent 
hoarseness. 

Tertiary syphilis appears in the larynx as a diffuse or circumscribed gummatous 
growth, which usually attacks the epiglottis, the cords, and the posterior wall 
of the larynx, causing thickening and infiltration of the tissues, and finally ulcera- 
tion of the surface in some instances. The cicatrization of the ulcers, or sclerosis 
of areas by infiltration, may cause stenosis and distortion of the laryngeal wall. 

Symptoms. — The symptoms are hoarseness and loss of voice, but pain is rarely 
present. 

Diagnosis. — The diagnosis is based on a history of syphilitic infection or by the 
finding of evidence of syphilis and by the relief which follows specific treatment. 
Tuberculous ulceration is not so rapid in its development and the patient reacts 
to tuberculin. Further than this, in syphilis the upper surface and in tuberculosis 
the lower surface of the epiglottis is usually affected. From malignant growth 
of the larynx syphilis is separated by the fact that the ulcer is solitary in epithelioma. 

Prognosis. — The prognosis is good if treatment is used early, before the stage 
of ulceration is well developed. After ulcers have become deep and severe they 
may be healed by treatment, but cicatricial contractions necessarily appear as 
healing goes on. 

Treatment. — The treatment consists of iodide of potassium, salvarsan, and the 
mercurials, as in other cases of syphilis. (See Syphilis.) 



DISEASES OF THE BRONCHI. 

ACUTE CATARRHAL BRONCHITIS. 

Definition. — Acute bronchitis is an inflammation of the bronchial tubes which 
is usually confined almost entirely to the mucous membrane lining them. 

History. — Bronchitis has been recognized as a distinct condition for many cen- 
turies. It was not, however, until the early part of the nineteenth century that 
this term was used to describe the condition now under discussion, when Badham, 
in England, and Franck, in Germany, first employed this term. As with many 
other diseases involving the thoracic organs, a clear description of the pathological 
condition was first given to us by the French physician Laennec. 



ACUTE CATARRHAL BRONCHITIS 371 

Distribution. — Acute bronchitis is a disease which occurs in all parts of the world, 
but it affects chiefly the inhabitants of those regions in which the climate is moder- 
ately cold and raw, and where the degree of humidity in the atmosphere is high. 
On the other hand, hot and dry portions of the earth's surface are usually free 
from this disease. Another important factor in its prevalence is sudden changes 
of temperature and the prevalence of cold winds laden with moisture. For these 
reasons the disease is most frequent at those times of the year when sudden changes 
of temperature are apt to occur, and therefore is commonly met with in the late 
winter and early spring months. 

Etiology. — The etiology of acute bronchitis, so far as external influences are con- 
cerned, has just been described. In a goodly number* of cases, practically in all, 
it is probable that micro-organisms have much to do with the development of 
the disease, and that the primary hyperemia and congestion of the bronchial 
mucous membrane is due to the exposure of the surface of the body to external 
influences and, to a slight degree, to the passage over the bronchial mucous mem- 
brane of an atmosphere which, because of its physical condition, is irritating to 
these parts. It is a well-known clinical fact that exposure of the surface of the 
body to cold seems to be followed by congestion of the bronchial mucous membrane, 
and that this actually takes place has been proved, first, by experiments upon 
animals, and, second, by observations upon man. Thus, it is possible by the 
external application, alternately, of heat and cold to the upper portions of the 
thorax to produce great changes in the capillary circulation of the larynx and 
trachea and probably the bronchial mucous membrane as well. 

Much depends, too, upon the general health of the patient who is exposed to 
the provoking causes which have just been named. Strong, hearty, or robust 
individuals who have a well-balanced circulation and elastic bloodvessels frequently 
suffer from no pulmonary inconvenience from exposure, but persons who have 
been enfeebled by disease, or by advancing years, or those who are very young 
frequently suffer from such a severe congestion, and it may produce fatal conse- 
quences. Bronchitis is also not rarely the result of an inflammatory process 
which begins higher up in the respiratory tract and extends to the tubes. Prac- 
tically all acute infections of the lung also produce some bronchial inflamma- 
tion. 

So, too, any condition of cardiac or renal disease which impairs circulatory 
activity is exceedingly prone to render the patient susceptible to this form of 
inflammation. We find, therefore, that acute bronchitis is a disease which is 
most prevalent in infancy and old age, and it is entirely competent, at these two 
periods of life, to produce death if it is present in a severe form. Those who have 
been attached to the departments for children in large hospitals cannot fail to 
have been impressed with the very great frequency of this disease in the winter 
months, and also with its rarity among the adults who come to the same institution 
for various ailments. 

Both sexes are equally prone to suffer from acute bronchitis, but it is more 
frequently met with in males because males are more exposed to the provoking 
causes than females. 

Certain of the acute infectious diseases very strongly predispose to this malady. 
Thus, it is nearly always present in a well-developed form in a case of measles, 
even when that disease is present in a mild form. Again, there are but few cases 
of typhoid fever which do not have a certain amount of bronchitis. 

The reason that bronchitis so frequently complicates cardiac disease depends 
upon the intimate relationship between the circulation in the lungs and the right 
side of the heart, for the bronchial veins open into the venae azygos and the superior 
intercostals, and so are intimately connected with the right side of the heart. These 
bronchial veins also anastomose closely with the pulmonary veins, and so valvular 



372 DISEASES OF THE BRONCHI 

disease which results in congestion of the right side of the heart naturally tends to 
produce a disturbance of the circulation in the bronchial mucous membrane. 

When emphysema of the lungs is present the coincident bronchitis is really 
due to two causes : first, the congestion of the right side of the heart which is so apt to 
ensue in emphysema, and, second, the pathological changes in the heart result 
in impairment of the bronchial circulation. On the other hand, bronchitis some- 
times leads to emphysema. These affections are therefore interactive. 

There are three other important etiological factors in the production of bron- 
chitis which must be considered. The first of these is the inhalation of irritant 
gases or vapors, producing what is known as acute traumatic bronchitis. The 
second is the inhalation of dust. These dusts may be vegetable, animal, or mineral 
in their origin. Sometimes all three forms are combined. Finally there can be 
no doubt that the inhalation of various micro-organisms may result in bronchial 
infection. 

Of the forms of dust which produce bronchitis we find that vegetable dust seems 
to be the most frequent cause. 

That form of bronchitis which most frequently follows the inhalation of irritant 
vapors or gases is seen in persons who have been exposed to ammonia fumes, 
irritating smoke, or to chlorine gas. Another form of local irritation producing 
bronchitis is that which is seen in large cities which are heavily veiled with smoke 
and fog. Thus, in the city of London the particles of moisture in the air become 
loaded with the sooty materials, and so evaporation, even in houses which are 
fairly well heated, is greatly impaired, and the fog penetrates in-doors. As a 
result the frequency of* acute bronchitis is greatly increased in London in those 
seasons of the year in which these fogs are prevalent, and the mortality of chronic 
bronchitis is wonderfully increased at these times. So powerful an influence do 
these deleterious factors exercise that it is a well-known fact that the mortality 
in the city of London may be doubled in those weeks in which the fog is present. 
Thus, on some occasions the mortality is as high as 46 per cent, as against an 
ordinary death rate of about 18 per cent. The deaths from diseases of the respira- 
tory organs rose on one occasion from 415 per week to 994 per week during the 
prevalence of a dense fog. Of these, 694 were due to bronchitis and 185 to pneu- 
monia. Probably most of them were bronchopneumonia complicating chronic 
bronchitis. That this increase was due to the fog and not to the other conditions 
of the climate is proved by the fact that a similar increase in mortality did not 
take place in surrounding provincial cities and towns. These facts are well empha- 
sized by West in his well-known book upon Diseases of the Organs of Respiration. 

The micro-organisms infecting the bronchial mucosa are the pneumococcus, 
which is most common; Friedlander's bacillus, the Streptococcus pyogenes, and the 
pyogenic staphylococci. The Klebs-Loeffler bacillus is usually present in the 
bronchitis which complicates diphtheria. In some cases of bronchitis additional 
micro-organisms have been found, such as the Bacillus typhosus, Bacillus coli 
communis, and various forms of fungi. In most instances, however, bronchitis 
is polymicrobic in origin, and it is often impossible to decide what organism is the 
primary infecting agent. 

Prevention. — Acute bronchitis can only be prevented by proper care of the 
general health, by proper clothing, and by the avoidance of climatic influences 
which are known to be deleterious. Persons who have learned by experience that 
they are peculiarly susceptible to the various provoking causes named, should, 
by change in climate or occupation, avoid these various causes of irritation. 

Pathology and Morbid Anatomy. — Acute bronchitis is characterized by hyperemia 
and swelling of the mucous membrane lining the bronchial tubes, accompanied 
by some infiltration of the submucous tissues. At first there may be an almost 
total secretion or undue dryness of the surface involved, but very soon the engorged 



ACUTE CATARRHAL BRONCHITIS 373 

mucous glands begin to pour out into the lumen of the tubes considerable quantities 
of mucus, which also soon contains epithelial cells coming from the lining of the 
glands themselves and from the surface of the mucous membrane as well. Leuko- 
cytes, which have undergone diapedesis, as they do in all acute inflammatory 
processes, are also present, and even red blood cells may be seen. A similar extra- 
vasation of red cells may also take place into the submucosa, and, escaping on the 
surface tinge the sputum. In the smaller bronchi the lining epithelium may be 
cast off in shreds, and if the inflammation is intense, we may find the tubes almost 
or completely closed, with resulting capillary bronchitis or suffocative catarrh. 
By the extension of the inflammation to the peribronchial tissues and the pul- 
monary alevoli there is developed a bronchopneumonia. (See Bronchopneumonia.) 
As recovery takes place the dead epithelium and extravasated cells are expelled 
from the tubes by coughing, and new epithelium is developed from deeper layers 
of cells. Sometimes, particularly when a large number of infecting micro-organisms 
are present, the sputum is distinctly purulent. When bronchial inflammation 
persists for any length of time, or the attacks are frequently recurrent, permanent 
thickening of the submucosa results. This fibrosis may extend to adjacent struct- 
ures (peribronchitis) or be continuous with the increased fibrous tissue of chronic 
interstitial pneumonia. 

. Symptoms.— The symptoms of acute bronchitis can be divided into three stages, 
namely, that of onset, the stage of profuse secretion, and the stage of convalescence. 

In the stage of onset there may be a chill, which usually is not severe; a short, 
dry cough which may, by its persistence, be annoying, and, owing to the dry and 
inflamed state of the mucous membrane of the bronchial tubes, be distressing 
because of the soreness or pain it produces under the sternum. If the degree of 
swelling of the mucous membrane is marked, there may be a sense of oppression, 
and the breathing may be a little quickened. The temperature of the body is 
usually not much above normal in the adult, but in children it is often as high as 
102° or even 103°, and the pulse is apt to be rapid in direct proportion to the degree 
of fever. Auscultation at this time reveals an increased roughness of the inspiratory 
or expiratory bronchial sounds, and perhaps a few dry rales between the shoulder- 
blades. 

In the second stage there is a disappearance of the soreness in the chest, but 
the cough may be persistent, and is more or less productive of expectoration of 
mucopurulent material. Febrile movement continues if that symptom has been 
present earlier. The pulse is but slightly quickened and auscultation reveals, 
particularly over the bronchial tubes posteriorly, large, moist rales and rhonchi. 

The duration of an attack of acute bronchitis rarely exceeds ten days to two 
weeks, and is often shorter than this. 

Treatment. — The treatment of acute bronchitis divides itself into two parts: 
that part which is devoted to allaying the inflammation in its early stages, and that 
which is directed toward the dissipation of the results of the inflammation after 
it has been present for some days. In the early stage no better remedy can be 
administered internally than a prescription which contains in each dose J drachm 
of syrup of ipecac and 1 teaspoonful to 2 teaspoonfuls of the official liquor potassii 
citratis of the United States Pharmacopeia. This should be administered every 
three or four hours. 

If cough is an annoying symptom, and there is much pain in the chest, Dover's 
powder may be given to an adult in the dose of 2 or 3 grains every three or four 
hours until 10 grains have been taken. A mustard plaster may be applied to the 
chest, back and front, or the thorax may be rubbed with ammonia liniment or 
with chloroform liniment. In children a very useful counter-irritant application 
to the chest is 1 drachm of the oil of amber in 2 tablespoonfuls of sweet oil. If the 
patient be a child, and if the air of the bed-room is particularly dry and irritating, 



374 DISEASES OF THE BRONCHI 

because it is furnace-heated, much relief can be obtained by disengaging a small 
quantity of steam. This may be given off from a tea-kettle which is kept boiling 
constantly, or may be obtained by dropping large pieces of unslaked lime into a 
tub of water. It is probable that when the latter procedure is resorted to the air 
of the room not only contains an extra amount of moisture, but fine particles of 
lime, which act advantageously upon the bronchial mucous membrane. 

If the evidences of bronchial irritation are very marked, the patient, whether 
he be an adult or a child, should sleep in a bronchitis tent. A bronchitis tent, it 
will be remembered, consists in a tent-like arrangement of sheets spread over the 
bed, and resting upon four corner sticks, one of which is tied to each corner of the 
bed. Under this canopy the patient will have plenty of air, and the steam from 
a kettle can be disengaged within its confines. If necessary, 1 or 2 grains of menthol 
may be added to the hot water every two or three hours. In other instances 
the bronchial irritation will be greatly soothed by pouring into the boiling water a 
tablespoonful of a mixture composed of equal parts of compound tincture of benzoin, 
oil of eucalyptus, and oil of pine. 

After secretion has begun to form in the secondary stage of acute bronchitis 
it then becomes necessary to administer not sedatives, but stimulant expectorants, 
and of these chloride of ammonium, without any doubt, is usually followed by the 
best results. From 5 to 10 grains of this drug may be given with equal parts of 
the fluidextract of licorice and water every four or five hours to an adult, and, if 
cough is excessive, \ grain of sulphate of codeine or 20 drops of paregoric may 
be added to each dose. Under the influence of this remedy the expectoration of 
yellow or mucopurulent sputum is at first increased, but at the end of twenty-four 
or forty-eight hours the quantity diminishes. 

When there seems to be lack of secretion, the compound licorice mixture of the 
United States Pharmacopoeia, which contains a small quantity of tartar-emetic, 
may be used in place of the plain extract of licorice just named. If for any reason 
the cough and expectoration persist and do not diminish under the use of the 
chloride of ammonium, we may give with advantage 5 to 10 minims of the oil of 
sandal-wood in capsules, three or four times a day. Other patients do well at 
this time if they receive 5 minims of the oil of eucalyptus in capsules three times 
a day. The latter remedy, however, is quite apt to disorder the stomach. Another 
very valuable remedy in the secondary stage of bronchitis, to promote expectora- 
tion, is terpin hydrate, which is best given in the form of an elixir, dose, a teaspoon- 
ful, and which may be much increased in its efficiency if to each dose is added T V of 
a grain of heroin, or J of a grain of codeine sulphate. The dose of terpin hydrate 
is from 2 to 5 grains four times a day, but in obstinate cases larger doses may be 
administered. Terebene may also be given in capsules in the dose of 5 minims 
three or four times a day. Oil of sandal wood is also useful. 

If the general nutrition of the patient is not good and he seems somewhat debili- 
tated, the employment of cod-liver oil, or syrup of iodide of iron, in moderate 
doses, will often produce the most advantageous results at this stage of the illness. 

CHRONIC CATARRHAL BRONCHITIS. 

Definition and Symptoms. — By chronic bronchitis is meant a condition in which 
there exists a chronic inflammatory process in the bronchial mucous membrane, 
as a result of which the patient suffers from cough and the expectoration of thick, 
mucopurulent sputum. When uncomplicated there is no febrile movement in 
association with this condition, nor is there, as a rule, any loss of flesh or impairment 
of the general health. It may be regarded as a subacute continuation of an acute 
cold. The chief objection to the term "chronic bronchitis" is that it so often is 
applied by the careless or ignorant, or by those who wish to use an euphemism, 



BRONCHIECTASIS 375 

to designate a far more serious condition, such as pulmonary tuberculosis or 
bronchiectasis. 

Treatment.— The treatment of chronic bronchitis is practically identical with 
that of the later stages of the acute form, which has just been described, but the 
most important thing for the physician to do, to whom is presented a so-called 
case of chronic bronchitis, is to carefully exclude tuberculosis or cardio-renal 
disease as causative factors in the case. Many cases of so-called chronic bron- 
chitis are treated for weeks with ordinary expectorants when tuberculosis is 
present or Bright's disease is the real cause of the disorder. 

BRONCHIECTASIS. 

Definition. — Bronchiectasis, as its name implies, is a condition in which the 
bronchial tubes are dilated. This dilatation may occur in three forms, namely, 
the cylindrical or fusiform, the saccular, and the trabecular or moniliform. The 
first of these is the only true type of bronchiectasis, but the other forms are those 
most commonly met with. 

The disease is not common in its well-developed form. If we combine the statis- 
tics of the Brompton Hospital, of London, with those of Biermer and Willigk, 
we find that in 8144 autopsies bronchiectasis was found in about 4 per cent. These 
are, however, postmortem figures, and do not represent a certain proportion of 
cases which do not come to autopsy because of a respiratory ailment. 

Etiology, Pathology, and Morbid Anatomy. — The saccular form is common in adults, 
and when it is present, the lung, at autopsy, contains one or more saccules, or 
globular cavities, which usually are not very large, but may be the size of a small 
lemon. These cavities or open spaces, when large, are due not only to simple 
dilatation of the bronchi, but to involvement of the surrounding tissues as well, 
and their walls are composed of parts of the bronchial tubes and thick connective 
tissue which has been formed in part as the result of chronic inflammatory changes, 
the lung tissue having undergone fibroid change. Sometimes these spaces are 
filled with thickened, inspissated secretion, and seem like closed cavities. It is 
readily seen, therefore, that the differentiation between this state and fibroid 
phthisis (see Tuberculosis of the Lung), so-called, may be by no means easy, par- 
ticularly as these pouches may become infected, ulcerate, and really form small 
abscesses. 

The trabecular form is still less a true bronchiectasis, and yet it is the condition 
most commonly met with, and to which the term bronchiectasis is most frequently 
applied. It consists in irregular cavities with smooth linings, which cavities are 
surrounded by dense walls of overgrown connective tissue which do not contain 
any signs of remnants of the tissues of the bronchial tubes. On the contrary, 
the only relation borne by the bronchial tube to such a cavity is that it forms 
the trabecular with the atrophied bloodvessels. These cavities are often joined 
one to another by openings, so that the lung may be thoroughly riddled with 
spaces more or less well filled with secretion. 

Cylindrical bronchiectasis (Figs. 69 and 70) is usually developed in children as 
the result of strain upon the bronchial tubes produced by the violent efforts in 
whooping-cough or measles. It probably depends .primarily upon inherent weak- 
ness of the muscular and elastic coats of the tubes. The affected bronchus is 
uniformly dilated in its entire circumference for a considerable distance, and this 
dilatation may be so great that its calibre is increased to twice or thrice the normal. 
In other instances it is dilated in sections, with a normal or nearly normal calibre 
between. 

When bronchiectasis occurs in the saccular and trabecular type it is a subacute 
or chronic disorder, and results from chronic inflammation of the bronchial tubes, 



376 



DISEASES OF THE BRONCHI 



with resulting atrophy of the elastic and muscular coats. Of the provoking causes 
influenza is an important factor. Another cause is the progress of cicatricial or 
cirrhotic change in the pulmonary parenchyma, which, as it proceeds, distorts 
the bronchial tubes, narrowing them in some places and widening them in others. 
In other instances it can be readily understood how chronic thickening of the visceral 
layer of the pleura may so result. In still others a localized bronchiectasis may 
be caused by the entrance of a foreign body. 

Fig. 69 




Bronchiectasis, originating in acute lobar pneumonia. Marked saccular and cylindrical dilatations 
with a large gangrenous cavity in the middle lobe. Duration eleven months. From a case under the 
care of Dr. MaguJre. Dr. Barty King. (Brompton Hospital Museum. Scottish Medical and Surgical 
Journal.) 



The influence of age in the development of the various types of bronchiectasis 
is quite noteworthy. Cylindrical dilatation is largely a condition limited to child- 
hood and the saccular and trabecular types are chiefly met with in adults. It 
has been thought by some physicians that the latter forms occur with increasing 
frequency as old age is approached, but the statistics of Barty King indicate that 
the age incidence of the pure type is from thirty to forty years. Thus, 53.1 per 
cent, of his case's occurred between twenty and forty years. The same observer 
places the proportions of the two sexes as 77 per cent, in males and 23 per cent, 
in females. 

Symptoms. — The symptoms of bronchiectasis naturally vary greatly with the 
form of the disease which is present. Cough of severe degree may be considered 
the most constant of them all. This cough is peculiar in that in many cases it is 
particularly severe in the morning, persisting until the patient has rid his dilated 
and feeble bronchi of the secretions which have accumulated in them during the 



BRONCHIECTASIS 



i t 



night. Not only is this cough peculiar in this respect, but it not infrequently 
happens that the patient, after a prolonged attack of coughing which is unpro- 
ductive, is enabled to get rid of a large quantity of sputum, which may come away 
in a gush or which may not be dislodged until by some change in posture drainage 
from the bronchiectatic area can take place. 



Fig. 70 




Cylindrical bronchiectasis. 



A typical case. Dr. Barty King. (St. Thomas' Hospital Museum. 
Scottish Medical and Surgical Journal.) 



The sputum is also somewhat characteristic, for it is often grayish-brown in 
appearance, somewhat fetid in odor, and separates when placed in a glass into three 
layers, the upper one brownish and thin, the second one mucoid, and the third 
granular and filled with dead epithelial cells and pus corpuscles. This lower 
layer also contains large crystals of the fatty acids and crystals of hematoidin. 
The sputum is so distinctly purulent that it may closely resemble that expectorated 
in cases of pulmonary abscess, a resemblance still further increased by the fact 
that it may be extremely fetid. It is not nummular, as in many cases of phthisis, 
and it rarely contains elastic-tissue fibres, which is of some importance in differential 
diagnosis. Fever is usually not present unless the purulent process in the bronchi 
is marked and septic absorption results. An additional symptom, sometimes 
met with, is hemoptysis from ulceration of a bloodvessel. 

The physical signs of bronchiectasis have little about them that is distinctly 
characteristic, and for this reason an absolute diagnosis may be difficult or impossible 
unless the lesions are so far advanced as to have affected the whole lung and caused 
alteration in the configuration of the chest. When the bronchiectatic spaces 
or cavities are large the physical signs are practically identical with those of pul- 
monary tuberculosis with cavity formation; but there is this important difference, 
namely, that the cavities in tuberculosis are commonly apical while the cavernous 



378 DISEASES OF THE BRONCHI 

breathing of bronchiectasis is usually most marked near the base. The physical 
signs of cavity formation also vary with the condition of the cavity — that is, whether 
it is full of secretion or empty, and therefore a change in the patient's position, and 
cough with expectoration, may cause very great changes in the results obtained by 
examination by auscultation and percussion. Loud, moist rales and amphoric 
breathing may be present. 

Diagnosis. — It is manifest from what has just been said that the differential 
diagnosis of bronchiectasis from pulmonary tuberculosis may be quite difficult 
and, indeed, impossible in certain cases, for it not uncommonly happens that a 
superficial dilated and sacculated area in the lung gives, on auscultation and 
percussion, physical signs which are identical with those which are produced in 
pulmonary tuberculosis with cavity. The presence of tubercle bacilli and of 
yellow elastic tissue in the sputum, of hectic fever, of rapid loss of flesh, and of 
night-sweats point to tuberculous infection. Another useful differential point is 
the fact that in tuberculosis the cavity is usually at the apex, whereas in bronchiec- 
tasis it is lower down in the lung. Still another point is that the patient is not as 
ill as in tuberculosis, and can get about year after year unless some acute inter- 
current pulmonary malady intervenes. 

On the other hand, bronchiectasis and pulmonary tuberculosis may exist simul- 
taneously. Thus, in 68 cases of bronchiectasis observed by Trajanowski, 21 
occurred in individuals who were affected with phthisis, and in 75 autopsies on 
individuals who died from phthisis Wilson Fox found bronchiectasis in 27 cases. 
Twenty-one were of the fusiform variety and six were saccular. 

Complications. — Hemoptysis, as a complication of bronchiectasis, is rarely severe 
and occurred in Barthez's cases 16 times out of 39 cases. Grainger Stewart met 
with it 3 times in 8 cases, and Fowler met with it 14 times in 35 cases. Three of 
these cases were tuberculous. 1 

Another complication is rheumatoid arthritis. I have recently had a case 
under my care in which, after many years of chronic bronchiectasis, a maiden 
lady developed multiple arthritis, and in the course of a few weeks became com- 
pletely disabled. Sometimes no more serious joint difficulties arise than swelling 
of the finger- joints and clubbing of the finger-tips, with incurvation of the nails, 
or the case develops true pulmonary osteo-arthropathy. The joint complications 
are probably septic in origin. Pulmonary gangrene may also develop, and Duret 
has operated on such cases with success. 

Brain abscess may arise from a septic focus in bronchiectasis. 

Cyanosis and dyspnea on exertion are such constant symptoms that they can 
scarcely be considered as complications. 

When we consider the state of the tissues involved we can readily understand 
how readily a septic bronchopneumonia may be developed in these cases, either 
as a result of direct extension of the inflammatory process from the area primarily 
involved, or by the inspiration into other parts of the lung of septic material during 
paroxysms of coughing. 

Prognosis. — This depends upon the state of the patient's health, the presence 
or absence of sepsis, and the presence or absence of tuberculous infection. In 
severe forms the health is greatly impaired. Recovery from the condition itself, 
if it be well developed, is manifestly impossible. Nevertheless, life may continue 
for many years. 

Treatment. — The treatment of well-developed bronchiectasis can be only pallia- 
tive. Once the condition of dilatation of the bronchial tubes has been established, 
it is evident that they cannot be brought back to their normal calibre. On the 
other hand, in the early stages of bronchiectasis, much can be done in the way of 

1 For some of the cases in French literature see Devic and Bertier, Lyon medical, January, 1904. 



FIBRINOUS BRONCHITIS 379 

palliative treatment. It is a mistake, however, to give sedatives to control the 
cough unless the cough is so excessive that it materially interferes with sleeping 
and eating, for cough is a measure designed by nature to rid the dilated tubes of 
the secretions which certainly do harm if they are retained. Ordinarily, expectorant 
remedies cannot be expected to do as much good as they do in ordinary cases of 
bronchitis. The best to be employed are creosote in doses of 3 to 5 minims three 
or four times a day; guaiacol in the dose of 3 minims three times a day, or guaiacol 
carbonate in the dose of 3 grains three times a day. In some instances much good 
follows the administration of a mixture containing iodide of ammonium. Still 
other cases are benefited by the chloride of ammonium. 

It must not be forgotten that many cases of bronchiectasis which have lasted 
for some years suffer as well from feebleness and dilatation of the right side of the 
heart, and the degree of cyanosis and dyspnea on exertion can be much decreased 
by the administration of small and continuous doses of digitalis or strophanthus, 
and, in some instances, by the proper use of strychnine. A certain amount of 
rest in bed or on a couch every day is very advisable; and if the patient seems to 
have great difficulty in expectorating the contents of certain cavities, experiments 
should be made with different postures to determine that in which the cavity is 
most easily drained, and he should be instructed to take this posture in order to 
avoid prolonged and exhausting spells of coughing. 

Within the last few years a number of clinicians have warmly advocated the 
employment of intratracheal injections of medicaments in cases of bronchiectasis. 
Various mixtures have been employed, of which perhaps the most popular have 
contained menthol, guaiacol, olive oil, or albolene. They do little good. In 
other instances, asserted good results, so far as elimination of the symptoms are 
concerned, have followed the inhalation of various drugs, such as the vapor of 
chloride of ammonium, creosote, and tar. 

So far as climatic treatment is concerned, these patients should carefully avoid 
high, dry altitudes, and should resort to hill altitudes or the seaside resorts, 
unless the latter are too damp, in which case the drier places must be sought, as, 
for example, Thomasville, Georgia; Lakewood, New Jersey, or some similar spot 
not too near the sea, where there is a sandy soil and a heavy pine growth. Such 
patients, too, should be warned of the danger of complications which may follow 
exposure to sudden changes of temperature and to wet, and should wear flannels 
next to the skin all the year round, if possible, to avoid chilling the surface. If 
these precautions are taken, the greater amount of time spent in the fresh air the 
better, as in-door life for these patients is disadvantageous if the climate is at all 
suitable to their condition. 

FIBRINOUS BRONCHITIS. 

Definition. — Fibrinous bronchitis is an exceedingly rare affection, characterized 
by the formation of a fibrinous exudate which makes a cast of the bronchial tubes. 
As ordinarily observed it is in no way related to diphtheria, in which disease, 
however, casts of the larynx and trachea and even of the bronchial tubes sometimes 
form. 

Etiology. — The cause of this strange affection is practically unknown. When 
it occurs as a complication or sequel of other diseases, it seems to bear no relation 
to them save that of coincidence. The condition is much more frequent in males 
than in females, and is not particularly prone to occur at any particular age. West 
states the youngest case recorded is four years of age, and the oldest seventy-two 
years. It has occurred more frequently after acute croupous pneumonia and 
during the progress of pulmonary tuberculosis and ordinary chronic bronchitis 
than in other maladies, but its occurrence in these affections is not sufficiently 



380 DISEASES OF THE BRONCHI 

constant to justify us in considering that these relationships are direct. In some 
instances it is associated with the presence of mitral disease of the heart. 

Pathology. — The casts when expelled are found to be composed of masses of 
gelatinous or pulpy-looking material which, when floated in water or carefully 
spread upon a glass surface, are found to be in the form of the bronchial tubes; 
sometimes even of the smaller tubes. The casts are tough and yellowish-white 
in appearance, and many are composed of fibrin in which may be found white 
blood cells and epithelium from the bronchial mucous membrane. Other casts 
contain no demonstrable fibrin, but are rich in mucin. Whether they are distinct 
forms or altered fibrinous casts is not known. The cast may be hollow or filled 
with gelatinous mucus. It is a curious fact that these casts may form without 
resulting in serious lesions of the lining membrane of the tubes, for even the epithe- 
lial lining of the bronchial tubes may not be found seriously impaired after a cast 
is thrown off (Fig. 71). 

Fig. 71 




Cast from a case of fibrinous bronchitis. 

As the affection is very rare, and still more rarely causes death, we know com- 
paratively little of its true morbid anatomy. Sometimes casts have been found 
at autopsy when the condition was not suspected to be present, and in other cases 
in which casts had been thrown off in life none have been found at the postmortem. 

Symptoms. — The symptoms of fibrinous bronchitis chiefly consist in severe 
attacks of cough and dyspnea, the cough being an effort to dislodge the membrane 
and the dyspnea the result of the obstruction to the respiration. Sometimes the 
dyspnea has been quite urgent, but it has usually been almost completely relieved 
after the cast is expelled. This expulsion of a cast may occur once in a lifetime, 
once in several weeks, once in several days, or several casts may be expelled in one 
day. Rarely the formation of a cast suggests periodicity. While the cough is 
usually severe in the effort to dislodge the exudate, the expulsion may be readily 
accomplished. Occasionally hemoptysis complicates the case, usually amounting 
to nothing more than slight streaking of the expelled membrane, but in other 
instances the bleeding is quite profuse. The blood comes from the bronchial, 



BRONCHIAL ASTHMA 381 

not from the pulmonary vessels. Fever may be present in the acute cases, but is 
usually absent in the more chronic ones. 

Diagnosis. — This condition must be separated from diphtheria, which can be 
done by the absence of false membrane in the fauces and larynx; from croupous 
pneumonia, which is possible by reason of the absence of the fever and other signs 
of that disease; and from foreign bodies in the air passages, which cause dyspnea 
and violent attacks of cough; by the history of the patient. 

Prognosis. — The prognosis as to return of the disorder is bad, as most cases 
suffer from recurrence, although acute cases in which complete recovery has occurred 
have been reported. In regard to the effect of the disease on life it may be said 
that this varies greatly with the general state of the patient's health and upon the 
gravity of the diseases which are associated with it. 

In cases with no grave complications recovery may be expected in a majority. 

Treatment. — The only plan of treatment which has proved itself of value in a 
sufficient number of cases to be regarded with any confidence is the use of iodide 
of potassium in full doses. Some patients seem to be made more comfortable 
by the inhalation of steam. Climatic change is often essential, and Southern 
California, or Florida, or Madeira, may be resorted to. 

BRONCHIAL ASTHMA. 

Definition. — Strictly speaking, the word "asthma" may be applied to any con- 
dition in which the respiration is labored and difficult, but in medicine it is most 
commonly used to describe a condition of difficult breathing due to constriction 
of the bronchial tubes and further narrowing of their calibre by swelling of the 
mucous membrane lining them. This state of spasm of the bronchial muscle 
fibres and hyperemia of the mucous membrane depends upon a neurosis. This 
neurosis may arise in turn from a large number of causes, all of which probably 
exercise their influence through the pneumogastric nerves. 

It is unfortunate that the term "asthma" has also been applied to labored 
breathing due to various toxemias, such as uremia and the coma of diabetes. 
Renal disease may, it is true, indirectly produce true asthma, but this word ought 
not to be applied to that form of labored breathing in which there is no swelling 
or spasm of the sort described in the preceding paragraph. The term asthma 
is, therefore, used in this article to mean bronchial asthma. 

Etiology. — The cause of asthma in many cases cannot be determined, and in 
some persons it is evidently due to some lack of stability in the nervous control 
of the bronchial tubes. In others the asthmatic attack arises because of the 
inhalation of bad air, which acts as an irritant to the respiratory tract, either 
because of the state of the atmosphere itself or because the air is laden with dust 
The influence exercised by the atmosphere in producing asthmatic attacks is 
very great and varies in different cases to an extraordinary degree. Mere impurity 
of the air has little to do with this influence in some cases. .Thus, I had under 
my care an old man, from a healthy country district in Pennsylvania, who came 
to Philadelphia to get relief from nightly attacks of asthma. Without any treat- 
ment the severity of the attacks diminished when he breathed city air on the level 
of the street, dust laden though it was, and his attacks ceased entirely so long as 
he remained in a private room of the fifth floor of the Jefferson Hospital, where 
there was less dust, but, perhaps, more smoke and gas from the neighboring chim- 
neys. In other instances gases or fumes, as from coal or arsenic, produce an attack, 
and in still others the patient only suffers at that season of the year when the pollen 
of certain plants or flowers is set free. For this reason, sufferers from "hay fever" 
often suffer from asthma, since the exciting causes of both states are present, 
namely, a respiratory neurosis and the irritants in the air. 



382 DISEASES OF THE BRONCHI 

In still other cases the cause lies in the system of the patient and does not come 
from outside. There is some justification for the view that the condition in certain 
cases is a form of anaphylaxis; that is, the patient is sensitized by heredity or 
acquirement to certain proteid substances. Thus an ethmoiditis or trouble in 
the frontal sinus with pus formation may cause the absorption of a minute amount 
of proteid that will induce an attack of anaphylaxis in a sensitized individual. 
Again certain persons who are sufferers from gout will occasionally have attacks 
of asthma, just as they have pain in the toe or soreness in the voluntary muscles; 
and, again, it not uncommonly happens that persons who have an unstable nerve 
supply to the bronchial tubes have an attack of asthma if exposed to great cold 
or if they have a slight bronchial congestion due to this cause. So, too, such persons 
may be seized with an attack as the result of great physical weariness or of nervous 
excitement, and it by no means rarely happens that feebleness of the heart, which 
results in poor circulation in the lungs, produces a seizure in susceptible persons. 
Such a case is called one of "cardiac asthma." In other instances deficient activity 
of the kidneys produces indirectly a similar seizure or so-called "renal asthma" 
In some cases great acidity of the stomach, and the various forms of indigestion, 
reflexly provoke an attack through the gastric fibres of the vagus nerves. 

The nervous mechanism whereby an asthmatic seizure is produced is supposed 
to be as follows: The control of the circulation in the bronchial mucous membrane, 
and of the muscular fibres controlling the bronchial tubes, resides in the vagus 
nerves, which possess efferent and afferent fibres, not only connected with the 
lungs, but with the stomach and heart as well. There are also, in all probability, 
fibres which indirectly connect the nasal mucous membrane with the vagus. 
Certain causes of irritation acting upon the respiratory, gastric, and cardiac fibres 
of the vagus give rise to an afferent impulse sent to the vagus centre, and this in 
turn results in the irradiation of an efferent impulse to the bloodvessels in the 
bronchial mucosa and to the bronchial muscular fibres, whereby the tubes are 
constricted, the mucous membrane becomes swollen, and, in addition, secretion 
takes place, which aids in obstructing still further the smaller tubes. 

Pathology and Morbid Anatomy. — The pathology of this condition has been 
described in part in the preceding paragraph. The morbid change which is mani- 
fest is the engorgement of the mucous membrane, the thick, viscid, bronchial 
secretion, and the spasm of bronchial tubes. 

The morbid anatomy, unless secondary conditions arise, is nil, for with the 
disappearance of the attack the lungs attain their normal state within a short 
time. It is only when repeated attacks of asthma occur that the patient as a 
consequence suffers from chronic bronchitis, emphysema, or bronchiectasis, 
although, if a single attack is very severe, he may develop bronchopneumonia, 
particularly if exposed to cold and dampness. 

The chest of the asthmatic patient, who has suffered from this disease for many 
years, is usually like that of pulmonary emphysema in its configuration, and if 
the disease be present in early life, when the chest is very pliable, a "pigeon-breast" 
may be developed, and a well-marked Harrison's groove may be seen. 1 

In most instances in which asthma has been present for years the heart undergoes 
dilatation and hypertrophy, particularly on the right side, and its beat may be 
quite feeble if hypertrophy has not fully compensated for the dilatation. Second- 
arily, these cardiac changes may result in hepatic and renal congestion. 

The scanty sputum which is expelled by asthmatic patients possesses in many 
instances peculiarities which are pathognomonic. This' sputum, if examined, 
is found to contain little lumps or balls, which, if they are teased out on a plate of 
glass placed on a black background, are found to consist of minute curls or twisted 

1 "Harrison's groove" is that depression which begins at the sternum at the attachment of the seventh 
or eighth rib, and extends backward in the line of the ribs toward the axilla. 



BRONCHIAL ASTHMA 383 

fibres, in form not unlike the curls of hair on a child's head. These curls are called 
" Curschmann's spirals," and in their folds are found crystals of the fatty acids, 
the so-called " Charcot-Leyden crystals." That fatty acids are present, however, 
is denied by many. Thus, Goodhart and Taslett think these curls are related 
to the casts of fibrinous bronchitis, and they point out that such casts frequently 
show twists or spiral terminations. Hoffmann thinks the terminal bronchioles 
are spiral in form. 

Before and during an attack of pure bronchial asthma there is an extraordinary 
increase in the number of eosinophiles in the blood. This eosinophilia is said 
not to occur in cases of renal and cardiac asthma. 

Symptoms. — The symptoms of spasmodic or bronchial asthma, in well-developed 
cases, are very typical. The patient usually retires to bed perfectly well and^wakes 
at midnight or in the early morning with a sense of intense dyspnea, oppression, 
which may be so severe as to seem to threaten death from asphyxia, but death 
never occurs in an attack from this cause. The attitude of the patient suffering 
from asthma is most characteristic. If he is in bed he sits up and places his hands 
back of him on the mattress, so as to support himself in that posture which will 
enable him to use his auxiliary muscles of respiration to the greatest possible 
extent. His respirations are labored, his brow is covered with sweat, and his face 
is at first anxious and pale, and then cyanosed and livid. The efforts at inspiration 
and expiration are forcible, but the chest has the appearance of distention, since 
the intercostal spaces are often unduly full, and the anterior portion of the thorax 
is elevated. The difficulty under which the patient labors is that he retains in 
his chest an excess of air which has become vitiated, but which he cannot expel, 
and therefore he has no room for fresh air. The condition is rather one of difficult 
expiration than of difficult inspiration. Owing to the great shortness of breath 
the patient is often unable to speak except in a whisper, and speaks but a word or 
two with each breath. The superficial veins are engorged. The urine during an 
attack is often scanty and heavily loaded with urates, but after the attack it is 
often passed in large quantities, and is clear and limpid. 

The attack may last from a half hour to several hours, and leaves the patient 
quite exhausted. In some instances, with the passing of the seizure, almost total 
respiratory relief follows, but in most cases some dyspnea persists for several 
hours, and cyanosis may be present till all respiratory difficulty is relieved. If 
the degree of relief is sufficient to permit sleep, the patient may be sufficiently 
rested to attend to business the following day, but in the majority of cases this is 
impossible, or at least inadvisable, because of the fatigue, the weak condition 
of the heart and lungs from the effects of the attack, and the presence of the bron- 
chitis and bronchial secretion, which may result in fatal bronchopneumonia if 
the patient is not very prudent as to exposure. 

Diagnosis. — The history of the attack, in its mode of onset and subsequent 
development, renders a diagnosis easy. The duty of the physician is to discover, 
if possible, the cause of the attack and remove it, resting confident that asthma 
is always a symptom and not a disease. The physical signs present in an attack 
are very characteristic. In the early stages auscultation reveals harsh bronchial 
breathing, with musical rales, which may be scattered here and there through 
the chest, and owing to the disturbed respiratory cycle it may seem as if one part 
of the lung does not expand simultaneously with the other parts. When the 
attack is well developed the difficult passage of air through the narrow tubes results 
in the still greater development of musical sounds, which may be described as 
resembling those made by a litter of mewing kittens or crying puppies. These 
to-and-fro, loud, musical rales, widely diffused through both lungs, are so character- 
istic of the asthmatic patient as to make the diagnosis certain in many cases. 

There is one condition from which asthma in the later stages must be carefully 



384 DISEASES OF THE BRONCHI 

separated, namely, that of pulmonary edema. Aside from the fact that the under- 
lying cause of pulmonary edema is often serious renal disease, and therefore a 
dangerous state deserving recognition, the history is often given of previous attacks 
of shortness of breath, or even of wheezing respirations; and the physical signs 
in the later stage of bronchial asthma, when widely diffused and musical moist 
rales are heard, may not differ materially from those of pulmonary edema, since 
musical moist rales and some impairment of resonance on percussion may be 
present in this condition as well. In spasmodic croup the obstruction to respira- 
tion is so clearly laryngeal and the chest is so free from widely diffused rales that 
the diagnosis is not difficult, and in laryngeal spasm due to locomotor ataxia the 
same freedom from musical rales in the chest again enables us to make a differentia- 
tion. Sometimes labored respiration resembling that of spasmodic asthma occurs 
in acute pneumothorax, but the physical signs are so different that no difficulty 
is experienced in separating these two conditions. 

Prognosis. — The prognosis as to recovery from an individual attack of asthma 
is very favorable, even if it be exceedingly severe, provided that no acute complica- 
tion arises. The prognosis as to recovery from the tendency to asthma is very 
bad, for the history of the vast majority of cases is that they have recurrences. 
It is only in those cases in which there is a manifest exciting cause, external or 
internal, which can be removed, that a favorable prognosis as to the future can be 
advanced. The tendency of spasmodic asthma to produce bronchopneumonia, 
emphysema, dilatation of the right side of the heart, and secondary circulatory 
feebleness must never be forgotten; but, on the other hand, it is remarkable that 
very many asthmatics live to moderate old age without being invalided. 

Treatment. — The treatment of spasmodic asthma may be divided into three 
parts : that devoted to the prevention of the attack, the relief of a paroxysm which 
is present, the removal of the underlying causes and of the sequelse which are pro- 
duced by the attack. It has already been pointed out that certain conditions of 
the atmosphere and the presence of certain kinds of dust in the air strongly pre- 
dispose certain individuals to attacks of asthma. On the principle that an ounce 
of prevention is worth a pound of cure, it is evident that asthmatic patients should 
be exposed as little as possible to such provoking causes, and if they must of neces- 
sity sleep in a room the air of which has been heated by a furnace, steam should 
be disengaged in the air of this room, so that it will not be unduly dry. Such 
patients should be subjected to a careful examination of the nasal, pharyngeal, 
and tracheal mucous membranes, with the object of discovering whether they 
suffer from any localized spot of hyperesthesia in these mucous membranes, for 
it not infrequently happens that foreign bodies or dry air may irritate these spots 
and so reflexly produce an attack. Indeed, in some cases of so-called "nasal 
asthma" it is possible by touching a hyperesthetic spot on the nasal mucous mem- 
brane to precipitate an attack of spasmodic asthma. Such hyperesthetic spots 
should be removed by the application of the cautery where it can be employed. 
Often permanent relief is obtained by change of residence. 

For the relief of the attack of asthma itself when it is threatened, nothing com- 
pares in efficiency to the hypodermic use of 5 or 10 drops of adrenalin solution 
1 : 1000, or a hypodermic injection of morphine and atropine may be given. 

When the attack is developed, an innumerable number of drugs have been 
recommended by various practitioners and by a still greater number of sufferers. 
Among the older remedies, without doubt, belladonna and its sister drugs possess 
the confidence of a large number of the profession; but none really exercise a power- 
ful curative influence, unless they are given in doses which are so large as to be 
almost capable of producing moderate poisoning. These drugs probably act by 
their depressant influence upon the vagus nerve, and by altering the circulation 
in the capillaries supplying the bronchial mucous membrane. They are particularly 



BRONCHIAL ASTHMA 385 

useful in those cases of asthma in which, during the attack, there is formed a 
considerable quantity of bronchial secretion, and they are the chief ingredients, 
with nitrate of potassium, of most of the proprietary cigarettes and powders which 
are burned in the patient's room. 

Of the so-called depressant remedies for asthma, we have lobelia, which is very 
highly thought of by many practitioners, particularly in England. On the other 
hand, some physicians are afraid of this drug, because of the depressant influence 
upon the heart. It is not to be employed when the heart is feeble. When the 
heart is strong, it should be given in full doses, if given at all. As much as J to 1 
drachm of the tincture should be given in one dose, and repeated in the dose of 10 
minims every half -hour or hour until the patient's circulation is markedly depressed 
and the skin is relaxed and perspiring. These doses may produce nausea and even 
vomiting, but the associated relaxation often will abort an attack, whereas smaller 
doses which do not produce vomiting may produce more profound circulatory 
symptoms, since all of the drug is absorbed and none lost by emesis. Pilocarpine 
may also be employed in those cases of spasmodic asthma in which there seems to 
be an excessive dryness of the bronchial mucous membranes. But the fact that 
this drug in some cases seems to depress the heart seriously, and in others cause an 
excessively profuse outpouring of bronchial secretion, has properly prevented its 
general employment. Many patients experience great relief in the early stages 
of an attack if they receive a hypodermic injection of J grain of morphine with 
y^-q grain of atropine. In a disease which recurs frequently, as does asthma, this 
use of morphine is always dangerous, in view of the possibility of establishing the 
morphine habit. Furthermore, the after-depressant effect of the drug upon the 
following day often renders the remedy almost as bad as the disease. 

For internal administration in the treatment of asthma, there is no drug which 
meets as many indications in as many cases as nitroglycerin. If the attack is 
threatened yfo or even 5^ of a grain may be given hypodermically, and the same 
dose may be repeated every hour or two, particularly if the patient is one of ad- 
vanced years and has a somewhat high arterial tension. In some cases the inhala- 
tion of a few minims of nitrite of amyl, poured upon a handkerchief, will serve to 
abort a threatened attack or to modify the severity of one which is already well 
developed. 

In those cases where there is great irritability of the nervous system underyling 
the asthmatic attack, the occasional use of the bromides may be advantageous, 
but they are of little value for the prevention of an individual attack, and their 
continued use between attacks is obviously unwise. The same opinion may be 
expressed in regard to the employment of chloral, which has the additional disad- 
vantage that the chloral habit may be instituted, or that the heart may be depressed 
to an undue degree. 

For many years the author has employed a compound in tablet or elixir in the 
treatment of asthma, both as a preventive remedy and as a cure for individual 
attacks, and has gotten results from it which cause him to regard this formula 
with considerable favor. It is now placed on the market by all large manufacturing 
druggists. 

1$ — Sodii iodidi gr. ij. 

Potas. bromidi gr. ij. 

Ext. euphorbise piluliferse . TTtiij- 

Nitroglycerini gr. ^0- 

Tinct. lobeliae . . ' mij.— M. 

Ft. in tabel. vel capsul. No. i. 

S. — One every four to six hours. 

It must never be forgotten, however, that asthma is a symptom rather than a 
disease, and that the remedies which prove useful in one case may in another 
25 



386 DISEASES OF THE LUNGS 

prove entirely useless, because in each instance the underlying cause of the malady 
is quite different. It is this fact which has probably caused some physicians to 
speak in high praise of certain remedies in the treatment of spasmodic asthma, 
while others with equal experience assert that they have gotten no good results 
from the employment of such drugs. 

Reference has already been made to the value of supplying asthmatic patients 
with moist air, particularly when they live in furnace-heated houses. It is the 
author's constant habit, when cases of astHma come under his care to place them 
in a bronchitis tent. To the air of this tent is supplied a small quantity of steam, 
with the result that the patient has a great diminution in the degree of dyspnea, 
and frequently gets some hours of refreshing sleep. An additional advantage 
in putting these patients in a bronchitis tent is that it requires them to remain 
in bed, and so gives rest to the heart, which organ is often sadly in need of relief, 
since the difficulty of breathing and the lack of sleep throws upon it, day after day, 
in some patients, a very severe strain. In some instances the addition of a few 
grains of menthol to the boiling water seems to increase the efficiency of the bron- 
chitis tent. In still others equal parts of oil of pine, oil of eucalyptus, and com- 
pound tincture of benzoin may be added, in the quantity of a tablespoonful or 
two to the boiling water, with benefit to the patient. In cases in which the bron- 
chial tubes are fullof liquid this tent is often not well borne. 

In all cases of asthma the physician should carefully examine the heart, and if 
there are any evidences of feebleness and dilatation of the right side of the heart, 
as manifested by venous engorgement, and the extension of cardiac dulness down- 
ward and to the right, small doses of strophanthus or digitalis should be given. 
In some cases in which the cardiac difficulty is marked during the attack, full 
doses, of Hoffmann's anodyne are advisable. These drugs may be assisted in 
their stimulating influence by one or two hypodermic injections of strychnine. 

It is also the duty of the physician in all these cases to carefully and repeatedly 
examine the urine, since renal disease sometimes produces true asthmatic seizures, 
and still more commonly produces attacks of dyspnea, which the patient may call 
asthma, but which are really those of true uremic poisoning. Then, too, if asthma 
is present with a moderate degree of albuminuria without casts, this albuminuria 
may aid the physician in determining that the heart is yielding under the strain, 
since this albuminuria is frequently due to renal congestion, resulting from a feeble 
circulation. The albuminuria disappears, the urinary flow becomes more profuse, 
and the heart's action gets better under the administration of digitalis or stro- 
phanthus, combined with rest, as already indicated. It is an interesting fact that 
persons who are susceptible to asthma seem to be very sensitive to antidiphtheritic 
serum. On the other hand it is undoubtedly a fact that certain asthmatics are fre- 
quently almost immediately relieved of their attack by the injection of diphtheritic 
antitoxin. So far we have no means of determining beforehand in which cases 
it will do good and in which it will do harm, but it is in any event a dangerous 
remedy for asthmatics, particularly when a second dose is given ten days after 
the first. 



DISEASES OF THE LUNGS. 



BRONCHOPNEUMONIA. 



Definition. — Catarrhal pneumonia, lobular pneumonia, or bronchopneumonia 
is an acute inflammation of the small bronchioles and of the tissues immediately 
surrounding them and their attached lobules, and primarily involves the lobules, 



BRONCHOPNEUMONIA 387 

rather than the lobes as does the croupous type of pulmonary consolidation. It 
is called bronchopneumonia because of this primary inflammation of the smaller 
bronchi, and it is called lobular pneumonia because it affects the lung by lobules 
rather than by lobes. More commonly still it is designated catarrhal pneumonia, 
since it usually follows inflammatory changes in the mucous membrane of the 
bronchial tubes. No single or specific micro-organism is the cause of broncho- 
pneumonia, but it is due to infection of the bronchi and adjacent tissues by many 
pathogenic germs. 

As with typhoid fever, so with bronchopneumonia: Gerhard, a Philadelphia 
student of Louis, in Paris, was the first person to clearly differentiate broncho- 
pneumonia from croupous pneumonia (1834), although as early as 1823 Seger 
had separated the croupous pneumonia of adults from this form, which is that which 
commonly affects children. 

Distribution. — Bronchopneumonia, because of its various causes, is found every- 
where throughout the world. 

Etiology. — Frequently bronchopneumonia is due to the micrococcus of croupous 
pneumonia, which for some unknown reason fails to produce a croupous exudate 
in a single lobe or in several lobes, as is usual when that organism enters the lung 
in an adult. In other instances pyogenic organisms such as the streptococcus or 
staphylococcus are responsible for the disease. Thus, in 103 cases of broncho- 
pneumonia examined by Netter, Weichselbaum, and Pearce, the streptococcus 
was found in about 30 and the pneumococcus in 29. When associated with other 
organisms the number of instances in which these cocci were found was much 
greater. Primary bronchopneumonia is usually due to the pneumococcus, and 
secondary bronchopneumonia to the streptococcus. 

When such a specific malady as diphtheria is the primary cause of the illness 
the Klebs-Loeffler bacillus is the most frequent cause of the pneumonic lesions. 
Thus, in 62 cases of bronchopneumonia following diphtheria examined by Pearce, 
this organism was found 52 times and the streptococcus 27 times. In still others 
the bacillus of Pfeiffer (that of epidemic influenza) brings on an attack. The 
tubercle bacillus not rarely is responsible for the inflammatory process, and almost 
any pathogenic organism entering the lower bronchial tubes may act as an exciting 
cause. Doubtless these organisms often gain access to the bronchioles in periods 
of good health without producing evil effects, but if by chance there is present a 
general or local impairment of vital resistance pathological changes ensue. 

Bronchopneumonia is usually said to be capable of division into two types, namely, 
the primary and secondary. The primary form is met with in children and adults 
who are usually in poor health with diminished vitality, and seems to have its 
onset with the development of an acute "cold." It is most commonly met with 
in infants, and in them, as has just been stated, is usually a pneumococcus infection, 
although true croupous pneumonia at this age is not common. The secondary 
type is much the more frequent of the two; indeed, it may be considered the rule 
that bronchopneumonia occurs as a secondary affection in the vast majority of 
cases, for nearly always there is a history of a previous acute or subacute bronchitis, 
or of some disease which predisposes to such a condition, as whooping-cough, 
measles, or influenza. 

In adults there is usually the history of a severe cold affecting the upper respi- 
ratory tract, or of the use of an anesthetic drug by inhalation, which has at one 
and the same time irritated the air-passages and permitted the entrance of saliva 
or particles of mucus or food containing many micro-organisms which produce 
infection. A similar result may accrue in instances in which no such drug is 
employed. Thus, in some asthmatics during the progress of an attack there 
may be drawn into the air-passages micro-organisms from the mouth or tiny 
particles of food. In individuals suffering from the coma of alcoholism, cerebral 



388 DISEASES OF THE LUNGS 

congestion, uremia, or apoplexy, with stertorous breathing, the same accident 
may ensue. Such a form of infection may occur in the coma following an epileptic 
seizure. In some instances the presence of an ulcerative laryngitis, due to syphilis, 
tuberculosis, or malignant disease produces an infection in this manner. Bulbar 
paralysis, or that due to diphtheria, may also provoke this type of pneumonia. 
In many cases of severe illness, as in typhoid fever, with foul secretions in the 
nose and mouth, this method of infection ensues because the ordinary sensitiveness 
of the glottic mucous membrane, and that of the trachea, is obtunded by the dryness 
of these parts or by the benumbing effects of the disease. This form of the disease 
is called aspiration pneumonia, or the " Schluck-pneumonie" of the Germans. 
Old age and debility are also predisposing causes. 

Prevention. — From what has been said it is evident that the secondary forms 
of bronchopneumonia are capable of prevention, at least to some extent. Perfect 
cleanliness of the mouth is one of the methods of prophylaxis, in that it prevents 
the inhalation from the oral cavity of infecting micro-organisms. So, too, during 
the course of measles and whooping-cough careful avoidance of exposure and the 
use of a bronchitis tent to allay bronchial irritation is preventive in its influence. 
If local lesions in the upper respiratory tract exist, they should be modified or 
removed by proper treatment. 

Frequency. — Bronchopneumonia is an exceedingly common disease, certainly 
outranking in frequency its sister malady, croupous pneumonia. As a terminal 
infection it causes death in many maladies otherwise almost never fatal in them- 
selves, such, for example, as whooping-cough and measles, both of which have a 
high mortality in very young children from this very cause. Thus, out of 446 
cases of bronchopneumonia in children cited by Holt, it followed or complicated 
whooping-cough 66 times and measles 89 times. It is a noteworthy fact that 
bronchopneumonia is the type which is particularly common in infancy, while 
croupous pneumonia is generally a disease of later life. In the child under five 
years it is very common, and fatal in direct proportion to the youth of the patient, 
whereas croupous pneumonia is rare in this period of life, and very rarely is fatal 
at this time. Out of Holt's 446 cases^ 53 per cent, occurred in the first year of 
life and 33 per cent, in the second year. 

Pathology and Morbid Anatomy. — This form of pneumonia, at least in its earlier 
stages, occurs in patches which cause the lung to present during life physical signs, 
and, after death, macroscopic appearances, ordinarily quite distinct from those 
of the solidified or hepatized lung of croupous pneumonia. Macroscopically 
the lung presents a mottled appearance because its surface represents three con- 
ditions of the pulmonary parenchyma, namely, (a) areas of consolidation, (b) 
areas of atelectasis or collapse, and (c) areas of emphysema, or enlargement, of 
groups of vesicles due to overdistention, resulting from collapse of adjacent lobules. 
The consolidated areas are pinkish, reddish, or grayish-yellow in hue, the emphyse- 
matous patches are paler and crepitate when touched, while the collapsed portions 
are bluish or mahogany in color and depressed below the rest of the cut surface of 
the lung. 

The inflammatory process usually begins in the smaller bronchi and extends 
from them to the tissues immediately adjoining, forming patches of consolidation, 
which are deep red in hue, and which extend farther and farther from their original 
site, until perchance they coalesce and form fairly large airless consolidations. 
As the margin of the inflammatory zone extends, the primary area of inflammation 
undergoes necrotic degenerative changes, loses its red appearance, and may become 
grayish, through granular and fatty degeneration of the exudate. This inflam- 
matory exudate not only invades the peribronchial tissues, but the vesicles as 
well, so that they are rendered airless. If the lung be cut across these patches of 
consolidation will project slightly, and in the centre of each can be seen the cross- 



BRONCHOPNEUMONIA 389 

section of the primarily involved bronchus, which looks whitish, and from which 
mucopus may exude. In some instances in which the infection is severe and the 
inflammatory process rapid, the mucopurulent character of the exudate into the 
bronchial tubes is very well developed, and this purulent process may extend 
into the peribronchial spaces and, in septic cases, cause small pyogenic foci. The 
exudate itself is composed, as would be expected from the character of the lesions, 
of serum, red cells, epithelial cells which have separated from the bronchial and 
vesicular walls, and a large number of leukocytes, and in varying numbers the 
associated bacteria. 

The exudate contains much less fibrin than it does in croupous pneumonia, 
often none at all, and a copious fibrinous deposit on the pleura is exceptional. 

If the inflammation of the walls of the bronchial tubes is severe they become 
thickened and swollen, and therefore their lumen is greatly decreased or even 
occluded. This result is greatly aided by their becoming plugged with the mucus 
and dead cells, and so it not infrequently happens that a certain area, or several 
areas of the vesicular portion of the lung is deprived of air and undergoes collapse 
or atelectasis. A marked polymorphonuclear leukocytosis and lymphocytosis 
is usually present. 

It is worthy of note that catarrhal pneumonia is in the great majority of instances 
present in both lungs, and that it is usually conspicuous in the bases posteriorly. 
The anterior portions of the lungs and particularly the apices, except in tuberculous 
cases, show little involvement unless the lesions are well developed elsewhere. 

The exudate in bronchopneumonia undergoes resolution, as do most inflammatory 
exudates, by the degeneration of the extravasated and desquamated elements 
and their speedy absorption or expectoration. With this process the material 
plugging the bronchial tubes disappears and the collapsed vesicles, upon receiving 
their normal supply of air, expand so that complete recovery ensues. 

When this does not take place we find the development of dense connective 
tissue about the air tubes and between the air spaces, which, as it increases in 
degree, causes thickening and induration. As this process increases the connective 
tissue distorts the lung so that the bronchi are twisted or bent, patches of vesicular 
tissue collapse, secretion is retained in the bronchial tubes, and as a result chronic 
bronchial inflammation, dilatation, or sacculation of these tubes occurs, and the 
patient becomes a sufferer from chronic bronchitis, with bronchiectasis or a chronic 
bronchopneumonia. 

In other instances old tuberculous lesions are rendered active by the acute 
bronchopneumonia, or a new tuberculous infection is superadded, so that the case 
speedily passes into a well-developed pulmonary tuberculosis. In still other 
instances the whole process from the very beginning is really due to the Bacillus 
tuberculosis, and the patient rapidly develops unmistakable evidences of tuberculous 
infection, the microscope showing, sooner or later, the presence of these organisms 
in the sputum. In such cases the exudate in the air cells goes on to caseation, 
and may become encapsulated or disseminated, depending upon the virulence 
of the organism and the resistance of the patient. 

Symptoms. — The symptomatology of bronchopneumonia varies with the primary 
cause. If it be primary it naturally presents symptoms which differ somewhat 
from those which it presents when it is secondary, and follows some more or less 
prolonged and exhausting malady. Then, too, the symptoms naturally vary with 
the age of the patient attacked, with the areas of the lungs which are involved, 
and with the severity of the illness which has preceded it. 

For the ready study of the symptoms of bronchopneumonia we may therefore 
form at least three classes of cases: those which are distinctly primary, those that 
are clearly secondary, and those which involve the small bronchioles very early 
in the attack, producing what is known as acute, suffocative catarrh. 



390 



DISEASES OF THE LUNGS 



When the child is attacked with the primary form of bronchopneumonia there 
is usually a chill at onset, which varies greatly in its severity, in some cases being 
so slight that it is scarcely noted, and in others amounting to a true rigor. Com- 
monly there is a history that the child has been exposed to cold and wet. As in 
all inflammatory conditions in childhood, there is a sharp rise in temperature, 
almost from the very first an increase in the respiratory rate, and, it may be, very 
considerable evidence of respiratory difficulty. 

It is curious to note how the severity of the symptoms of catarrhal pneumonia 
vary in different children. Some become dyspneic very early, and others suffer 
very little respiratory embarrassment through the whole course of the malady. 

So sudden may be the onset in this primary form of bronchopneumonia that 
it may be practically impossible for the physician to separate it from croupous 
pneumonia, particularly as children suffering from the latter disease rarely bring 
up rusty sputum, and also because they frequently have a pulse rate which is 



Fig. 72 




Lung of a child. Catarrhal pneumonia following measles. In the upper left quadrant is part of the 
wall of a small bronchus, the epithelium of which is desquamating (A) ; several air vesicles containing 
catarrhal exudate are shown (B). The connective tissue of the bronchus and the intervesicular structure 
are slightly edematous and the seat of considerable leukocytic infiltration ((7). 



higher in proportion to the respirations than that ratio which is common in croupous 
pneumonia in adults. Cerebral symptoms may also be present, just as they are in 
croupous pneumonia; and this is not surprising in view of the fact already pointed 
out, that the pneumococcus is the micro-organism most frequently responsible 
for both forms of pneumonia in children. For this reason, probably, primary 
catarrhal pneumonia in children not infrequently ends by crisis, and recovery 
may speedily take place after a very few days of illness. Indeed, the outlook in a 
case of this kind in an otherwise healthy child, which is not very young, is usually 
favorable. 

The symptoms of the onset of secondary bronchopneumonia vary greatly from 
those just described. Instead of having a sharp onset the onset is insidious. A 
child having been ailing from some other malady for a number of days or weeks, 
is found to have an accession of fever, to be languid, to have a rapid pulse, to have 
a very marked increase in respiratory rate, and the skin is found to be hot and dry. 
The speed of the pulse is often excessive, reaching 150 to 200 a minute; but in 



BRONCHOPNEUMONIA 391 

this disease, as in all others, its quality is of as great importance as its speed. An 
irregular pulse is of evil import. The cough is fairly constant and sometimes 
produces pain, and if the area involved is at all large respiratory embarrassment 
is early manifested. This is shown by the increased number of respirations, by 
the fact that they are somewhat labored, and also by the fact that the intercostal 
spaces are frequently drawn in by the suddenness of the inspiratory movement. 
Auscultation will probably reveal in the smaller bronchial tubes some fine rales, with 
exaggerated inspiratory and somewhat prolonged expiratory sounds. The breathing 
is of the exaggerated, puerile type; the cough is unproductive. Percussion for 
the first twenty-four hours of the attack may reveal practically nothing. This 
is in part due in children to the resiliency of the entire chest, so that, unless very 
gentle percussion is exercised, the resonance of neighboring parts may cover the 
impaired resonance of the consolidated area. Again, those areas which have 
undergone compensatory dilatation possess a hyperresonance which may cover 
the impairment. If, however, the pathological lesion is well developed, at the 
end of twenty-four or forty-eight hours careful percussion will usually reveal 
distinct impairment of resonance, particularly if the lesions are, as is common, 
chiefly at the bases posteriorly. 

If the disease is severe the symptoms of dyspnea may become distressingly 
well marked, and cyanosis may become constant, the child being so short of breath 
that it ceases to cry, and, indeed, may have difficulty in taking liquids because 
of its dyspnea; that is to say, it is so short of breath that it cannot take time to 
swallow. Usually at this time the expression is somewhat anxious. If the dyspnea 
has been prolonged enough to exhaust the child, and the accumulation of carbon 
dioxide in the blood has been sufficient to benumb its sensibilities, it is markedly 
apathetic. These symptoms last a variable number of days, but usually a change 
for the better in a mild case begins to be noted by the end of the fifth, sixth, or 
seventh day, and with the beginning of improvement in the general symptoms 
auscultation will reveal that the rales in the chest are more moist, that on coughing 
they alter in quality more than before, and, further, air will be found passing through 
portions of the lung which heretofore have seemed devoid of it. 

In other instances the disease runs a much longer course, and the child, after 
hovering between life and death for a number of days, slowly emerges from its 
illness, and the physical signs in the lungs equally slowly disappear. 

In young children it is by no means an uncommon occurrence for the disease to 
spread in a violent form into the smaller bronchioles, and by the swelling of the 
mucous membrane, the copiousness of the exudate, and the wide area involved, 
produce what is known as acute suffocative catarrh, a condition which at one time 
was considered as a separate entity from bronchopneumonia, but which is now 
recognized as being simply a malignant form of the disease involving a large number 
of the smaller bronchioles, and so greatly interfering with respiration. Another 
term which has also been used to describe this condition is "capillary bronchitis;" 
in other words, this name is meant to bring out the fact that the finer bronchioles 
are involved. A very excellent term to describe this form of the disease is "acute 
disseminated bronchopneumonia.' ' 

Capillary bronchitis, or acute suffocative catarrh, is one of the most distressing 
acute maladies which affect young children. Its onset is usually very rapid, and 
within twelve or twenty-four hours the child may be suffering intensely from 
dyspnea. At first, the dyspnea and inability to get a sufficient quantity of oxygen 
render it fretful and restless; but very soon it becomes weary, and with weariness 
of the general system there develops a weariness of the respiratory centre, which 
fails to send out sufficiently powerful influences to cause the remaining healthy 
portion of the lung to be completely filled at each inspiration. Very speedily, 
too, carbonic acid gas accumulates in the blood and benumbs the respiratory 



392 DISEASES OF THE LUNGS 

centre, so that within twenty-four or thirty-six hours after the beginning of the 
malady the child may lie in its mother's arms limp and motionless except for the 
rapid respirations which are required to maintain life. I have not infrequently 
seen a child in this condition as limp as it is when under the influence of ether or 
chloroform, and only semiconscious. The finger-nails are livid, the lips much 
darker than normal. The mouth is apt to be excessively dry, owing to rapid 
evaporation of moisture from the high fever and rapid breathing. 

During a portion of the attack the respiratory rate may become as high as 60 
or even 70 a minute, and not infrequently death comes on as a combined result 
of the infection, of the dilatation of the right side of the heart, of the accumulation 
of carbon dioxide in the blood, and of general nervous exhaustion. 

Probably the most characteristic symptom of capillary bronchitis is the intense 
dyspnea, which is quite as acute in some cases as it is in diphtheria with laryngeal 
obstruction. Indeed, I have known intubation to be done in a case of capillary 
bronchitis, it being thought that the child had laryngeal trouble in addition to 
its pulmonary difficulties, although no laryngeal lesion was actually present. 

The temperature in cases of capillary bronchitis varies very greatly. At the 
time of death the temperature may, superficially at least, be subnormal, although 
the rectal temperature may be high. The general run of the temperature pursues 
no definite course as it is wont to do in croupous pneumonia, but progresses very 
irregularly. 

The degree of fever in bronchopneumonia of the secondary type is of little value 
for the purpose of determining the severity of the disease. Sometimes when the 
infection is quite severe the temperature may not rise above 101° or 102°, whereas 
in other cases which are really less ill, it may reach 105° or 106°. 

Duration. — The duration of bronchopneumonia varies very greatly with the 
condition of the child at the onset of the disease. In primary bronchopneumonia, 
occurring in an otherwise healthy child, the malady may last for but a few days, 
and it is a noteworthy fact that it may be arrested in any stage of its development, 
so that recovery may speedily take place. 

In secondary bronchopneumonia the duration is apt to be very much longer 
than in the primary form. Under these circumstances it commonly runs a course 
of from ten days to two weeks, and if the condition of the patient is seriously 
impaired at the time of its onset, it may last for three or four weeks. Usually, 
however, during the last ten days or two weeks of a prolonged attack of this char- 
acter, the symptoms are much modified and the temperature is but a little above 
normal. Whooping-cough, which is a very frequent cause of bronchopneumonia, 
runs a course of from six to twelve weeks, and if bronhcopneumonia develops 
early in the attack of whooping-cough the persistency of the spasmodic seizures, 
with their accompanying bronchitis, naturally prolongs the duration of the pul- 
monary disorder; whereas, in another disease like measles, which runs a much 
shorter course, the pulmonary disorder may disappear almost as soon as the erup- 
tive disease, although very often it persists for a week or ten days, and convalescence 
from measles is well established. Much depends, too, as to the duration of the 
malady, upon the size of the areas of consolidation and the presence of more slowly 
liquidated exudates. Commonly, the greater the area infected, the greater the 
length of the disease. 

Complications. — The complications of bronchopneumonia are not numerous. 
As already pointed out, it occasionally happens that tuberculosis develops in the 
area which is diseased. More rarely still the infection of the peribronchial tissues 
is so severe that pulmonary abscess results. Pleuritis is rare unless there happens 
to be a patch of consolidation close to the pleura, in which case a small area 
may be involved. This rarely spreads and still more rarely is accompanied by 
marked effusion, but it sometimes results in empyema. 



BRONCHOPNEUMONIA 393 

Diagnosis. — Bronchopneumonia is to be differentiated from ordinary severe 
bronchitis by the presence of patches of impaired resonance on percussion, and 
by the fact that during the course of an acute bronchitis an exacerbation of tem- 
perature and of the general symptoms of severe illness ensue. Beyond these points 
it may be practically impossible to separate the two maladies. It is not to be 
forgotten that bronchitis is not associated with hyperresonance in any portion 
of the chest as a rule, but catarrhal pneumonia is frequently associated with this 
physical sign. Percussion in capillary bronchitis may therefore give exaggerated 
resonance owing to the emphysematous state of the vesicular parts of the lung, 
for, as in asthma, the difficulty, which often exists, is an inability to expire some 
of the air which has been taken in by forced inspiration. As has already been 
stated, hyperresonance may completely take the place of impaired resonance due 
to consolidation. 

From croupous pneumonia bronchopneumonia is to be separated by the fact 
that its onset is more gradual or insidious, by the intermittent character of the 
fever, and by the irregular distribution of the physical signs in the chest. Another 
important differential point is the fact that catarrhal pneumonia is usually bilateral 
and joined at the bases, whereas croupous pneumonia is not; that bronchopneu- 
monia is usually well diffused, and in both lungs, whereas the croupous type is 
usually but not always unilateral, and commonly limited to one lobe. Croupous 
pneumonia usually ends by crisis, whereas bronchopneumonia may end by lysis. 
The predominance of severe cerebral or meningeal symptoms is rather in favor of 
the croupous type of the disease. 

In many cases it is impossible to determine whether the bronchopneumonia 
is due to the pneumococcus or some other coccus, or is the result of the infection 
by the tubercle bacilli. In the absence of enlargement of the mesenteric glands 
and of other signs of tuberculous infection, the differential diagnosis between 
bronchopneumonia of tuberculous origin and that due to ordinary causes is prac- 
tically impossible, until the disease has advanced so far that other systemic mani- 
festations of tuberculous infection are evident. 

Sometimes the intermittent and irregular temperature curves of bronchopneu- 
monia suggest the possibility of malarial infection. The differential diagnosis 
in a case of malarial infection, with bronchial symptoms like those of bronchopneu- 
monia, can of course only be made by careful examination of the blood, and by a 
more careful study of the temperature chart than is usual in the ordinary case. 
Then, too, in the malarial forms of the disease the symptoms will be modified 
or arrested by the use of quinine. 

As already pointed out, the symptoms of bronchopneumonia, in children in 
particular, vary to an extraordinary degree with the primary illness from which 
the patient has been suffering. Thus, in whooping-cough the onset of the disease 
is often so insidious as to be easily overlooked because the rales are mistaken for 
those of the usual mild bronchitis. In other instances the symptoms may be 
those of tuberculous or acute meningitis, particularly in rachitic infants. 

Not rarely an acute diarrhea may be present, the stools being green and containing 
much mucus, some of which is due to a coincident gastro-intestinal catarrh, and 
some of it being from the bronchial tubes, for a child rarely expectorates, and 
usually swallows what he coughs up from the chest. Because of the associated 
indigestion there may be vomiting and distention of the abdomen by gas, which 
factors all aid in increasing the adynamia, and in interfering with the cardiac 
and pulmonary activity. These facts emphasize a fact too frequently overlooked, 
namely, that the condition of the lungs should always be carefully investigated 
in all cases which present signs of illness elsewhere, since it may be found, to the 
physician's surprise, that the pulmonary condition is the primary underlying 
cause. 



394 DISEASES OF THE LUNGS 

Prognosis. — The prognosis of bronchopneumonia varies very greatly with the 
underlying cause of the disease and with the age of the patient. In young infants 
it is an exceedingly fatal malady, whether it is primary or secondary, and during 
the first year of life, if the disease is well marked, the prognosis is always unfavor- 
able. The favorableness of the prognosis increases with each year of age. Another 
important factor in the prognosis of these cases is the general vitality of the patient. 
Children who are naturally strong and healthy, and are provided with good air 
and sunshine, have a better opportunity than those who live in poorly constructed 
dwellings with bad ventilation, and whose primary vitality is necessarily limited. 
This question of the vitality of the patient is a most important factor from a prog- 
nostic stand-point, and therefore if the child has been much weakened and devi- 
talized by prolonged illness, or has had its heart seriously weakened by the 
prolonged strain of severe whooping-cough, the outlook is much less favorable 
than if the disease attacks the child who is suffering from a mild attack of 
measles. 

The mortality of bronchopneumonia in very young children in private practice 
is probably about 30 per cent.; whereas in asylum practice, where it is impossible 
to provide them with the same amount of fresh air and careful nursing, and where 
the health is often previously impaired, it is not infrequently as high as 65 or 70 
per cent. While it is true that poorly nourished, rachitic children are very apt 
to fall victims to the disease, it is also a fact that well-nourished, stout, fat children 
sometimes have marked difficulty in surviving its attack; and this is particularly 
true if they are "condensed-milk babies," for such children usually have low vital 
resistance. The complicating maladies, as, for example, active diarrhea and 
indigestion or vomiting, of course make the prognosis very uncertain, and if they 
resist treatment are still more cause for anxiety. 

Treatment. — In the treatment of bronchopneumonia it is of the greatest impor- 
tance that the child should be in a well-ventilated room which receives as much 
sunshine as possible, for bronchopneumonia is essentially a disease of bad ventila- 
tion. The temperature of the room should be kept constant, and every care 
should be exercised that it is not damp. If possible, it should be heated by a stove, 
or by an open fire, rather than by furnace-heated air, and if it is necessary to heat 
it by means of a furnace, care should be taken that the air of the room should not 
be allowed to become unduly dry. This may be prevented by having the air from 
the furnace flue pass over the surface of a pan of water, and if the air is very hot 
and thoroughly dried it is better to set free in the air of the room a certain amount 
of steam from a tea-kettle, a pan of boiling water, or by occasionally immersing 
a large piece of quicklime in a bucket of water. 

There can be no doubt that the influence of dusty, impure, or dry air upon the 
bronchial mucous membrane in cases of this disease is most deleterious, and I 
believe that in many instances much better results can be obtained if it is possible 
to place the child in a bronchitis tent, or to provide the air of the room with a 
sufficient degree of moisture to make the apartment the equivalent of a bronchitis 
tent. This can readily be accomplished in the way just suggested, or by the use 
of what is known as a " croup kettle," which continually sets free a small quantity 
of steam. To the water which is placed in the croup kettle 1 or 2 grains of menthol 
may be added every two or three hours, and in some instances, for their soothing 
influence, a few drops of oil of eucalyptus and compound tincture of benzoin may 
be so employed. As far as possible the patient should be kept quiet in bed, or, 
in the case of little children, should be moved as little as is consistent with com- 
fort; but if the child is very ill, it should not be allowed to lie in one posture hour 
after hour, but occasionally be changed, lest hypostatic congestion occur. Easily 
digested, nutritious food should be given in small quantities every two hours. No 
medicine which may disturb digestion should be given. 



BRONCHOPNEUMONIA 395 

In the way of external applications to the chest, the child's back, sides, and 
front may be rubbed with a mixture of a teaspoonful of turpentine and three 
tablespoonfuls of sweet oil. In other instances a weak ammonia liniment may be 
used, or in still other cases oil of amber, in the strength of a teaspoonful to two 
tablespoonfuls of sweet oil. These methods of treatment provide sufficient counter- 
irritation and do not maintain the febrile temperature as do the poultice or cotton 
jacket, both of which forms of application have now deservedly gone out of use, 
as it is inconceivable that they can favorably affect the lesion in the lung, and they 
certainly increase the discomfort, the fever, and the irritation of the child's nervous 
system. 

Stimulants are not needed in all cases of bronchopneumonia, but are used wisely 
in a larger proportion of patients than in those who suffer from the croupous variety 
of the disease, because bronchopneumonia, as has already been pointed out, usually 
attacks the feeble and therefore those who commonly need stimulation. The 
quantity of stimulant which is given varies of course with the feebleness of the 
heart sounds, the condition of arterial tension, and the degree of general nervous 
prostration. One of the best stimulants which can be used is the carbonate of 
ammonium in the dose of 2 or 3 grains every three or four hours to a child of a 
year or two, usually giving it in the syrup of acacia and water. Carbonate of 
ammonium, however, acts best when it is given for comparatively short periods 
of time, and for a constant stimulant during the greater portion of the disease 
it is probable that brandy occupies the first place. Care should be exercised that 
the brandy is at least five years old, and that it is as bland as possible. It should 
be given very well diluted by water, and a child of a year may take as much as half 
an ounce to an ounce in twenty-four hours with advantage, 30 drops being given 
every two or three hours. 

As a rapidly acting diffusible stimulant to meet critical periods of depression Hoff- 
mann's anodyne in the dose of 5, 10, or 15 drops may be employed in young children. 
In other instances yto grain of strychnine may be used, or a larger dose than this, 
it being always borne in mind that the nervous system of a child is exceedingly 
susceptible to this drug. Like the carbonate of ammonium, strychnine is only to 
be used when it is necessary to bridge an exceedingly critical period. If the dose 
of strychnine is to be repeated, ^-q of a grain is a sufficiently large amount. This 
quantity may be given twice, thrice, or four times in twenty-four hours, but, as a 
rule, it is unwise to continue its use for a longer period than this. 

Where the quantity of bronchial secretion is considerable, particularly in many 
cases of suffocative bronchitis, a critical period may be weathered by the use of 
small doses of atropine; from 10 1 00 to -gfo of a grain may be given every two or 
three hours by the mouth, or, if need be, 5-^ to -g-g-gr may be given hypodermically, 
if there seems to be danger of the child drowning in its own secretions. Oxygen 
may be taken by inhalation in some cases with advantage. 

The use of antipyretic drugs is to be absolutely condemned. They are even 
more dangerous in this disease than in croupous pneumonia. If the temperature 
is so high as to be dangerous in itself, it may be controlled by cool or tepid spongings, 
with gentle friction; by the use of cool cloths to the forehead, or an ice-bag applied 
to the head if cerebral symptoms are marked. 

When the symptoms of respiratory oppression are marked and the fever is 
high, it is often advantageous at a critical period to dip the child alternately in 
cool and hot water, the water being hot enough to produce distinct counter-irritation 
on the skin, and, reflexly, to arouse the dormant nervous system. Under these 
circumstances the child often rallies, takes deep inspirations, dislodges the mucus 
which is otherwise obstructing its breathing, and at the same time has a reduction 
in its temperature. Such an alternate hot and cold plunge bath should only be 
resorted to when conditions are desperate, and should not be repeated too fre- 



396 DISEASES OF THE LUNGS 

quently. A tepid bath, the patient being immersed or simply sponged, will also 
very frequently allay restlessness and permit quiet sleep. 

In the protracted cases it is exceedingly important that pure air and good food 
should be provided. Not infrequently the child which fails to improve in the city 
may, when carried in its nurse's arms to the sea-shore or the mountains, change 
for the better to a remarkable degree within a very short period of time. This is 
particularly true if the weather is oppressively hot. Such patients also may 
be benefited in some instances, particularly during the winter months, by cod-liver 
oil inunctions, and, if the digestion will stand it, by the administration of small 
quantities of cod-liver oil or the syrup of iodide of iron by the mouth. Sometimes 
such patients are also greatly benefited by the administration of the hypophosphites. 

During the acute stage of bronchopneumonia there is little use in employing 
the ordinary expectorants. During the stage of resolution, if the secretion is 
profuse, small doses, such as 1 or 2 grains of chloride of ammonium, with fluid- 
extract of licorice and water, may be given twice or thrice a day. Rarely in young 
children is there much expectoration, either in the sense of expelling mucus from 
the mouth or coughing it up into the pharynx. The younger the child the less 
chance there is of freeing its bronchial tubes of secretion by coughing, and care 
should always be taken that the administration of an expectorant, which is not 
of very great importance, does not disorder the digestion, which is of far greater 
importance to the maintenance of the child's health and strength than any medicine 
can be. 

The bronchopneumonia of adults usually follows asthma or the inspiration 
of irritant materials, and must be treated in much the same manner as that just 
described for bronchopneumonia in children, except that the doses should be 
larger in proportion to the age and size of the individual. In nearly all cases 
active stimulation is required, and. digitalis and strychnine are particularly useful. 
Counter-irritation, freely applied to the chest, seems to be of advantage in some 
instances, but here again the cotton jacket or the poultice ought not be resorted 
to, as they simply oppress the patient and do little good. 

METASTATIC PNEUMONIA. 

Definition. — By the term metastatic pneumonia is meant a condition of consolida- 
tion of part of one lung, or more rarely parts of both lungs, as the result of the plug- 
ging of one or more of the pulmonary vessels by an embolus which is of septic 
origin. 

Etiology and Pathology. — As elsewhere, emboli reaching the lung may be (1) 
simple or bland, (2) septic or infective; either of these may be massive or small. 
A large mass thrown into the pulmonary artery at once arrests the flow of blood, 
the patient gives a few gasps, possibly has a convulsion, or at least convulsive 
movements, and dies. Smaller emboli, if numerous (an embolic shower), may 
induce similar phenomena. The simple or bland embolus occludes one or more 
vessels, and leads to the formation of a hemorrhagic infarct. These irregularly 
shaped or conical areas vary in size, depending upon the magnitude of the occluded 
vessel and the efficiency of the collateral circulation. They may be central or 
peripheral, massive or small, single or multiple. 

The question of autochthonous embolism is of pathological rather than clinical 
interest. 

The affected area is airless, denser than the uninvolved pulmonary tissues, and 
near the centre it is dark purple or almost black in recent infarcts, black or brownish- 
black in older areas, and it may be surrounded by a zone of reactionary inflamma- 
tion. If the lesion is peripheral the indurated area rises above the level of the 
pleura and is frequently covered by a delicate stratum of fibrin. Certain pleurisies, 



BRONCHOPNEUMONIA 397 

particularly those following operations, have been attributed to pulmonary infarc- 
tion. Histologically such areas when recent show air vesicles occupied by blood 
cells and fibrin and more or less interstitial extravasation. Later the erythrocytes 
are fragmented, the leukocytes increased, phagocytes abundant, and evident 
reparative processes in progress. 

The sputum is more or less blood-stained, and when the infarcts are large or 
numerous it may be intensely so. In fat embolism, such as may accompany 
fractures of the long bones, oil globules may be demonstrable in the sputum. 

Whether the process arises to the dignity of a pneumonia depends, of course, 
upon the amount of accompanying inflammation. It is evident that a few small 
infarcts irregularly distributed may give rise to no symptoms because of the insig- 
nificant lesions induced; or, on the other hand, large, or multiple, areas may be 
accompanied by evident lung symptoms. Whether inflammation be marked 
or slight is so largely dependent upon the presence of infection that in the absence 
of bacteria the name metastatic pneumonia is scarcely applicable. 

Embolism due to fragments of neoplasms entering the lungs usually escapes 
notice until the proliferating cells give rise to metastatic tumors. 

The most important and gravest type of metastatic pneumonia is that seen 
in pyemia. 

During the course of a septic process in any part of the body, even though it 
may be so minute as to escape notice unless carefully sought, it is possible for a 
small clot (embolus) infected by micro-organisms to enter the circulation and, 
being carried to the lung, to plug one of the vessels. The difference between the 
infarct resulting from an ordinary embolus and the lesion ensuing from one of 
septic origin is very marked, for in the latter condition there speedily develops 
an acute local process due to the rapid extension of the infection from the embolus. 
In this way the immediate neighborhood of the closed vessel becomes engorged; 
polymorphonuclear leukocytes accumulate in the infected area, which rapidly 
undergoes liquefaction, necrosis, and an abscess is formed. As such emboli are 
rarely solitary, multiple foci are prone to develop; these may, by extension, 
become confluent, or successive embolic showers may cause closely approximated 
lesions of different ages. 

As the quantity of infective material and its distribution constantly vary, 
the anatomical result of such conditions can rarely be the same in any two cases. 
There may be a single area of infection, or the lung may be riddled by abscesses, 
the "pyemic pneumonia" of old writers. 

The area of solidification in the lung may resemble the patchy state seen in 
bronchopneumonia or the hepatized appearance of croupous pneumonia. There 
is, however, this important difference in the further progress of the local lesions 
between the two diseases named and that under discussion, for in metastatic 
pneumonia the inflammatory process usually goes on to suppuration, the entire 
infected area becoming crowded with pus cells and cocci, the walls of the vesicles 
and the connective tissue of the lung breaking down instead of remaining intact 
as in most cases of ordinary pneumonia. As a result we find, one or more abscesses 
of the lung which may rupture into a bronchus, into the pleural cavity, or even 
through the diaphragm, and are practically always accompanied by marked septic 
fever. 

The pleura rarely escapes, and empyema, in patients surviving sufficiently 
long, is not uncommon. As the abscesses open into the bronchi and eroded vessels 
give way, pulmonary hemorrhage is prone to occur. Large areas of pulmonary 
tissue may undergo necrosis and further complicate the case by the addition of 
pulmonary gangrene. 

Symptoms. — The symptoms of metastatic or septic pneumonia present so little 
that is characteristic that they are often overlooked. This is because the lesion 



398 DISEASES OF THE LUNGS 

in the lung is secondary to some inflammatory process already present, which 
is responsible for much of the fever and other signs of an infection. In the midst 
of these symptoms, if they are severe, the slight exacerbation produced by the 
embolism is not recognized. It is only in those cases in which the area of the lung 
involved is very considerable that pulmonary signs are forced upon the physician, 
projecting themselves, as it were, above those already present. When the pulmo- 
nary symptoms are marked they so closely resemble those of an acute pneumonia 
that not infrequently the diagnosis of an intercurrent pneumonia is made, only to 
be modified when repeated chills, sweats, and a temperature chart indicative of 
sepsis show that the process in the lung is septic. (See Pyemia.) 

When the embolus is a large one and plugs the pulmonary artery at its bifurca- 
tion, death suddenly ensues. 

The physical signs of metastatic pneumonia are practically identical in the 
early stages of the affection with those of bronchopneumonia or croupous pneu- 
monia, for the consolidated portion of the lung produces dulness on percussion, 
bronchial breathing, and increased vocal fremitus and resonance. Later, when 
the consolidated area breaks down and begins to undergo suppuration, the physical 
signs may be those met with in beginning resolution in ordinary croupous pneumonia. 

Prognosis. — The prognosis in metastatic pneumonia is bad because it is a septic 
process and also because it is a serious complication added to a process which is 
already more or less severe. It usually ends in abscess or gangrene, and these 
affections, particularly the latter, are fatal in the great majority of cases. In the 
rare instances in which recovery takes place the health of the patient is, as a rule, 
permanently impaired. I have, however, seen two instances followed by abscess 
end in complete restoration to health. 

Treatment. — There is no specific treatment of this condition unless it be known 
that the streptococcus is the cause of the infection, in which case antistreptococcic 
serum may be employed. Even in these instances, however, it cannot do much 
good because, after the pulmonary vessel is mechanically closed by an embolus, 
no treatment can bring about its relief. The most that the serum can do is to 
limit the degree of general toxemia. 

Ordinarily the treatment must consist in the use of as much easily assimilated 
food as the patient can take without disordering his digestion, the administration 
of proper quantities of stimulants, and the careful control of such symptoms as 
may become excessive, as, for example, the reduction of high temperature, if it is 
persistent. 

PNEUMONOCONIOSIS. 

Definition. — This term is applied to a state of the lungs in which, by reason of 
exposure to, and inhalation of, various kinds of dust, a deposit of the foreign body 
takes place in the pulmonary tissues and produces secondary changes. When the 
individual is exposed to coal-dust in sufficient amount and for a long-enough period 
to cause its accumulation in the lung, the state of the lung is called " anthracosis;" 
when the dust is derived from the grinding of iron or steel, it is called " sidcrosis;" 
when the dust arises from stones, the term "lithiasis" or " chalicosis" is employed. 
Still another type of foreign body capable of causing pneumonoconiosis affects 
those who work in large textile industries and shoddy mills. The minute particles 
of wool and cotton, and of the clay used for "sizing," often cause bronchitis and 
favor the occurrence of phthisis. The dust can often be found in the sputum of 
such patients. Reference to this type of the disease is made in the author's Fiske 
Fund Prize Essay for 1885. Still another form of exposure gives rise to "grain- 
shovellers' disease," and to "potters' rot." 

Etiology. — Under ordinary circumstances the respiratory tract is able to get 
rid of minute foreign bodies which may enter it. This is accomplished by the 



PNEUMONOCONIOSIS 399 

arrest of the dust in the nasal and pharyngeal mucus, and by the action of ciliated 
epithelium lining the larynx, trachea, and bronchial tubes, which continually 
passes along toward the mouth for expectoration any dust particles which may 
enter. If these protective measures are insufficient because of the great quantity 
of dust inhaled, or where after a time this ciliated epithelium is destroyed, some of 
the particles are carried through the mucous membrane and are arrested in the 
nearby connective tissue; but if the amount of dust is so large that even this third 
barrier is passed, then the dust particles are taken up by the lymphatics and carried 
to the bronchial lymph nodes, or to the interlobular pulmonary septa under the 
visceral layer of the pleura, or to the substernal lymph glands, where they are 
deposited and remain fixed. Very rarely the fine particles may enter the circula- 
tion and be deposited in the liver and spleen, as in a case reported by Welch, or 
they may be even excreted in the urine. 

Pathology. — Up to this stage these results may possess no pathological signifi- 
cance, but in some instances the presence of large quantities of these foreign bodies 
produces a low-grade inflammatory process in the lung tissues which results in 
overgrowth of connective tissue; that is, a chronic productive interstitial pneumonia 
or pulmonary sclerosis. Occurring independently of the interstitial change, or 
associated with it, there is quite constantly a subacute or chronic bronchitis and 
emphysema, and finally areas of softening take place, in the fibroid portions of the 
lungs, which are small in size and filled with dust-stained fluid. Sometimes these 
communicate with a bronchial tube and may then become infected and ulcerate. 
These ulcerated patches or spots of softening may or may not be due to infection 
by the Bacillus tuberculosis. It is by this process that we have established " miners' 
phthisis" or " grindstone consumption" and " gold-dust complaint" of the lung. So 
common is this condition in Sheffield, England, that it has been called "knife- 
grinders' rot." 

Symptoms. — As a rule symptoms of pulmonary trouble do not come on in serious 
form until the individual has been exposed for some months or years, when chronic 
cough, dyspnea, and loss offiesh call attention to the insidious changes in the lungs. 
A macroscopic or, when this fails, a microscopic examination will usually reveal 
the dust in the sputum, and the history of the case renders the diagnosis easy. 

Prognosis. — In an investigation carried on at Solingen, Germany, by Moritz, 
it was found that there were no fork-grinders above forty-five years of age and no 
sword-grinders above fifty. Of the total number of knife-grinders employed, 
only 5.5 per cent, were over forty years of age. Of the scissors-grinders there were 
8.4 per cent, above forty. The fork- and sword-grinders work with dry grinding 
stones, while the knife- and scissors-grinders work with grinding stones which are 
constantly kept moist. The relatively greater number of scissors-grinders who live 
to be over forty is explained by the fact that the knife-grinders sit closer to their 
machines than the scissors-grinders, and thus inhale more dust. 

Peabody, in some investigations made at Sheffield, England, found that the 
average period of knife-grinders who are able to continue their work is thirteen 
years. In South Africa, Fox states that the duration of life in gold mines where 
there is much dust from blasting is only four years. Out of 1377 rock-drill miners, 
225, or 16.34 per cent., died in two and a half years. 

Treatment. — The treatment is removal from exposure and the use of the medicinal 
measures advised in the articles on Chronic Bronchitis and Emphysema. It is 
the duty of all employers of labor in dusty places to provide free ventilation, both 
to dissipate the dust and to diminish the chance of tuberculous infection. In 
many industries the employers should use moist respirators to catch the dust in 
the respired air. Moist or wet grinding should be used instead of dry grinding 
to prevent dust, and workmen known to be tuberculous should be excluded from 
the workshop. 



400 DISEASES OF THE LUNGS 

EMPHYSEMA OF THE LUNGS. 

Definition. — The term emphysema, as applied to disease of the lung, signifies 
a condition in which the air content of the organ, in a large or small area, is in 
excess of the normal. Systematic writers ordinarily make it include (1) essential 
hypertrophic or large-lunged emphysema; (2) atrophic or senile emphysema; 
(3) compensatory emphysema, a form of vesicular overdistention due to inexpan- 
sion, or absence, of pulmonary parenchyma in some juxtaposed or, less commonly, 
a distant area, and (4) a form of what occurring elsewhere is ordinarily termed 
"surgical emphysema/' but in the lung is called "interstitial," "interlobular," 
or " intervesicular" — names that indicate the location of the air and differentiate 
the condition from the first-named states or those forms in which the abnormal 
air content is intravesicular. 

Emphysema has also been divided into an acute and chronic form. In point 
of time the interstitial is always acute, the essential and atrophic always chronic, 
while the compensatory may be either. Some writers apply the term "acute" 
to that condition in which rapid overdistention of relatively large areas. occurs as a 
result of violent inspiratory efforts, or obstructed expiration, such as occurs in 
cardiac asthma, bronchial obstruction, and allied conditions. 

Briefly described, vesicular emphysema is a state in which there is atrophy of 
the septa between the air cells so that a number of vesicles coalesce. As a result 
we find in the lung many small, bladder-like spaces containing air. Associated 
with this minute change the entire lung increases in bulk and the thoracic cavity 
is usually much increased in all its diameters, especially the anteroposterior and 
the vertical, producing the so-called "barrel-shaped chest." 

Etiology. — Much difference of opinion exists as to the primary cause of pulmonary 
emphysema. It is universally acknowledged that the condition develops as a 
result of inadequacy, either congenital or acquired, of the supporting elastic tissue 
between the vesicles , but one school of pathologists maintains that the giving way 
of the vesicular walls depends upon mechanical stress, while another school asserts 
that such a result ensues only when the normal support is removed through failure 
of nutrition in these parts so that atrophy results. The author is convinced of 
the correctness of the latter view, namely, that the coalescence of the vesicles 
takes place only after the elastic connective tissue has become wasted as the result 
of impaired circulatory supply. It is perfectly true that great pulmonary stress 
tends to produce emphysema of the lung, but it only produces this state when the 
connective tissue is unable to provide proper vesicular support. 

Probably in a large proportion of cases the tendency is hereditary, the defect 
is congenital, and the tissues succumb as soon as any great stress is put upon them. 
If this primary nutritional feebleness be admitted as the fundamental cause of 
the condition, it is easy to understand how it is that persons so affected fall victims 
to emphysema when attacked by spasmodic asthma, or when following occupations 
which produce pulmonary stress, and it also makes manifest why it is that other 
persons exposed to equally severe exciting causes escape. 

Frequency. — The frequency of true pulmonary emphysema is difficult to deter- 
mine because many of the mild cases are overlooked, and patients do not present 
themselves for treatment until the disease is far advanced. To show how widely 
statistics may vary according to the method of their collection, it is interesting 
to note that Lebert states that pulmonary emphysema forms about 5 per cent, 
of all diseases, while Virchow found in nearly 200,000 cases, admitted to the Charite 
in Berlin, that the percentage of emphysema was only 0.3, a result confirmed by 
West at St. Bartholomew's in London. The disease is met with three times as 
frequently in men as in women, probably because they are exposed to its secondary 
causes more constantly, and it occurs chiefly between'the ages of thirty and sixty 



EMPHYSEMA OF THE LUNGS 401 

years. It occurs in children, but rarely before they are ten years of age, although 
cases as young as two years of age have been recorded. 

Pathology and Morbid Anatomy. — It has already been stated that the essential 
characteristic of pulmonary emphysema is the wasting of the interalveolar tissues 
so that coalescence of the vesicles takes place. As a result small, bladder-like 
spaces are formed, the lung loses its elasticity, and so fails to expel the air on expira- 
tion, with the result that the quantity of residual air is greatly increased. This 
results in dyspnea in two ways: first, there is an impaired circulation of fresh air 
in the lung, and, second, there is a decrease in the area of the vesicular tissues, so 
that a much smaller surface is afforded for the absorption of oxygen. 

When the thorax of a case of essential emphysema is opened the lungs do not 
retract as do healthy lungs. Indeed, they may project into the opening which has 
been made. The left lung extends so far forward as to cover the heart, and the 
right lung may overlap the edge of the left. Often the epiclavicular spaces are 
distended by lung tissue, and if the disease be marked the convexity of the dia- 
phragm is reduced, with consequent displacement downward of the adjacent 
abdominal viscera, particularly the liver. 

The chest is changed in appearance because with the increase in the size of the 
lungs the ribs become more horizontal and the intercostal spaces more bulging, 
the sternum and costal cartilages are projected forward, and the normal dorsal 
curvature of the spine is exaggerated. 

When the lungs are removed from the chest it is found that they possess four 
peculiarities aside from their great size: they are pale gray in color, unusually 
free from blood, dry, and when pressed between the fingers they lack the crepitation 
met with in normal lung tissue. A noteworthy change is the presence of dilated 
pouches or bladder-like protuberances on the surface of the lung, and particularly 
at its margins. If the lung be cut, somewhat smaller spaces will be found scattered 
through it. It is noteworthy that in emphysema these open spaces are surrounded 
by thin walls which readily collapse, whereas the sacculations of saccular bronchi- 
ectasis are surrounded by areas of thickening and inflammatory change. 

With the coalescence of the air spaces the capillaries which usually pass between 
the vesicular walls disappear, and this in turn diminishes the number of pathways 
by which the blood can pass from the right to the left side of the heart. As a 
result three chief circulatory changes ensue. Some of the blood finds its way by 
large anastomotic channels from one side to the other, and so is imperfectly oxidized. 
The increased obstruction to the flow results in distention and arteriosclerotic 
changes in the pulmonary artery, in dilatation, with more or less hypertrophy, of 
the right ventricle and finally in dilatation of the right auricle. Eventually, 
when the pathological process is far advanced we find that the liver is greatly 
engorged with blood, ascites may develop, the cardiac failure rapidly progresses, 
and death results from the various sequences of the primary lesions. 

Associated with emphysema there is usually more or less well-developed chronic 
bronchitis. 

Symptoms. — The symptoms of emphysema may be best divided into the objective, 
or those that can be seen by the physician, and the subjective, or those described 
by the patient. 

Physical Signs. — The most noteworthy objective signs are the increase in 
the diameter of the chest, so that the anteroposterior diameter equals the lateral; 
the fulness or bulging of the intercostal spaces; the impaired respiratory movement 
of the thorax, which may seem quite fixed; the well-filled or distended cervical vessels, 
and the presence in the epigastrium of the apex beat of the heart. If the case 
is severe we see in addition to these signs pulsations of the jugular reins, labored 
breathing, cyanosis of the lips, fulness of the abdomen, due to the displaced and 
engorged liver, and the accumulation of fluid in the peritoneum. Not infrequently 
26 



402 



DISEASES OF THE LUNGS 



inspection of the upper part of the epigastrium reveals a network of enlarged capil- 
laries in the skin. These are the chief signs on inspection. 

On further careful physical examination we find on palpation that the apex 
beat cannot be felt at the normal area near the nipple because it is displaced and 
covered by the enlarged lung. The lower margin of the liver may be felt as low 
as the navel. Palpation of the chest while the patient speaks reveals a marked 
decrease in vocal fremitus. Percussion gives 

a high-pitched resonant note all over the Fig. 74 

chest, particularly over the upper lobes; 
reveals a decrease of the normal area of 
cardiac dulness; shows the liver to be as 
low as palpation indicated it to be, and 
gives flatness in the flanks and in the 
suprapubic area if ascites is present. 
Auscultation reveals a feeble vesicular 
murmur, marked prolongation of expir- 
ation because of the inelastic state of the 



Fig. 73 





Section of anterior margin of the lung from a case 
of essential emphysema, showing the wasting and 
absorption of the vesicular walls. 



2cm. 



Lung, anterior aspect, from a case of essen- 
tial emphysema. The large bullae on the 
anterior margin of the middle lobe are nearly 
two centimeters in diameter. Smaller vesicles 
are present on the anterior margin of the upper 
lobe and along the diaphragmatic harder of the 
lower lobe. The apex is but slightly involved, 
but in some cases it is markedly affected. 



lung, and sometimes there can be heard rales, which are due to the associated 
bronchitis. A curious crackling sound, the cause of which is not certain, is also 
heard sometimes. It is not due to pleurisy and is probably produced by the air 
in the bladder-like dilatations in the margins of the lungs. This sound is usually 
best heard at the apices. 

Subjective Signs. — The symptoms from which the patient complains are 
chiefly those connected with respiration. The shortness of breath varies greatly 
in different cases. In some it is constant. In others it is only developed when 
exercise is taken, and the difference in its degree on exertion varies widely in different 
individuals. Often dyspnea is only felt on warm, oppressive, or humid days, 
while in other cases any exertion whatever produces such severe dyspnea that the 



EMPHYSEMA OF THE LUNGS 403 

patient is forced to rest. This dyspnea, as already stated, depends upon deficient 
oxygenation of the blood, upon the interference with the action of the right side 
of the heart, and upon the inability of patient to take fresh air into his lungs in 
large quantity because of the excess of residual air which is present. 

The cough in some cases is so constant as to greatly annoy the patient. In 
other instances it is almost entirely absent. The development of this symptom 
largely depends upon the degree of bronchitis which is associated with the emphy- 
sematous change. If marked bronchial irritation is present, the cough is not 
only annoying because of its persistency, but also exhausts the patient, and aids 
in the dilatation and fatigue of the right side of the heart. The sputum which 
results from the cough varies in quantity with the severity of the bronchitis which 
is present, and is not peculiar in appearance unless by chance the patient is also 
a sufferer from asthma, when the characteristics of asthmatic sputum may be 
manifest. The digestive disorders sometimes complained of by the patient depend 
chiefly upon the impairment of the circulation in the liver, stomach, and intestines, 
produced by the secondary cardiac lesions. Sometimes, too, the urine is scanty, 
owing to congestion of the kidneys from the same cause. 

Diagnosis. — From what has just been said of the symptoms and typical signs 
of pulmonary emphysema it is evident that the diagnosis is not difficult. Indeed, 
in a well-developed case there is probably no pulmonary condition so easily recog- 
nized. The bilateral increase in the size of the chest, the narrowing of the inter- 
costal spaces, the dyspnea, the cyanosis, the prolongation of expiration, the hyper- 
resonance on percussion are all to be noted in forming a positive conclusion as to 
the character of a case. It is not necessary for the diagnosis of emphysema that 
deformity of the chest be present. Sometimes a marked degree of pulmonary 
change exists without any change in the shape of the thorax. 

Emphysema of one lung is practically never seen, and therefore pneumothorax 
can be easily separated from emphysema. 

Prognosis. — The prognosis of emphysema is always unfavorable; at least, so far 
as complete recovery is concerned. In many cases, however, the progress of the 
disease is so slow that the patient may live for years with a fair degree of comfort. 
Indeed, in some instances the pathological process becomes stationary. Patients 
with well-developed emphysema are, however, rarely fortunate enough to develop 
this arrest of the disease, and equally rarely live until advanced old age, usually 
because with advancing years the muscle fibre of the right side of the heart 
becomes less and less able to stand the strain which is thrown upon it. 

It is vitally important, so far as prognosis is concerned, for patients suffering 
from pulmonary emphysema, to avoid exposure to sudden changes of temperature; 
for such changes may produce a severe bronchitis or pneumonia, conditions which 
the patient is ill able to withstand. The presence of a persistent chronic bronchitis 
renders the prognosis more grave than if this complication does not exist. Death 
rarely comes on suddenly in these patients, but slowly, as a result of constantly 
increasing circulatory failure. Lebert asserts that one-third of these cases die 
from cardiac dropsy, and the rest from pulmonary congestion and gradual 
feebleness, with slow suffocation, increasing cyanosis, and constantly developing 
bronchitis. 

Treatment. — The treatment of pulmonary emphysema is, unfortunately, very 
limited. There is no curative treatment. The. most that the physician can do 
is to improve the condition of the circulation and the nutrition of the patient, and 
to prevent him from throwing severe strain upon his pulmonary tissues and his 
circulatory apparatus. Where the patient follows an occupation which is manifestly 
injurious, he must be advised to give it up, and, for that matter, to avoid all violent 
muscular effort which will throw a strain upon his heart and lungs. Incipient 
attacks of acute bronchitis should be treated at the earliest possible moment, and 



404 DISEASES OF THE LUNGS 

if chronic bronchitis is present, the remedies which are commonly given for that 
disorder should be employed, care being taken, however, that no drug is given 
which tends, on the one hand, to act as a circulatory depressant, and, on the other, 
to promote too free bronchial secretion, for it must always be borne in mind that 
drugs of this character may precipitate an attack of profuse bronchial secretion, 
in which the patient may drown in his own fluids. 

Many of these patients will be benefited by the administration of 5 grains of 
carbonate of ammonium and 5 grains of chloride of ammonium given in a cachet, 
or capsule, or in fluidextract of licorice and water, three or four times a day. In 
other instances, if the bronchitis is chronic and well marked, creosote or guaiacol 
may be used; but care must be exercised that they do not disorder the stomach. 
If the secretion is thick and tenacious, iodide of ammonium, or iodide of sodium, 
in the dose of 5 grains three times a day, is useful, care being taken, however 
that the administration of this remedy does not produce too free bronchial secretion. 
It must also be borne in mind that bronchitis complicating emphysema is not 
infrequently the result of impaired cardiac action, and, therefore, that the best 
treatment for the bronchitis is the administration of cardiac tonics, such as small 
doses of digitalis, 3 to 5 minims twice or thrice a day, or the tincture of strophan- 
thus, or, in other cases, the administration, for a few days, of moderately large 
doses of strychnine or nux vomica. 

When the patient's means permit him, it is important that he should avoid 
extreme climatic changes. High altitudes are, of course, not only disadvantageous, 
but even dangerous to patients suffering from pulmonary emphysema, because of 
the dyspnea which such altitudes produce and because of the strain which is thrown 
upon the dilated right heart. 

In cases of emphysema suffering from an unusually severe attack of dyspnea, 
with great congestion and engorgement of the venous system, it is often advan- 
tageous to resort to venesection, removing as much as 20 to 30 ounces of blood; 
but it is manifest that this method of treatment can only be resorted to on a few 
occasions, and when the symptoms of dilatation and distention of the right side 
of the heart and of the liver are very well developed. Sometimes in these cases, 
if there is evidence of hypostatic congestion of the lungs, the application of wet 
or dry cups, posteriorly, near the bases is advantageous. 

For many years various text-books have recommended the employment of 
the iodides in their various forms in the treatment of pulmonary emphysema, 
with the idea that they distinctly modify the pathological process going on in 
the lungs, and to a certain extent arrest the destruction of the elastic tissue which, 
by its failure, results in the coalescence of the vesicles. It must be manifest that 
even that wonderful drug, iodide of potassium, must be quite useless for this 
purpose in many instances. Any advantage which follows its employment probably 
depends upon its influence upon the associated bronchitis, or upon the effect which 
it produces upon the vascular system by diminishing the tendency to atheromatous 
change, and by reducing high arterial tension if it is present, and so relieving 
the heart of unnecessary burden. Still another advantage in the iodides may be 
that in some cases they act as a diuretic and so help to relieve the tissues of an 
undue quantity of fluid if dropsy be threatened. 

Compensatory or Acute Emphysema. — This is an unfortunate use of the word 
emphysema, as the condition is not a true emphysema, but simply an abnormal 
distention of each individual air vesicle by active efforts at forced respiration, 
so that the entire lung may be increased in size and the areas of pulmonary resonance 
greatly increased. Usually in this state some high-pitched rales are audible in 
the chest. The condition may be seen in cases which have suffered from stridor 
due to laryngeal obstruction, or more commonly in those who are recovering 
from an acute asthmatic attack. It is also found in those parts of the lungs 



GANGRENE OF THE LUNG 405 

which have endeavored to compensate for other parts affected, as, for example, 
by pneumonia. 

Small-lunged Emphysema. — Small-lunged emphysema is sometimes called senile 
or atrophic emphysema, or senile atrophy of the lung. It resembles ordinary 
emphysema, as just described, in the fact that there is a wasting of the walls of 
the air vesicles, so that several vesicles form a larger cavity; but instead of the 
lung being larger and more voluminous than normal, it is shrunken and small, 
so that the heart is uncovered, the diaphragm raised in well-marked cases, and the 
whole thorax distinctly decreased in size. The expansion of the vesicles, as in 
large-lunged emphysema, is most marked at the apices and the edges of the lung. 
Inspection of the chest in such a case shows the intercostal spaces obliterated by 
the drawing together of the ribs, while the epiclavicular and episternal spaces are 
exaggerated and the respiratory movement is feeble and very shallow. On percus- 
sion the chest is found to be hyperresonant everywhere, but there is a great increase 
in the area of cardiac dulness, due to the retraction of the lung. On auscultation 
little that is abnormal is heard, save that expiration may be prolonged. 

Except there be an associated bronchitis, the patient with this type of emphysema 
rarely suffers from much inconvenience as a result of the pulmonary disease, and 
life is not materially shortened. 

Treatment. — There is no curative treatment for this type. The physician can 
only order rest, good food, proper clothing, and the avoidance of exposure. 

Interstitial Emphysema. — In interstitial emphysema the pathological condition 
is not like that of ordinary pulmonary emphysema, for the lung is riddled with 
tiny globules of air which find their way between the lobules and underneath the 
visceral layer of the pleura, where they may form quite large blebs. The condition 
arises whenever air escapes into the pulmonary tissues, as after tracheotomy, 
when it extends down along the trachea into the lung itself; fractures of the ribs 
with puncture of the lung; other wounds of the lung; rupture of air vesicles by 
great thoracic compression, as in sand crushes, even without injury to the skeleton, 
and occasionally results from violent abnormal respiratory action, as in whooping- 
cough, strangling, and sneezing. It has been observed after severe convulsions 
in epileptics and eclamptics. 

GANGRENE OF THE LUNG. 

Etiology. — This condition arises in individuals whose general vitality is greatly 
impaired by some primary disease, with the result that various micro-organisms, 
putrefactive and otherwise, produce death of part of the pulmonary parenchyma, 
and so a slough is formed. Manifestly, the causes of gangrene and abscess must 
be nearly related, and why gangrene rather than abscess should develop in any 
particular case is difficult to determine. Infarction of the lung, or pulmonary 
hemorrhage, may, by affording a nidus for the development of putrefactive germs, 
result in this state, and so may croupous pneumonia; yet it is a curious fact that 
bronchopneumonia, which is often due to profound debility and secondary infection, 
rarely so results. Equally curious is it to note that pulmonary tuberculosis in 
all its forms is rarely complicated in this manner. 

The most common cause of pulmonary gangrene is embolism and thrombosis, 
after this croupous pneumonia, and, thirdly, injuries to the lung through the chest 
wall, as in gunshot injuries. It may also arise from foreign bodies in the bronchi. 
It may also be due to pressure produced by an aneurysm, or tumor, or by an exten- 
sion of an infective process to the lung from the esophagus, pleura, vertebra?, 
mediastinum, or ribs. It may also follow the inspiration of particles of food. 
Rarely it is due to pressure of an aneurysm or to perforation of the esophagus 
when that tube is affected by cancer. 



406 DISEASES OF THE LUNGS 

Frequency. — Pulmonary gangrene most frequently attacks males in middle 
life — that is, from twenty to forty years of age — and is undoubtedly a very rare 
affection. In a large hospital service only a single case may be met with in many 
years. 

Pathology and Morbid Anatomy. — No description of pulmonary gangrene is 
better than that given by Laennec, who, nevertheless, in an experience of twenty- 
four years, saw only 2 cases. He divides the condition into three stages: (1) 
that of early mortification, in which the pulmonary tissue is edematous and of 
dark brown or greenish hue, the sloughing area looking shreddy and water-soaked; 
(2) that of deliquescence or liquefaction, the part of the lung affected becoming 
still more soft and flabby; and (3) that of excavation or abscess formation, in which 
the lung undergoes the separation of the slough and the formation of a line of 
demarcation to limit the pathological process. At this line of separation a con- 
solidation takes place, the sphacelus breaks down, and suppuration rapidly results 
in the coughing up of the dead tissues. As a matter of fact, it is incorrect to speak 
of a single sphacelus, for the cavity usually contains separate masses of shred-like 
tissue. 

Finally the limiting wall may undergo fibroid contraction, as it does in abscess, 
and the area be more or less closed, a focus usually remaining, from which more 
or less foul pus is constantly discharged. In the majority of cases this reparative 
process does not occur, and the patient dies. Over the seat of the process the 
pleural membrane is usually thickened and may be covered by a fibrinopurulent 
exudate, while if the pleura be perforated a putrid empyema may develop. In 
such cases pyopneumothorax may also manifest itself. Extensive suppuration 
of the bronchial glands may occur. 

Pulmonary gangrene affects the lower lobes oftener than the upper. 

Symptoms. — The symptoms of pulmonary gangrene in the early stages are not 
very definite. They depend, to some extent, upon the severity of the lesions and 
upon the micro-organisms which produce it. The patient is markedly prostrated, 
the heart's action is feeble and rapid, the skin leaky, the face anxious and thin, and 
the tongue dry and coated. The temperature runs the typical course of hectic 
fever, and it is a noteworthy fact that the exhaustion seems out of proportion in 
its severity to the febrile movement. Sometimes these symptoms are ushered 
in with severe chills, which recur at irregular intervals. The respirations are 
quickened, and there may be cough and expectoration, but until the break-down 
goes on so far as to result in. suppuration there may be but little material expec- 
torated. If a cavity forms, the ordinary signs of excavation, with those of sur- 
rounding consolidation, may be developed upon auscultation and percussion. 

One of the most characteristic symptoms of pulmonary gangrene is the odor 
of the patient's breath and of the materials which he expectorates. There is 
probably no discharge from the human body the odor of which is so penetrating 
and disgusting as is that of pulmonary gangrene. Not only does it render the 
patient disgusting to everyone who comes near him, but it penetrates every part 
of the room in which he exists, and often can be smelled throughout the whole 
house. On some days it is worse than others, but the variation of the quantity 
of expectoration does not necessarily mean a variation in its fetid character. The 
quantity of material which is expectorated does not give any very definite concep- 
tion of the size of the lesion of the lungs. West quotes a case of Godlee and Williams 
in which the patient expectorated a quart daily, and yet the autopsy revealed a 
gangrenous cavity which was not large enough to contain more than an ounce of 
fluid. 

The sputum is peculiar, in that on standing it separates into three layers. The 
upper layer is apt to be yellowish-green and opaque; the middle layer is opalescent 
and turbid, and resembles saliva when a considerable quantity is gathered in a 



PULMONARY ABSCESS 407 

glass. The lowest layer consists in a mass of greenish or brown-looking material, 
which constains considerable quantities of pus, altered red blood cells, and fragments 
of connective tissue. A careful microscopic examination of this sputum will 
show that it is filled with an immense number of micro-organisms, and crystals 
of leucin and tyrosin can be seen in large numbers. Various fatty acid crystals 
are also present. The sputum, at first alkaline, becomes acid, and seems to exercise 
a peculiar digestant or disintegrating influence upon the shreds of connective tissue 
which it contains. 

The cough in a case of pulmonary gangrene varies greatly according to the 
amount of material which is expectorated, and also with the degree of bronchial 
irritation which coexists. Sometimes, after a prolonged spell of coughing, a con- 
siderable amount of material from the gangrenous area comes away in a gush. 
Sometimes, too, the fluid which is expectorated is distinctly blood-tinged, due to 
the ulceration of small bloodvessels in the part surrounding the affected part. 
Not only may free hemoptysis develop, but septic emboli may be carried elsewhere, 
as, for example, to the brain or liver, and so cause secondary abscess. 

If by chance the patient swallows any of the sputum, septic diarrhea may 
be established and the stools may also become excessively offensive. The degree 
of exhaustion gradually increases, the heart becomes more and more feeble, the 
patient more and more emaciated, and, finally, dies of asthenia. 

Diagnosis. — The diagnosis between a moderate degree of pulmonary gangrene, 
pulmonary abscess, and bronchiectasis may be almost impossible, since, if bronchiec- 
tasis exists, the fetor of the sputum may be very marked. If the sputum under 
the microscope shows a large amount of connective tissue, the diagnosis is largely 
in favor of gangrene. The absence of tubercle bacilli in the sputum and the presence 
of the various bodies already named as appearing in this fluid will also aid in differ- 
entiation of the case. When the grangrene cavity is small, a positive antemortem 
diagnosis may not be possible, the more so because of the presence of acid-resisting 
bacilli, which may be mistaken by the novice for tubercle bacilli. 

Treatment. — The treatment of pulmonary gangrene is not promising. It is 
the duty of the physician to maintain the strength of the patient, as far as possible, 
by the administration of nutritious food given at frequent intervals, in small 
quantities, so that the digestion will not be overloaded; to give stimulants, as 
alcohol ; and occasionally, if the circulation becomes feeble, to administer strychnine 
hypodermically, or by the mouth. Bitter tonics may also be prescribed for the 
purpose of maintaining digestive activity. The employment of antiseptic inhala- 
tions, as suggested in the treatment of pulmonary abscess, may also be resorted 
to, but at most only do good by soothing the irritation of the bronchial mucous 
membranes and cannot, of course, influence the pulmonary parenchyma where 
the disease exists. 

If the evidences of sepsis are marked and anemia is present, the tincture of 
chloride of iron is to be administered, and the heart supported by alcohol, digitalis, 
and occasionally by caffeine. The internal use of creosote, carbolic acid, and 
similar substances, with the idea that they exercise a beneficial influence upon the 
gangrenous portion of the lung, is futile. 

A few cases of gangrene of the lung have been treated surgically, with success, 
by incision and drainage. For these methods the reader is referred to surgical 
treatises. 

PULMONARY ABSCESS. 

Etiology. — Abscess of the lung is always due to invasion of its tissues by one or 
more forms of pyogenic micro-organisms. Single large abscess occurs very rarely, 
but it is met with as a sequel of lobar pneumonia, bronchopneumonia, and as a 
result of injury to the lung by the entrance of foreign bodies through the chest 



408 DISEASES OF THE LUNGS 

wall or by the respiratory passages. Most commonly small abscesses are the 
result of septic emboli. Abscess may be due to the extension of a septic process 
from the mediastinal tissues or of the liver. So, too, a suppurative process in 
the deep tissues of the neck may result in secondary infection of the lung. 

When pulmonary abscess ensues after an attack of croupous pneumonia or 
bronchopneumonia, it is usually not single, but multiple, the area of consolidation 
being the seat of several foci of purulent material. These formations are not by 
any means so rare as in the larger variety. Holt states that he found them in 
about 7 per cent, of the autopsies of young children dying of pneumonia. Such 
foci are really not true abscesses; that is to say, they have no true abscess wall. 
When these formations are numerous, as they usually are, and of considerable 
size, the patient may maintain a high temperature for a long time after the acute 
primary disease has passed away, and may, by causing septic absorption, ultimately 
produce the patient's death. It may be difficult, even at autopsy, to state positively 
whether the purulent infiltration of the later stages of both forms of pneumonia 
is present, or if there is a true suppurative abscess in the lung. In both cases the 
areas of softening are found to be infected by the streptococcus, staphylococcus, 
or other pyogenic organism. 

When the foci are of large size, and are multiple, the prognosis is bad, for wide- 
spread suppuration in the lung is always fatal when the breaking-down process 
involves the exudation of pneumonia. If there be a single, large, localized abscess 
involving the area of pneumonic exudate, the prognosis is less grave, but it is 
exceedingly bad, nevertheless. To sum up, therefore, we find that suppuration 
takes place in the lung in three degrees or forms after pneumonia: (1) as a mild 
suppurative process, which is really nothing more than a rapid breaking down of 
the exudate of the disease; (2) as a more severe process, partaking more of the 
character of true suppuration, in which multiple and large foci of pus form; and 
(3) of a single large suppurative process; in other words, a single abscess of the lung. 
As already stated, these so-called "abscesses" rarely have a true abscess wall. 

Abscess, multiple or single, when it arises from the entrance of a foreign body, 
occurs only if that body enables infecting micro-organisms to enter the surrounding 
tissues. Thus, a marble, or small stone, entering a bronchus may be there for a 
long time without causing abscess; whereas, the entrance of a piece of food, a straw, 
or a fragment of cork, or other organic matter may speedily cause a septic suppura- 
tive pneumonia and death. An abscess may follow a gunshot injury. 

If by chance the patient recovers from the acute illness, there may be left a 
constantly discharging focus of pus. 

Again, we find pulmonary abscess forming as the result of a septic embolus 
entering the lung. About the site of its lodgement an inflammatory exudate 
rapidly forms, and this speedily proceeds to suppuration. Pus and yellow elastic 
tissue are expectorated, and the patient dies of septic poisoning and exhaustion, 
or if recovery takes place there is formed around the zone of necrotic tissue a wall 
of inflammatory exudate, which prevents further destruction of the parts, and, with 
recovery, proceeds to organization, finally developing into more or less well-formed 
fibrous tissue, which gradually contracts until the cavity disappears or is greatly 
decreased in size. . We have in this type what may be called the true form of abscess 
as it occurs in other tissues; whereas, the ordinary suppurative foci hitherto de- 
scribed are hardly to be regarded as true abscesses. Occasionally the abscess 
cavity persists for months, and we have then a chronic pulmonary abscess. 

When abscesses elsewhere than in the lung break into its tissues the result is 
not always a pulmonary abscess by any means. It is often extraordinary how 
much foul pus may pass from an empyema or hepatic abscess through the lung, 
and be expectorated, without causing any severe lesions in these organs. 

Sometimes suppuration takes place in an echinococcus cyst in the lung. 



CONGESTION OF THE LUNGS 409 

Symptoms and Diagnosis. — The diagnosis of pulmonary abscess in its early 
stages may be practically impossible, for there may be present no other signs than 
cough, fever, and scanty expectoration, with patches of impaired resonance on percus- 
sion. In unresolved pneumonia the physical signs may be identical, but the 
leukocyte count is rarely above 15,000 or 20,000, whereas in abscess from 30,000 
to 50,000 white cells may be present. As the pus is freely formed, much aid may 
be gained from the temperature chart, which may show the long sweeps of septic 
absorption. There may be sweats, chills, and some hectic flushing; but these do 
not necessarily point to abscess of the lung, for they may be due to empyema 
or an abscess elsewhere, or be a result of tuberculosis. If the sputum becomes 
distinctly purulent, and the microscope shows abundant pus and masses of connec- 
tive tissue without tubercle bacilli, the diagnosis is readily made. About this 
time it may be possible, too, to discover the physical signs of cavity. 

When a single large abscess is present the positive diagnosis may be made evident 
by the sudden rupture of its contents into a bronchus, and the expelling through 
the mouth of a considerable quantity of pus. I had under my care recently a 
young woman, aged twenty years, who, after an attack of typical croupous pneu- 
monia, developed a more and more septic temperature, and, finally, expelled at 
one time nearly a pint of pus from the right lung. Constant expectoration of pus 
persisted for several days, and then an equally large amount was expelled, nearly 
causing death by strangulation. After a long convalescence she reached perfect 
health. In this case the fluoroscope revealed the site of the abscess very clearly. 
Care must be taken that the purulent expectoration and fetid breath of a case of 
bronchiectasis is not considered an indication of true pulmonary abscess. 

Prognosis. — The prognosis in these cases is always very grave. Death may 
ensue, not only from septic absorption, but from the gradual exhaustion due to 
prolonged suppuration or from the ulceration of the wall of a bloodvessel with 
consequent severe hemoptysis. Again, a secondary pneumonia may develop 
from the primary suppurative process. 

Treatment. — The treatment of abscess of the lung divides itself into three parts : 
the support of the patient's strength by good food and the moderate use of stimu- 
lants; the resort to as much fresh air and sunshine as possible; the inhalation of 
gentle antiseptic balsams which do not really influence the abscess, but perhaps 
benefit the associated bronchitis; and, lastly, by the use of the knife, bone forceps, 
and the actual cautery, to open the abscess through the chest wall and lung. 

As supporting drugs, iron and arsenic, whiskey and port wine, are particularly 
valuable. Easily digested semiliquid foods, with digestants to aid their speedy 
absorption, are valuable, and in the way of an inhalation equal parts of oil of 
eucalyptus, oil of pine, and compound tincture of benzoin may be added to the 
water in a croup kettle, and so dissipated through the air of the room. Codeine 
and cannabis indica may be used to relieve excessive, painful cough; but large 
doses of these drugs should not be used, because they prevent the expectoration 
of the pus, and if the patient sleeps soundly while under their effects, rupture of 
the abscess may cause fatal asphyxia. 

CONGESTION OF THE LUNGS. 

Definition. — Strictly speaking, there is a congestion of the lungs whenever severe 
exercise is taken, but this, of course, is not referred to here; nor is it the intention 
to consider that form which constitutes the early stage of croupous pneumonia, 
and which ends in the formation of a croupous exudate. The form of congestion 
here referred to is that due to mechanical causes which interfere with the proper 
passage of blood through the pulmonary vessels (passive congestion), or that due 
to intense irritation caused by inhaling irritant vapors or fumes. 



410 DISEASES OF THE LUNGS 

Etiology and Pathology. — The most common cause of pulmonary congestion 
is progressive valvular inadequacy at the left auriculoventricular orifice, or, in 
other words, mitral disease, either obstructive or regurgitant. These lesions dam 
the blood back into the lungs, and the right ventricle undergoes hypertrophy in 
an endeavor to drive it onward. As a result the pulmonary capillaries are placed 
under abnormal strain, increased hemolysis occurs, and when the condition becomes 
chronic there is produced what is known as brown induration of the lungs. At 
autopsy they appear of a dull reddish-brown hue, the incised surfaces becoming 
brighter red after exposure to the air. The supporting tissue of the lung is thickened 
and less elastic than normal, and the organ is heavy, as shown by the fact that when 
placed in water it does not float so high as normal lung tissue. Microscopically 
the connective tissue and the alveolar epithelium, some of which is desquamated, 
contain granules of brownish pigment derived from the hemoglobin content of the 
disintegrated red blood cells. 

The bloodvessels are tortuous, and the capillaries which line the walls of the 
alveoli project in loops or tufts into the air spaces. Sometimes hemoptysis of 
moderate degree arises from rupture of these vessels or those which are in the 
bronchial tubes. It can be readily understood why it is that a person with 
these lesions is a ready victim for pneumonia, hypostatic congestion, and infarc- 
tion. 

Acute pulmonary congestion resulting from sudden failure of the left ventricle 
is often the cause of sudden death in the course of an attack of sunstroke or after 
the inhalation of irritant gases. 

Closely connected with this form of congestion from an etiological stand-point 
is hypostatic congestion of the lungs. In this state the lower portions of the lungs 
are commonly affected because the patient is usually in the dorsal decubitus and 
the blood accumulates in the most dependent part of the organs. Associated with 
this accumulation of blood in the vessels of the lung, an excess of serum collects 
in the intervesicular structures, producing edema, or, passing into the vesicles, 
causes the affected part to become essentially airless. 

The causes of hypostatic congestion are not very different from those of ordinary 
congestion as just described, save that the failure of the right side of the heart 
is more marked and the condition is more frequently met with as the result of 
profound asthenia occurring in the course of some malady like severe typhoid 
fever or advanced renal disease. That the dorsal decubitus is not the chief cause 
is proved by the fact that many persons suffering from certain maladies which 
require the maintenance of this posture do not suffer from hypostatic congestion. 
That posture exercises some influence, however, is shown by the fact that if the 
patient remains on one side the stasis is often unilateral. 

Autopsy in cases of hypostatic congestion reveals the involved area as darkened 
in color, often black or purplish-black in hue. They may be airless, with frothy 
accumulations in the bronchial tubes, loss of crepitation on pressure, and a doughy 
condition when one finger is pressed upon the lung, resembling the sensation 
produced by edema elsewhere. In some cases, not only a serous exudation takes 
place into the vesicles, but red and white blood cells are extruded, which may 
render the lung so red that it looks somewhat as if true croupous pneumonia were 
present. To this -state has been applied the term " splenization," or " hypostatic 
pneumonia," in distinction from the red solidification in true pneumonia called 
" hepatization." Still less frequently actual hemorrhage into the lung occurs as 
the result of giving way of the walls of small vessels. 

The causes being identical on both sides of the chest, it is natural that hypostatic 
congestion should usually be found to be bilateral. It begins at the bases and 
slowly creeps upward, until it may involve the lower lobes of each side, and even 
the middle lobe on the right side and part of the upper on the left. 



CONGESTION OF THE LUNGS 411 

Symptoms. — The symptoms of that form which is due to valvular disease at 
first are those of shortness of breath, with repeated attacks of bronchitis, which 
may become chronic. The mucus expectorated may contain tiny clots of blood 
arising from the dilated vessels just described. An infarct of the lung may develop 
into an area of consolidation and hemoptysis may occur. Sometimes this accident 
follows an improvement in the condition of the heart, which is produced by rest 
and tonics, because the renewed strength of the right ventricle ruptures a weak 
and tortuous vessel. 

The symptoms of hypostatic congestion differ greatly with the rapidity with 
which the condition develops, and the underlying cause. When the exudation 
rapidly takes place evidences of respiratory embarrassment develop and dyspnea 
and cyanosis are often marked. If the condition is slow in onset as in most 
instances when it complicates some state of adynamia, no symptoms may be 
present until a large area of lung tissue is affected. Cases of the acute type are 
seen chiefly as the result of renal disease and cardiac failure. 

The physical signs of hypostatic congestion are not well marked in the early 
stages. Careful light percussion may reveal slight impairment of resonance, and 
auscultation may discover a few moist rales, which are chiefly bronchial, forming 
small rhonchi or sibilant sounds. These are the signs which it is important to 
recognize, since it is at this time that the physician can do much, in many cases, 
to limit or even prevent the spread of the condition which is beginning to develop. 
Later on the condition is so well marked that the merest tyro can recognize it by 
reason of the bronchial breathing, the moist rales, and the absence of vesicular 
sounds which have been put aside by exudation. The only thing to be done at such 
a late hour is to endeavor to support the circulation, so that the lesions will not 
spread and so that the patient may be kept going till absorption or resolution 
occurs. 

The presence of hypostatic congestion is often not recognized, because the 
physician does not carefully examine the lungs. In many cases, too, it is agonal, 
particularly if death comes slowly. 

Diagnosis. — Hypostatic congestion must be separated from catarrhal and croupous 
pneumonia, and from pleural effusion, serous or purulent. An important point 
in the differentiation is the fact that in both forms of pneumonia the temperature 
is usually febrile, and if they complicate some pre-existing state the fever is usually 
exacerbated when the pulmonary condition develops, whereas distinct febrile 
movement is unusual in hypostatic congestion unless it is in turn associated with a 
true pneumonic process. The sputum, if any is raised, is frothy in cases of con- 
gestion, but is sticky and rusty in croupous pneumonia, and perhaps mucopurulent 
in the catarrhal form. The cough is loose and productive (juicy) and not hard 
and difficult as in pneumonia. Then, too, the onset of congestion is not character- 
ized by a chill nor by pain in the chest. Pleural effusion may be separated from 
hypostatic congestion by a change in the level of dulness on percussion when the 
patient changes his posture, by the fact that the percussion note in congestion 
is rarely as flat as in effusion, by the fact that pleural effusion is rarely bilateral, 
and if at all profuse usually displaces the heart to the left if it be on the right side 
and downward if it be on the left. 

Prognosis. — This depends largely on the promptness with which hypostasis 
is discovered and treated, the cause of the condition, and the vitality of the patient. 
When due to renal disease and associated with a general tendency to edema, the 
prognosis is bad. So, too, if it ensues in a prolonged exhausting fever the prognosis 
is bad because it indicates great feebleness. In old persons and in young children 
it is very often the cause of death during the course of other diseases. 

Treatment. — This consists in preventive measures, such as changing the posture 
of the patient every hour, in the use of cold sponging if fever is present, to readjust 



412 DISEASES OF THE LUNGS 

the circulation, and in the proper use of stimulants. As soon as any signs of the 
malady appear, the patient should be made to lie on one side and then on the 
other and not upon the back. Two or three dry cups should be applied to the 
chest over the base of each lung posteriorly, or in their place a mustard plaster 
may be used. If the heart is feeble, strychnine, digitalis, and belladonna are 
useful. It may be wise in urgent cases to give strychnine and atropine hypoder- 
mically and to use Hoffmann's anodyne in the dose of a drachm every hour for 
several doses. Sometimes if the patient is strong enough to stand active purga- 
tion, colocynth or elaterium are valuable cathartics, the latter being given in the 
dose of | grain, but when the symptoms are urgent and the venous system is 
engorged free venesection should be practised. 

Manifestly it is the physician's duty in all these cases of exhausting disease to 
carefully listen to the chest at every visit during an illness, to note the first sign 
of this insidious state. 

TUMORS IN THE LUNGS. 

Tumors in the lungs are rarely met with. They may be benign or malignant, 
but are usually the latter, and occur as primary or secondary growths; tumors 
secondary to growths elsewhere being much the more frequent. The benign 
tumors are chondroma, fibroma, osteoma, and dermoid cyst. The malignant 
tumors are sarcoma, carcinoma, and occasionally endothelioma. The sarcoma 
and carcinoma usually occur as nodular masses which as they grow push the lung 
tissue aside, or more rarely they occur as infiltrating growths which extend along 
the bloodvessels or bronchial tubes. If the tumors are placed peripherally or 
are primary, it may be difficult to determine whether they are pleural or pulmonary. 
In cases of lymphosarcoma and in leukemia typical masses of lymphomatous 
tissue are quite frequently found infiltrating the lung, and they may cause consoli- 
dation throughout considerable areas. 

When the malignant growths are secondary they are usually found in both 
lungs unless the tumor is the result of extensive infection, as in the case of tumor 
in the chest wall directly involving the lung tissue through the pleura. In such 
an instance the growth at first is single, whereas when it has spread by metastasis 
it is multiple. Secondary cancer of the lung is more frequent in women than in 
men because of the frequency with which women suffer from carcinoma of the breast. 

Symptoms. — The symptoms are not characteristic. They depend largely upon 
the situation of the growth and upon the degree of pressure which it exercises 
upon surrounding tissues. If it presses upon nerve trunks it causes severe pain; 
if upon a large bronchus it produces cough and expectoration; and if a consider- 
able area of lung tissue is involved it causes dyspnea, particularly if the growth 
or growths press upon the bloodvessels and so cause pulmonary congestion or 
stasis, so that as the disease advances pulmonary edema aids in decreasing the 
area for the oxygenation of blood. Great and manifest engorgement of the super- 
ficial veins of the neck and head is sometimes present as the result of pressure on 
the superior vena cava, and if the vagus or the recurrent laryngeal nerves are 
pressed upon cardiac neuroses and laryngeal spasm or paralysis may ensue. 

Diagnosis. — The diagnosis of tumor of the lung when no primary growth exists 
elsewhere is extremely difficult. The presence of thoracic pain, in the absence 
of signs of aneurysm, and inability to discover cardiac disease, aortitis, or disease 
of vertebrae should arouse the suspicion of the presence of a growth, which may be 
confirmed by the presence of dulness on percussion in the area affected. When 
these symptoms develop in a patient who has a growth elsewhere, or has had a 
growth elsewhere which has been excised, as in carcinoma of the breast, they 
possess much more diagnostic value. Stokes considered that prune-juice sputum 
was a very typical sign of malignant growth in the lung. Emaciation may be a 



PLEURITIS 



413 



marked symptom, as it is so often in cases of malignant growth elsewhere in the 
body, but the maintenance of flesh by the patient does not negative malignant 
growth, as sometimes little weight is lost. 

It is hardly necessary to add that the malignant tumors are more frequently 
met with in middle life or in advanced age than in youth. 

No treatment is of any avail so far as cure is concerned. The most that can 
be done is to support the system by good food and relieve pain by morphine. 



DISEASES OF THE PLEURA. 



PLEURITIS. 



Definition. — The term pleuritis, or pleurisy, is applied to an inflammation, 
either acute or chronic, of the serous membrane which lines the thoracic cavity 
and in its reflections covers the lung; the so-called parietal and visceral layers 
of the pleura. This inflammation is always the result of an infection by some 
pathogenic micro-organism. It occurs in four forms, namely, as dry or fibrinous, 
serofibrinous, purulent, when it is called empyema, and that due to tuberculosis, 
or tuberculous pleurisy. Sometimes malignant disease affects this membrane, 
and this may be considered a fifth form of pleural inflammation (Tig. 75). 

Fig. 75 




Carcinomatosis of the costal pleurae. (Kast and Rumpler.) 

Etiology. — As just stated, pleurisy is practically always due to an infection 
by some micro-organism. In a large number of cases it arises as the result of an 
invasion of the lung by the pneumococcus, with or without an associated pneumonia. 
In other instances it is due to the entrance of pyogenic organisms such as the 



414 DISEASES OF THE PLEURA 

staphylococcus and streptococcus, and in still other cases from invasion by tubercle 
bacilli. Infection of the pleura may also take place through the pericardium, 
the mediastinal tissues, the vertebrae, and the diaphragm. Sometimes, though 
rarely, it is from the chest wall itself, after injury to the thorax or by extension 
from the mammary gland. Pulmonary abscess may, by the extension of the 
inflammatory process, produce pleuritis, or a bronchopneumonia may cause a 
secondary infection. In some cases, however, the inflammation of the pleura is a 
primary lesion without any pathological change in the lung except as a secondary 
condition. 

The relative frequency with which acute pleurisy is produced by each specific 
micro-organism is unknown, since recovery takes place in mild cases and no oppor- 
tunity of determining the provoking cause presents itself. The pneumococcus 
and tubercle bacillus, however, are the causes in the majority of cases. 

When empyema follows pleurisy the necessity of setting free the pus enables 
us to determine the character of the infection in the great majority of cases, and 
the statistics derived from this source give us some conception of the relative 
frequency with which pleurisy follows infection by different organisms. (See 
Empyema.) 

Frequency. — Pleurisy is most commonly met with between the ages of twenty 
and forty, but it is by no means confined to these decades of life. On the contrary, 
it is very frequent in young children — at least, as a complication of pneumonia 
in its various forms — and is also not rarely met with in persons of advanced years. 
In adults pleurisy occurs more than twice as often in males as in females, but in 
early childhood this predominance does not occur. As an illustration of these facts 
it is interesting to note that in 651 cases in St. Bartholomew's Hospital, London, 
465 were in males and only 186 in females. The distribution -of these cases as 
to age was as follows: five years and under, 25; ten years, 59; fifteen years, 50; 
twenty years, 54; thirty years, 179; forty years, 149; fifty years, 85; sixty years, 35; 
over sixty years, 15. 

Pleurisy occurs most frequently in the early spring and late autumn, when 
great changes in temperature take place. This does not mean that exposure 
to cold produces pleurisy directly, but rather that the exposure reduces vital 
resistance to such an extent that infection takes place. 

So, too, a number of acute and chronic diseases result in pleurisy, not because 
they have any direct effect on the pleural membrane, but because they lower 
vital resistance at the same time that they expose the pleura to infection by their 
specific germ. Thus, pleurisy may be indirectly produced by the acute specific 
fevers and by Bright's disease, the first of which provide a predisposing cause and 
a specific germ, while the latter lowers vital resistance in general. So, too, it is 
possible for damage to the chest wall to result in acute pleuritis and its conse- 
quences. 

It is to be constantly borne in mind that of all specific infections that by the 
tubercle bacillus is the most important, because of the prognosis, because it is 
often insidious, and because it is probably one of the most frequent causes of 
pleurisy. 

The pathology, morbid anatomy, symptomatology and treatment of the various 
forms of pleurisy are best considered under the specific description of each type. 

Dry Pleurisy. — Dry pleurisy, as its name indicates, is an inflammation of the 
pleural membrane with a minimum amount of serous exudate. It may be circum- 
scribed or localized, as over a tuberculous cavity, or may be diffused over a large 
area, as in croupous pneumonia. The pathology and morbid anatomy of pleurisy 
of the dry type may be described as follows: As in all inflammations of serous 
membranes, there is an acute hyperemia followed by infiltration and exudation 
of blood cells, fibrin, and, it may be, serum. The pleural membrane is lustreless 



PLEURITIS 415 

in appearance, and roughened or granular, and is somewhat thickened, partly 
because of infiltration, but chiefly by reason of the fibrinous exudate on its surface. 
This exudate is a primary factor in the formation of adhesions between the visceral 
and parietal layers of the pleura. Sometimes the exudate is remarkably profuse 
or perhaps a number of layers are formed, so that the pleura may exceed a quarter 
of an inch in thickness, and is somewhat reticulated or uneven on the surface. 
Such an exudate is rarely completely absorbed after the attack has passed, and it 
often organizes and produces impaired resonance on percussion and other morbid 
physical signs during the lifetime of the patient. 

Symptoms. — The onset of acute dry pleurisy is characterized by a severe pain, 
or "stitch," in the side and by the development of some fever. The pain in the 
side is sharp and stabbing in character and the patient " catches his breath," to 
use a popular expression, when he endeavors to inspire. Speaking, coughing, 
or any movement which causes increase in the thoracic movement, greatly increases 
the pain, which can, however, be markedly relieved, as a rule, by strapping the 
side of the chest which is affected, and so diminishing its freedom of movement. 
The pain which is developed by pressure on the chest wall is sometimes of two 
types, namely, severe pain produced by deep pressure, and exquisite tenderness 
of the skin over that part of the pleura which is inflamed. In the great majority 
of cases the patient states that the greatest pain is between the mammary line 
and the posterior axillary line, but it may be complained of in many other parts 
of the chest, particularly if the disease be due to tuberculosis. Young children 
who have not been trained in the localization of pain often state that the suffering 
is in the epigastrium, or in the left or right hypochondrium, and even in adults 
I have more than once seen physicians misled into a diagnosis of appendicitis 
because of the pain referred by the patient to this region, when in reality the cause 
was acute pleuritis. In all cases of pain below the diaphragm it is a good rule 
for the physician to examine the condition of the thoracic viscera before asserting 
that abdominal disease is present. As severe stabbing pain in the thorax is some- 
times due to aneurysm, muscular rheumatism, or intercostal neuralgia, these 
possibilities must be excluded before we can decide that the cause is pleuritis. 

The most important physical sign which determines the diagnosis of this 
affection is the so-called "friction sound" produced by the rubbing of the visceral 
layer of the pleura upon the parietal layer, both layers being roughened and dried 
by the early stage of the inflammation. This friction sound is usually best heard 
just below and just back of the nipple on the side involved. (See Fig. 76.) In 
persons who have very thick chest walls and who breathe superficially, by habit 
or because of the pain, it is often necessary that they take a deep breath before 
a friction sound is produced. Sometimes the friction sound is so creaking and loud 
that it sounds like the noise made by a new leather saddle when it is first used; 
at other times it is so soft that only the most careful auscultation will reveal it, 
and it may resemble the fine rales of croupous pneumonia. In other cases this 
creaking can be felt by the hand of the physician. If the pleurisy be situated 
near the heart the action of that organ may cause the pleural friction sound to 
occur as often as the heart beats, and so lead one to the diagnosis of pericarditis. 
This is called a pleuropericardial friction sound, and may also depend upon a simul- 
taneous development of pericarditis and pleuritis. 

A second important physical sign is the diminished respiratory movement on the 
side of the chest which is affected, as may be seen by the eye and recognized by the 
feeble respiratory sounds when auscultation is performed, the semifixation of the 
chest being an effort to decrease the thoracic movement, and so limit the degree 
of pain. My colleague, Coplin, has suggested that the fixation is in part due to 
changes in the intercostal muscles themselves. (See article on Croupous Pneu- 
monia.) This fixation may extend to one side of the diaphragm, and so result in 



416 



DISEASES OF THE PLEURA 



decreased abdominal movement on that side. The rate of respiration may be 

increased in order to compensate for the shallow breathing, but it is never the 

hurried or urgent respiration met with in cases of real dyspnea. 

There are two other signs of pleurisy which are of some diagnostic value, namely, 

the suppressed cough, which the patient attempts to stifle in order to prevent pain, 

and the attitude of fixation of the body, so that inadvertent movement by the 

patient or change in his position made by his attendant may not produce pain. 

Sometimes if the skin is not hyperesthetic the patient lies on the affected side to 

render it fixed, or he may lie on the well side to avoid pressure on the involved 

pleura. 

Fig. 76 




Area in which a right-sided pleural friction sound is usually heard best. 

The fever in acute pleurisy is rarely high in adults, although it may be in young 
persons. Often it never rises above 102°, and the pulse is usually only increased 
by reason of the fever; so that it bears no direct relationship to the disease. There 
is usually marked leukocytosis. 

Diagnosis. — Dry pleurisy is separated from muscular soreness due to strain by 
the facts just given and by the history of an injury; from muscular rheumatism 
by the fact that signs of this malady are to be found elsewhere; from intercostal 
neuralgia by the inconstancy of that affection, and by the fact that ordinary 
breathing does not increase the pain in the majority of cases, and, further, that all 
three of these conditions are not accompanied by any febrile movement or evidence 
of general systemic disturbance. Acute pleurisy of the dry type lasts from a 
few days to two weeks. A longer attack than this should arouse the suspicion 
of the presence of a more persistent disease, such as tuberculosis. 

Prognosis. — Barring complications the prognosis is favorable. (See Empyema, 
and Pleurisy with Effusion.) 

Treatment. — The treatment of dry pleurisy consists in applying adhesive strips, 
two inches wide, and overlapping one another one inch, from the middle line of 



PLEURITIS 417 

the vertebra? to the middle line of the sternum, not following the line of the ribs, 
but passing from behind forward horizontally. They should be applied from below 
upward, and with a sufficient degree of pressure to produce almost complete fixation 
of that side of the chest. The pain, if it is extensive, may be further controlled 
by the administration of 3-grain doses of Dover's powder every two or three hours. 
If necessary, a hypodermic injection of morphine may be given. If the fever is 
high an ice-bag may be applied to the head, and tepid or cold spongings over the 
entire body may be employed. An ice-bag may also be applied to the side of the 
chest which is inflamed, for the relief of pain. 

In the earliest stages of an acute dry pleurisy, in a strong, healthy individual 
of a pleurotic type with a bounding pulse, there can be no doubt that the adminis- 
tration of sufficiently large doses of the tincture of veratrum viride or the tincture 
of aconite is advantageous, as it may diminish the local hyperemia in the pleura 
and decrease the action of the heart so that it pumps less blood into the inflamed 
area, thereby causing determination of blood to the peripheral capillaries. This 
vascular relaxation, associated with sweating, tends to still further relieve the local 
congestion, and altogether exercises a beneficial influence upon the local lesion. 
These depressant drugs, however, are distinctly contra-indicated unless the patient 
is strong and hearty, and after the first twenty-four hours of the illness they are 
probably useless. Indeed, after this time they may do harm. If they are used 
at all, they should be given freely. Thus, 6 minims of the tincture of veratrum 
viride may be given every half-hour until the patient is very slightly nauseated 
or until his skin becomes moist, when the drug should be stopped. A similar 
method of employing aconite may also be practised. 

The employment of a poultice, or cotton jacket, in the treatment of pleurisy 
is less and less resorted to at the present time. There is no reason to believe that 
its influence is advantageous, and it very greatly increases the discomfort of the 
patient because of the heat and consequent sweatings which are produced. Further 
than this, there is always danger of the patient taking cold by the poultice becoming 
chilled, or during the removal of the poultice or cotton jacket for cleansing purposes. 

It is important to remember that the presence of a moderate pleural effusion 
does not require the physician to institute measures for its immediate relief, because 
in a very considerable proportion of cases absorption will take place by natural 
processes, and so nature will produce a cure. 

Finally, all patients convalescing from an attack of dry pleurisy should be 
instructed to present themselves to the physician several times at intervals of a 
few days, in order that he may have the opportunity of determining whether the 
pathological condition has entirely disappeared. It happens, all too frequently, 
that such patients are discharged "cured," when they actually have an insidious 
tuberculosis, the primary pleurisy having been due to this cause. 

Pleurisy with Effusion. — While a large proportion of cases of acute pleurisy 
are dry, in the sense that no excess of serum is poured out by the inflamed serous 
membrane, it is not to be forgotten that a considerable number of cases of pleural 
inflammation terminate in more or less profuse outpouring of fluid into the 
pleural sac. This forms what is sometimes called "pleurisy with effusion," or 
"pleuritic exudation." While the dry type often involves only a patch, or small 
part, of the pleural membrane, that form which is accompanied by effusion, unless 
limited by adhesions, usually affects the entire pleura of one side, and, indeed, 
it may be bilateral, although this is, fortunately, a rare occurrence. 

The exudate is composed of two parts: (1) a solid portion, consisting of fibrin 
and cells, which is attached to the surface of the pleura and which constitutes 
the basis by which adhesions binding the two layers of the pleura together may 
be formed, and (2) serum or fluid exudate, which may be so abundant that the 
pleural sac is completely filled. This fluid is always turbid or cloudy from the 
27 



418 DISEASES OF THE PLEURA 

presence of degenerated and exfoliated endothelial cells, particles of fibrin and blood 
cells, particularly leukocytes. It is worthy of note that the pleura in cases of 
pleuritis, accompanied by serous effusion, is usually not so markedly infiltrated 
as in the dry type. 

These effusions are usually the result of infection by the pneumococcus, the 
staphylococcus pyogenes, and the tubercle bacillus. The latter infection is always 
to be suspected in subacute cases with much fluid and little plastic exudate. 

An examination of the literature on the bacteriology of this state shows that a 
large number of organisms have been found in pleural effusions and also that in 
many cases the effused fluid is sterile. (See Empyema.) For example, Lemoine 
made cultures from the fluid of 38 cases of serofibrinous pleurisy, and found it 
sterile in 28 instances. 

Recovery, which takes place in the majority of cases, occurs by the absorption 
of the serum and the partial absorption and shrinkage of the fibrin, but the chief 
change in the plastic exudate is organization brought about by the formation of 
granulation tissue, which finally becomes dense and cicatricial in character. 

There is probably no form of pleural effusion so prone to confuse the clinician 
as loculated or ensacculated effusions. These may form between lobes, between 
the base of the lung and the diaphragm, or on the mediastinal aspect of the organ. 
Their localization is maintained by marginal adhesions that prevent the diffusion 
of fluid throughout the pleural cavity. Empyema, similarly limited, offers identical 
difficulties in diagnosis. (See Interlobar Empyema.) 

The lung may be markedly distorted, displaced, or compressed by the adhesions, 
and even the heart may be forced from its normal position. 

Symptoms. — The symptoms of pleurisy with effusion are not very characteristic, 
except in so far as the physical signs are concerned, but these are typical, and some 
of them pathognomonic. If the onset of the attack of pleurisy has been sharp 
the severe pain already described passes away as the effusion takes place and so 
separates the inflamed layers of the pleura, at the same time probably depleting 
them. The fever often diminishes or disappears when the stage of effusion is 
reached. Dyspnea may or may not be present, according to the size of effusion, 
the spaciousness of the chest, and the ability of the healthy side to do enough 
work to compensate for the part which is impaired in function. Strong, hearty 
individuals often seem to be more dyspneic than feeble ones, probably because 
in the former case the effusion is more rapid and the restricting adhesions are more 
firm. Cough in this stage of effusion is usually not severe, and may be absent, 
except on exertion. It is often due to an associated bronchitis. 

The posture of the patient, if the effusion be large, is usually characteristic, 
in that he persists in lying on the affected side, in order to permit the healthy lung 
to have full play. Turning him on the affected side may cause urgent dyspnea 
and a sudden change to the erect posture may do likewise, since the pressure of the 
fluid on the diaphragm interferes with its movements or with the action of the 
heart. If it be on the right side the apex beat is displaced to the left. 

Physical Signs. — The physical signs of pleural effusion are as follows : Inspection 
shows decrease in respiratory movement on the affected side, with increased 
activity on the healthy side; bulging of the entire chest on the diseased side, with 
fulness of the interspaces and some fulness it may be in the hypochondrium. Pal- 
pation reveals an absence of vocal fremitus on the affected side, and if the effusion 
be on the left side the apex beat of the heart is displaced downward and to the 
right. If it be on the right side the apex beat is displaced to the left. 

Percussion elicits flatness, or marked dulness, except at the apex above the 
fluid, where the percussion note is peculiarly high-pitched, and almost tympanitic — 
the so-called Skodaic resonance. Percussion of the liver, if the effusion be on the 
right side, may show that the lower margin of liver dulness is abnormally low. 



PLEURITIS 



419 



If the effusion is on the left side, percussion shows dulness in Traube's semilunar 
space. (See Fig. 77.) 

Auscultation discovers that there is an absence of breath sounds in the area 
where percussion gives flatness, except it may be for distant and transmitted 
bronchial breathing. Along the vertebral column and near the inner edge of the 
scapula on the affected side egophony, or the "bleating voice" sound, may be 
heard if the patient speaks, while vocal resonance in the apex of the lung, where 
Skodaic resonance is present, is greatly increased, even to the degree of pectoriloquy. 
At this place above the effusion bronchial or tubular breathing may be very marked. 
Sometimes the breath sounds are even amphoric in character. 

Fig. 77 





Showing at x maik the so-called area called Traube's semilunar space, where, in health, percussion 
gives a tympanitic note, which becomes flat in left-sided pleural effusion. The solid block represents 
hepatic and cardiac dulness. 



Occasionally, as the result of the formation of adhesions, pleural effusion is 
circumscribed within narrow limits, and the presence of an inflammatory exudate 
produces an area of dulness which is much larger than that space occupied by 
the fluid. The introduction of an aspirating needle for diagnostic purposes may, 
therefore, readily mislead the physician, since a dry tap will often occur unless 
the needle happens to enter that portion of the area of dulness which actually 
contains the fluid. The mere introduction of the needle into the centre of the area 
of dulness is not necessarily followed by the withdrawal of fluid, since it not infre- 
quently happens that a considerable mass of inflammatory exudate lies to one side 
of, or above or below, the fluid. These loculated effusions are more common 
in cases of empyema than in ordinary cases of pleurisy with effusion. (See 
Empyema.) 

The rate at which effusion takes place varies very greatly. Rarely the chest 
may become filled in a few days; more commonly it takes a week or even three 



420 DISEASES OF THE PLEURA 

weeks. Rapid effusion is more dangerous than the delayed type, because the 
thoracic viscera in the former case do not have time to adjust themselves to the 
altered conditions. I have seen a case of rapidly forming pleural effusion in which 
sudden death followed the turning of the patient on his well side. 

The duration of pleural effusion varies very greatly. Small effusions are often 
absorbed with surprising speed within a few days, but large ones are often very 
slowly absorbed and may not be absorbed at all until some of the pressure is removed 
by aspirating the chest. 

Diagnosis. — It is a noteworthy fact that while the diagnosis of pleural effusion 
is very readily made in some cases, in other instances it is so difficult as to baffle 
the most experienced clinician. 

Pleurisy with effusion is to be separated from pneumonia, from tuberculous 
consolidation, from pulmonary edema and hypostatic congestion, from new growths 
in the lung, pleura, and mediastinum, and from pleurisy with great fibrinous 
exudation and thickening. 

If on examining one side of the chest it is found to present impaired movement, 
impaired percussion resonance, and absence of breath sounds, it is fair to suppose 
that the cause is effusion, if in addition we find, in disease of the right side, displace- 
ment of the apex beat to the left, or, if it be left-sided, obliteration of Traube's 
semilunar space. This opinion is still further confirmed if the area of dulness on 
percussion varies with a change in the posture of the patient, and if Skodaic reson- 
ance is present above the area in which resonance is impaired. On the other hand, 
it is not to be forgotten that high-pitched resonance is often met with in that part 
of the lung which is over an area consolidated by pneumonia. In many cases of 
pleural effusion Grocco's sign is present. This consists in a triangular area of 
dulness on the healthy side of the chest in the paravertebral line. The base of 
this triangule is on a line from the spine outward; its side extends up the spine 
and the hypothenuse of the triangle from the outer part of the base line to the 
upper end of the spinal line. The hypothenuse is often curved slightly outward. 
The degree of dulness is not as great as that over the effusion, and when the patient 
lies on the affected side the dulness in Grocco's triangle usually disappears. In 
pneumonia distinct bronchial or tubular breathing is usually heard throughout the 
consolidated area, and this, of course, is not so markedly the case in effusion; but 
if the bronchial tubes become plugged by secretion in pneumonia, this important 
differential point is destroyed. Again, it sometimes happens that if the physician 
auscults the chest with the unaided ear he can readily hear bronchial breathing 
even if an effusion be present, although if he uses a stethoscope bronchial breathing 
seems absent. In pneumonia, however, bronchial breathing is usually associated 
with rales which are absent in effusion. 

Very useful in the differentiation of the two affections is the history of the patient, 
in whom the early symptoms of the two diseases are usually quite at variance, 
unless the case has been one of primary pleuropneumonia. 

In cases of tuberculous consolidation the appearance of the patient and the 
history of onset may be valuable differential points, and if loss of flesh or fever is 
present these facts are still further emphasized. 

When pulmonary edema is present the presence of moist rales, the feeble heart 
action, and the discovery of some prolonged preceding illness, or of renal disease 
predisposing to pulmonary edema, and bilateral dulness, are the points of value in 
making a diagnosis. 

In cases of acute pleurisy with great thickening of the pleural membrane there 
may be marked impairment of resonance on light percussion, and a friction sound 
may be heard, but deep percussion may elicit normal pulmonary resonance. 

Growths in the lung, or pulmonary abscess, usually are so peculiarly placed 
and surrounded by healthy tissue that careful examination of the chest and a study 
of the patient's history will be sufficient to make the differentiation. 



PLEURITIS 421 

Pneumothorax is separated from pleural effusion by its high-pitched resonance 
on percussion and the other physical signs of that condition which are only partly 
modified if the pleura is chronically thickened. 

There still remain two important diagnostic points in these cases which have 
to be studied before diagnosis can be reached, viz.: Are the physical signs due 
to the possible presence of subphrenic abscess, which, pushing the diaphragm 
upward, encroaches upon the thoracic space, or are they due to abscess or hydatid 
cyst in the liver? These conditions become manifest if the patient is carefully 
examined for them. Further, their rarity is a point against their presence. 

Lastly, it is important to determine the size of the effusion in order that the 
danger to the patient may be appreciated. It is not possible to even approxi- 
mate the actual quantity, because the capacity of the chest varies greatly in 
different cases, but the extent of the effusion can be decided by the line at which 
percussion dulness first changes to impaired resonance, and further up to high- 
pitched resonance. 

After a diagnosis of pleural effusion has been made, the question which arises 
is whether the effusion is serous or purulent, and if serous whether it is the result 
of inflammation or transudation. This is a most important question, since the 
treatment is quite different in each instance. 

This may be determined by performing paracentesis thoracis and to a great 
extent by an examination of the fluid after it is withdrawn by aspiration. Its 
specific gravity, if the cause be of an inflammatory nature, varies from 1.010 to 
1.018, and it contains large amounts of fibrin and albumin. On the other hand, 
the fluid due to transudation in dropsy shows a specific gravity of only about 
1.008 and contains little fibrin and albumin. (See Hydrothorax.) When the 
effusion is due to tuberculosis the specific gravity is very high (1.012 to 1.024). 
The symptoms and diagnosis of empyema will be found discussed below. 

Cytoscopy in Pleural Effusion. — In 1900 Widal and Ravaut called attention 
to the cytological examination of the fluid of pleural effusion, asserting that the 
nature of the pleurisy can be determined by the organized elements held in sus- 
pension in the exudate. According to their observations, since confirmed by others, 
the fluid of tuberculous pleurisy is characterized by the presence of an excess of 
lymphocytes, that of the acute infective pleurisies by polymorphonuclear leukocytes, 
and that of the pleurisies dependent upon new growths and the aseptic pleurisies 
accompanying renal and cardiac disease, by shreds of endothelium. These facts 
are not, however pathognomonic, for Naunyn found that the effusions complicating 
Bright's disease often contain lymphocytes instead of endothelium shreds, and 
Tarchetti and Rossi found lymphocytes in only a portion of the tuberculous effusions 
which they examined. The discovery of a marked lymphocytosis in the fluid is 
certainly of some value as indicating tuberculosis, particularly if it is associated 
with other signs, but it is not to be forgotten that in certain non-inflammatory 
exudates a very extraordinary degree of lymphocytosis may be present. So, too, 
a high count (60 to 90 per cent.) of polymorphonuclear cells is indicative of an 
infection by the pneumococcus. 

Prognosis. — The prognosis in cases of pleural effusion is favorable, except in two 
conditions. If the formation of the fluid is very rapid and very copious, pressing 
upon the heart and lungs and seriously impairing their action so that dyspnea 
becomes urgent, the prognosis is, of course, grave, unless relief is given by thoracen- 
tesis. Again, if the effusion is primarily due to tuberculosis, or to nephritis, which, 
by decreasing vitality, has permitted infection to take place, the prognosis must 
be correspondingly grave as to ultimate recovery. 

Treatment. — When the effusion has formed in such large quantity that it produces 
pressure upon a vital organ, or, again, when it remains unabsorbed for a consider- 
able period of time, the physician should undertake measures for its removal. 



422 DISEASES OF THE PLEURA 

The only measure of any value when the pressure is sufficiently great to be 
producing serious symptoms is "tapping" the chest by means of an aspirator. 
The skin over the affected side should be first thoroughly cleansed, as if for the 
performance of a minor surgical operation. A hollow needle having a moderately 
wide calibre, and attached to a rubber tube three feet long, which is filled with 
fluid, is then pushed into the pleural cavity in the sixth or seventh interspace in 
the midaxillary line. Care should be taken that the aspirating needle should be 
kept well down on the upper surface of the nether rib, in order to avoid injuring 
the intercostal artery, and the physician should grasp the needle with his thumb 
and forefinger not far from its point, so that after it pierces the skin it will not 
suddenly plunge into the chest for several inches, and so, perhaps, do damage to 
deep-lying tissues. No sooner does the needle enter the pleural cavity than the 
end of the rubber tube is lowered to a level with the floor and the contents of the 
pleura is in this way siphoned out of the chest. The advantage claimed for this 
method of treatment is that the degree of suction is at no time great, and, further- 
more, it is constant. Again, there is no danger of the fluid being withdrawn with 
too great rapidity. 

A very much more frequently resorted to measure of performing panacentesis 
thoracis is to attach a large needle, or trocar and cannula, to a piece of rubber 
tubing, which, in turn, is attached to a tube running through the cork of a bottle 
in which a vacuum has been produced by a small hand-pump. The entrance to 
the bottle is guarded by a small stopcock. After the needle has been placed in 
the chest, the trocar is withdrawn, the stopcock is turned,- and the fluid is drawn 
by the vacuum from the chest into the bottle. It is rarely, if ever, proper to com- 
pletely empty the chest by this means at one sitting, particularly if the effusion 
has been a large one. Too rapid withdrawal of the pressure in the thorax may 
cause serious disturbance of the action of the heart, or too rapid an expansion of 
that portion of the lung on the affected side which has been compressed by the 
fluid, with the result that damage is done to the pulmonary tissue, or that a peculiar 
form of gelatinous exudation into the lungs takes place, which is only relieved by 
constant and exhausting cough, and sometimes results fatally. 

Should constant cough develop during paracentesis, it is best to discontinue 
the operation at once. 

It is also important to remember that not infrequently the withdrawal of a 
small quantity of the effusion, by the relief of pressure and the establishment of 
normal lymphatic and blood circulation in the chest wall, may result in the natural 
absorption of the remaining fluid with a very considerable degree of rapidity, so 
that even if the chest is not emptied by the aspiration it may become so in a few 
days by a natural process. This holds true with particular force in those cases of 
large pleural effusion which do not require interference because of pressure symp- 
toms, but which do not undergo absorption by natural means until after absorption 
has been stimulated by the performance of paracentesis. 

It is necessary that the physician should exercise care in inspecting his needle 
before he employs it. Experienced clinicians have frequently been humiliated by a 
dry tap when they were skilful enough to diagnose an effusion, but careless enough 
not to notice that their needle was plugged. 

A pleural effusion should not be permitted to remain too long in the chest, since 
its presence tends to increase the organization of the inflammatory process on the 
surface of the lung, or results in the formation of such firm adhesions that decortica- 
tion of the lung by the surgeon is necessary if recovery is to ensue. 

The employment of purges, diuretics, or diaphoretics in cases of pleurisy with 
effusion, with the object of causing an absorption of the fluid, is, for very good 
reasons, futile in almost every instance. It has already been pointed out that in 
this disease the pleura is almost invariably covered by a dense fibrinous exudate, 



PURULENT PLEURAL EFFUSION, OR EMPYEMA 423 

which is plastic in character and mechanically interferes with the absorption of the 
exudate. Even if the physician is able, by the administration of powerful hydra- 
gogue cathartics, to cause a concentration in the blood, this concentration does not 
result in the absorption of the pleural effusion, because of the obstruction just spoken 
of, and also because absorption takes place from the pleura chiefly by the lymphatic 
vessels, and not by the bloodvessels. The only result of administering powerful 
diaphoretics and cathartics to patients suffering with effusion following pleurisy 
is to exhaust their vitality without materially influencing the local condition. 

The application of blisters to the chest, with the hope that they will stimulate 
absorption, is probably quite as futile as the employment of purgatives, although 
they may indirectly aid in the absorption of fluid by stimulating the removal of 
the film of plastic exudate which covers the pleural membrane. 

The condition in pleural transudations following, or accompanying, cardiac 
or renal dropsy is quite a different one from that due to inflammation. In the 
latter condition there is not any fibrinous exudate, and the effusion takes place 
by a process of transudation from the vessels, the fluid being quite different in 
its character from that found after the acute inflammatory process just discussed. 
It usually contains much less fibrin. Purgatives may therefore do good. 

Aside from the operative measures, which are necessary in about one-half the 
cases of pleurisy with effusion, the physician should administer mild tonics, with 
the object of aiding digestion, and he should support the system by the administra- 
tion of proper quantities of nutritious food. If after tapping the fluid it recurs, 
it should be withdrawn a second time. Such a recurrence rarely takes place in 
the effusion following pleurisy, although it is not infrequently met with in cases of 
ordinary transudation into the pleural cavity in other pathological states. 



PURULENT PLEURAL EFFUSION, OR EMPYEMA. 

Definition and Etiology. — By empyema we mean a condition in which pus has 
accumulated in the pleural space or spaces. It was taught at one time that such 
an effusion might primarily be serous and by infection become purulent, but this 
rarely occurs. Empyema occurs as a sequel to infection from the lung in the great 
majority of cases, but it may arise from primary infection of the pleura. The con- 
dition is far more common in children than in adults (Fig. 78). In children it is 
generally the result of the presence of the pneumococcus, which commonly causes a 
bronchopneumonia or a croupous pneumonia first and empyema afterward, but 
in adults the streptococcus is usually the exciting cause. The condition occurs 
much more frequently in boys than in girls. 

In 69 cases of empyema in children, P. S. Blaker found the pneumococcus in 
62 cases; the streptococcus in 3; the pneumococcus and streptococcus in 3, and the 
staphylococcus in 1. In 40 cases in children reported by Bythell, 26 were due to 
the pneumococcus and 9 to the pneumococcus and some other organism (Fig. 79). 

Empyema is sometimes due to infection by the Bacillus tuberculosis, and it is a 
fact worthy of note that the pus in such cases is usually sterile, only revealing the 
presence of tubercle bacilli when by chance some of the exudate which lines the 
pleura is obtained through the aspirator. In other words, sterile pus from an 
empyema raises a suspicion of tuberculous infection. Bacteriological examination 
of pus from 311 cases of empyema, occurring in hospitals in the United States, 
Canada, England, France, Germany, Austria, and Italy, showed that the pneu- 
mococcus was the infecting organism in 92 cases; the streptococcus in 58; the 
tubercle bacillus in 30. In the remaining cases the pus was sterile, or more than 
one micro-organism was found. If children are excluded from these statistics, the 
streptococcus becomes the most common infectious agent. 



424 



DISEASES OF THE PLEURA 



When no pulmonary lesion can be discovered in a case of empyema, it must be 
recalled that a very small and insignificant lesion in the lung, and, therefore, one 
which is easily overlooked, may be the focus for a very severe pleural infection, 
and, therefore, the inability of the physician to find a primary pulmonary lesion 
does not prove that it has not existed. 



Fig. 78 



UJ 

O 
< 

H 
Z 

LU 

o 

0£ 
LU 

a. 


UNDER 
10 YEARS 
OF AGE 


Z o 

LU CM 

LU Q 

£ z 

1- < 

LU o 
CO - 


Z o 
UJ <*> 
UJ Q 

h- < 
LU o 


Z o 

UJ ^~ 
UJ Q 

1- < 
UJ o 


Z o 

LU "> 
LU Q 

M 

LU o 
CQ ■=*" 


Z o 

UJ ^o 
LU Q 

1- < 
LU o 


40 














































































































39 














































































































38 










\ 




































































































37 










\ 




































































































36 










] 


\ 


































































































35 












\ 


































































































34 












\ 


































































































33 












1 


\ 
































































































32 














\ 
































































































31 














\ 
































































































30 
















\ 






























































































29 
















\ 






























































































28 
















1 






























































































27 


















\ 




























































































26 


















\ 




























































































25 


















1 


r 


























































































24 




















V 


























































































23 




















\ 


























































































22 






















\ 
























































































21 






















\ 
























































































20 






















\ 
























































































19 
























\ 






















































































18 














































































































17 
























\ 


\ 




















































































16 














































































































15 


























\ 




















































































14 
































































i 












































13 










































































































12 


























































i 
















































11 
























































- 






\L 












































10 








































































































9 














































































































8 














































































































7 














































































































6 














































































































5 














































































































4 














































































































3 














































































































2 














































































































1 















































































































Chart showing morbidity percentage of empyema due to all causes at different ages, based on 403 
cases occurring in five hospitals in the United States and England. 

The character of the pus found in cases of empyema varies considerably in differ- 
ent cases, the variation depending in part upon the micro-organism which has 
produced the condition, and upon the duration of the malady at the time the effusion 
is examined. Usually it is creamy and homogeneous; in other cases it is thin 
and separates on standing into a thick and thin layer. When the effusion is an 
old one, the pus may be quite thick and curdled in its appearance, containing clot- 
like masses or shreds of fibrin, which plug the aspirating needle and make aspiration 
impossible. While the color is commonly a creamy yellow, it is sometimes slightly 
pinkish in appearance, and may be greenish in hue, and in still other cases, when a 
considerable amount of blood has been extra vasated into the effusion, it is a dirty, 



PURULENT PLEURAL EFFUSION, OR EMPYEMA 



425 



pale cocoa color. In some instances, as in cases due to infection by the pneu- 
mococcus, the pus is almost odorless, while in others, particularly if the empyema 
has ruptured into a bronchus, it is fetid. 

Purulent effusion in the pleural space is usually profuse. Indeed, it has been 
taught that as a class these collections are larger than are serous effusions, which 
is not, however, always true by any means. On the other hand, they are very 
much more likely than are serous effusions to be walled off and encysted by reason 
of adhesions, thereby forming a small pocket of pus. 































Fig. 


79 


































< 

H 
Z 

LU 

o 

CE 
LU 
Q- 


LLl 

2 < 

LL 

K O 

UJ 

Q <0 

>- 


z ° 

LU Q 

M 

LU o 

CO r- 


z ° 
Lu " 

UJ Q 

M 

LU O 


z ° 
LU D 

H < 

LU o 
CQ CO 


z ° 

LU Q 

H < 

LU O 
CO «- 


Z ° 
LU «3 
LU Q 

£ z 

H < 

LU q 
00 LO 


z ° 
S3 ^ 

LU Q 

£ z 

1- < 

LU 

0Q io 


32 








































































31 








































































30 








































































29 








































































28 








































































27 








































































26 








































































25 








































































24 








































































23 








































































22 








































































21 








































































20 








































































19 








































































18 








































































17 








































































16 








































































15 








































































14 








































































13 








































































12 








































































11 








































































10 








































































9 








































































8 








































































7 








































































6 








































































5 








































































4 








































































3 








































































2 








































































1 












_L 



























































Chart showing morbidity percentage of empyema due to the pneumococcus at different ages, based 
on 286 cases collected by Netter. Large percentage in childhood. 

Symptoms. — If after an attack of pneumonia the temperature does not fall, or 
if, after it has been normal or near normal, it begins to rise again, and the patient 
has chills or chilly sensations, empyema should be sought for. 

The symptoms of empyema in general are those of impaired health. The patient 
is, as a rule, pale and ill-looking, suffers from loss of weight, and sweats, which are 
particularly prone to come on when he sleeps. 

A moderate fever may be present, and suppressed or even well-developed chills 
may recur. It is important, however, to remember that in some cases none of 
these constitutional symptoms are manifest, the fever in particular, being so mild 
that it fails to attract attention, so that the condition of empyema is suspected 
only when some shortness of breath calls attention to the thorax. 

The pus in cases of empyema sometimes becomes so completely walled off from 
the surrounding tissues that it remains for weeks without producing any signs of 
its presence, but in other cases — and these are the more numerous — it causes such 



426 DISEASES OF THE PLEURA 

severe pressure symptoms or so much evidence of sepsis that relief is demanded by 
the patient. In other cases — and these are often those in which the empyema 
has not been recognized — the pus burrows its way out, rupturing into a bronchus 
or perforating the chest wall. Very much more rarely it empties into the peri- 
cardium, or even into the esophagus. In other instances it has perforated the 
diaphragm, although this process is, curiously, much more rare than the rupture 
of a subdiaphragmatic abscess into the pleural cavity. 

Statistics as to the relative frequency with which rupture into a bronchus takes 
place are not in accord. Thus, of 195 cases of empyema occurring in St. Thomas' 
Hospital, London, and in the Leeds General Infirmary, 11 ruptured into the 
lung, a percentage of 5.64; while an analysis of a large number of cases of empyema 
collected by Netter gave a percentage of 26.2 rupturing into the lung. These 
latter figures certainly must be far too high. 

The physical signs of empyema have already been discussed when describing 
those of serous effusion, for in both states they are practically the same. Sometimes 
the presence of pus may be shown by an edema of the superficial tissues, which is 
often met with over deep-seated suppurations. Empyema is also apt to produce 
more bulging of the intercostal spaces than is serous effusion, perhaps because 
there is more wasting, and so the bulging is more readily observed. In some 
instances of empyema, however, the contraction of the thickened pleura draws 
the edges of the ribs so closely to one another that bulging of the interspaces is 
obliterated. 

When pulsation is transmitted to the purulent effusion, so that the impulse 
is manifest through the interspaces, it is called " empyema necessitatis." 

Complications. — The chief complications of empyema have already been named, 
viz., sepsis and perforation. The signs of sepsis are similar in this state to those 
produced by accumulations of pus elsewhere, and require no further discussion. 
The symptoms of perforation into a bronchus consist of an attack of violent cough- 
ing, during which the patient expels, in large, or sometimes in small amount, a 
quantity of almost pure pus. After the pus first appears, it is commonly brought 
up in mouthfuls several times a day, and more rarely in such large quantities as 
to threaten the patient with suffocation. This drainage of pus through the lung, 
curiously enough, rarely causes serious permanent damage to the lung, which may 
ultimately entirely recover if the physician will but provide an opening in the chest 
wall for proper drainage. 

When the pus escapes externally by burrowing, it most frequently does so about 
the sixth intercostal space in the axillary area, but it sometimes burrows a great 
distance and escapes by way of numerous openings. In other instances it burrows 
far down the trunk and discharges as low down as the pelvis. Indeed, Barton 
has reported a pulsating empyema in the left lumbar region. These openings may 
persist for many years, and if the suppurative process persist, amyloid disease of 
the liver and kidneys may ensue. 

Diagnosis. — The differentiation of empyema from serous effusion is to be made 
by the presence of the septic symptoms just named, and by the use of an aspirating 
needle to determine the character of the fluid. The localized types of empyema 
are those which offer real difficulty in diagnosis, since the pus may be between two 
lobes of the lung, or at the base of the lung next the diaphragm, or be extended 
over a considerable area although very shallow, or, again, the inflammatory process 
in the adjacent lung tissue causes the presence of the physical signs of consolidation 
of the lung or of large effusion, when in reality the purulent collection is a small one. 
In these cases the introduction of the aspirating needle may fail to reveal the pres- 
ence of pus, because the instrument does not happen to strike the purulent focus. 

When the pus is localized by adhesions in the neighborhood of the heart, this 
organ may be displaced by the pressure and transmit its impulse to the effusion, 



CHRONIC PLEURISY 427 

so giving rise to the belief that a purulent pericarditis is present; the absence of 
this more serious state being revealed only when the pus is set free. 

A still more difficult condition to discover is interlobar pleurisy with effusion. 
In such cases if the accumulation is pus, it may rupture into the bronchi and give 
rise to the belief that the patient has true pulmonary abscess. 

Prognosis. — The prognosis in empyema in children, over three years of age, 
if the condition is due to the pneumococcus, and if the pus is allowed to escape 
before it has done much damage, is surprisingly good, both as to rapid and complete 
recovery. Not only do many of these cases soon cease to form any more pus, but 
the compressed lung expands with remarkable rapidity, and may, in the course 
of a few months, fill the pleural cavity so well that nearly all traces of the disease 
may disappear. When the disease affects infants the outlook is bad, because 
of their susceptibility to wasting processes and their low vital resistance. 

In streptococcus infection the prognosis is not so favorable, nor is it good in 
tuberculous empyema, for in the first type the formation of pus is persistent and 
the deformity of the chest is very apt to be great, while in the second type a primary 
infection elsewhere is usually present. 

It has been stated by some authors that an empyema may undergo absorption. 
While a decrease in the size of the effusion may result from the absorption of some 
of its fluid constituents, true disappearance of pus from the thorax does not take 
place unless it is let out or escapes spontaneously. It may, however, become 
inspissated and encysted. 

Treatment. — There is but one thing to be done in cases of empyema, and that 
is to let out the pus, treating the case as one of ordinary abscess. If the quantity 
of the fluid is sufficiently large to compress and displace adjacent organs, particularly 
the heart, it is better to first relieve some of this pressure by aspiration, as in a 
case of serous effusion, removing enough of the pus to permit the heart and vessels 
to slowly regain their normal position. As the pus in these cases is often under 
great pressure, so that it squirts several feet when an incision is made, I am con- 
fident that this preliminary modification of the pressure is wise in most cases. On 
the following day or, if need be, immediately after aspiration, an incision should 
be made between the sixth and seventh, or seventh and eighth, ribs in the posterior 
axillary line, and this opening should be maintained by the insertion of a doubled, 
or extra large, drainage tube or by a gauze drain. If the ribs have been drawn so 
closely together by the contraction of the parietal pleura that free drainage cannot 
be obtained, then the upper surface of the lower rib should be cut away until 
drainage is free, or, if need be, several inches of the rib or of several ribs should be 
resected. This is usually necessary in streptococcus infection. As a rule, in 
children all that is necessary is to introduce a large drainage tube by means of a 
large cannula and keep it in place with a safety-pin and adhesive strip. This tube 
is connected by means of a short glass tube, whereby the flow can be watched, 
with a piece of rubber tubing long enough to reach a bottle placed below the bed. 
In this manner adequate drainage can be maintained without subjecting the child 
to the hardship of an incision and the excision of a piece of rib, but if the formation 
of pus persists resection should always be performed. For the details as to the 
exact technique of these operative procedures reference should be made to a surgical 
work. 

CHRONIC PLEURISY. 

Definition. — Chronic inflammation of the pleura may be nothing more than a 
sequence of some of the acute conditions already discussed. If a fluid accumulation, 
serofibrinous or purulent, be allowed to remain within the chest cavity, important 
alterations take place in the serous membrane. With the subsidence of infection 
reparative efforts lead to the production of fibrous tissue, which greatly thickens 



428 DISEASES OF THE PLEURA 

both parietal and visceral layers and ensheaths the collapsed lung, eventually 
forming such a dense investing membrane that re-expansion becomes impossible. 
In other cases the fluid is absorbed and the pleural surfaces coated by inflammatory 
products come in contact, coalesce, and become fused by permanent organization 
of the exudate. In the latter group of cases the pleural cavity may be obliterated, 
or partial adhesions only may form. In some cases unattended by frankly expressed 
acute inflammation, hyperplastic thickening of large or small areas, usually with 
adhesions, occurs. In such cases the newly formed inflammatory tissue may attain 
a thickness of 1 cm. or more and not infrequently contains calcareous plaques. 

The third form is called "primitive dry pleurisy" in the sense that it begins 
without effusion and often without pain, and is not associated with fever. The 
patient may himself feel the pleural friction. Finally, limited adhesions occur 
between the layers of the pleura, but they do not cause marked interference with 
the lung nor deformity of the chest. 

The fourth type is the so-called "primitive dry pleurisy" described by Sir Andrew 
Clarke, in which the layers of the pleura become adherent and thickened as in 
the forms just described. From the visceral layers of the pleura bands of connective 
tissue penetrate and traverse the lung almost as if they were true trabecular. The 
effect of these bands as they contract is to produce bronchiectasis and some distor- 
tion of the lung in its lower lobe, where the process is nearly always situated. The 
condition is really a pleurogenous interstitial pneumonia. These cases are not 
identical in character with those due to old empyema. 

Occasionally in chronic pleurisy large calcareous plates are developed in the newly 
formed inflammatory tissues. 

HYDROTHORAX. 

This condition is to be clearly separated from ordinary pleural effusion due to 
inflammatory changes. Pleural effusion due to inflammation is usually unilateral, 
but hydrothorax is often bilateral. The fluid in the pleural cavities is present 
as a result of transudation in cases of renal disease, cardiac disease, profound 
anemia, or any cause which tends to impede circulation or to increase the readi- 
ness with which the serum can escape from the bloodvessels. Thus it may develop 
in cases of thrombosis of the vena azygos during the course of typhoid fever. 
While it is true that hydrothorax is often bilateral, it sometimes happens that 
it is unilateral, if perchance the obstruction to the flow of blood or lymph is 
produced by some lesion which affects only one side of the chest. This occurs 
much more frequently on the right side than on the left, in those cases in which the 
cause is cardiac disease. Fetterolf and Landis have shown that such effusions 
come from the visceral layer of the pleura and are due to pressure of a dilated 
heart on the pulmonary veins. When the effusion is right-sided the pressure is 
due to a dilated right auricle. When on the left side it is due to pressure by dilata- 
tion of the left auricular appendix and of the left ventricle. 

When it is present in the course of cirrhosis of the liver it is probably due to 
the presence of associated pulmonary tuberculosis. Osier asserts that such an 
effusion may occasionally occur in what he designates as "perfectly healthy men." 

The fluid in hydrothorax is usually of low specific gravity (see Pleurisy with 
Effusion), and clear or but slightly opalescent, yellowish or straw-colored. It is 
not rich in cells, and those cells that are present consist largely of relatively volu- 
minous flat endothelial cells. Fibrin is usually absent. If an injury^or obstruction 
of the thoracic duct is present, the fluid may be chylous in character. 

Again, if such a patient is given iodide of potassium and the fluid is withdrawn 
by aspiration iodine will be found in it, whereas if the fluid is due to inflammation 
iodine is absent. The fluid is placed in a test-tube, a few drops of fuming nitric 



PNEUMOTHORAX, HYDROPNEUMOTHORAX, PYOPNEUMOTHORAX 429 

acid are added, and then it is shaken with some chloroform, when if iodine is present 
a red color will appear, which sinks to the bottom of the tube with the chloroform. 

Hydrothorax can often be relieved by the free use of a saline purgative, such as 
half an ounce of magnesium sulphate given every morning before breakfast and 
by cardiac tonics if they are needed. If it causes symptoms by pressure it must 
be removed by aspiration. (See Pleurisy with Effusion.) 

Bloody effusion into the pleura is met with in cases of cancer of the pleura and 
of Bright's disease. It is more indicative of the presence of the former malady. 
I have more than once seen a simultaneous pleural and abdominal bloody effusion 
due to a general carcinomatosis. 

When pleural effusion is tapped a second time, or when the needle has been 
introduced more than once in the search for fluid, it not infrequently happens that 
the liquid obtained is blood-stained, owing to wounding of a bloodvessel by the 
instrument. Of course, this possibility must be remembered when a bloody 
effusion is found. Sometimes a true hemothorax arises from this cause, or it is 
due to a leakage from an eroded bloodvessel. 

PNEUMOTHORAX, HYDROPNEUMOTHORAX, PYOPNEUMOTHORAX. 

Definition. — Pneumothorax — that is, the presence of air in the pleural spaces — 
is rarely present as the result of disease unless it is associated with fluid (hydropneu- 
mothorax) or pus (pyopneumothorax). As the result of injuries to the chest and 
to the lungs it not rarely appears as true pneumothorax, as after the fracture 
of a rib, or as the result of a stab wound. 

History. — As long ago as the time of Hippocrates a succussion sound on shaking 
a patient suffering from empyema or pleural effusion was recognized, but it was 
not until the time of Laennec, about 2200 years later, that the value of this sign 
was appreciated as indicating the presence of both fluid and air in the chest. 

Etiology. — The most common cause of pneumothorax is pulmonary tuberculosis, 
and it arises as a result of the perforation of the pleura through the visceral layer. 
In order that air may enter the pleural space the tuberculous cavity must directly or 
indirectly communicate with a patulous bronchus, thereby affording a communica- 
tion between the lung and the thoracic cavity. West believes that fully 90 per 
cent, of the cases are due to this cause. In many cases this accident is prevented 
by an acute or subacute pleurisy occurring at the area diseased, so that the pleura 
is thickened or the two layers glued together. This is particularly prone to be the 
case when a cavity has formed; and were it not for this protective process the 
condition of pneumothorax would be commonly met with. In still other cases, 
however, these very adhesions result in pneumothorax, for during some severe 
exertion they are torn, and so the air finds an opening through which to escape. 

As a rule, the perforation occurs in the lower part of the upper lobe, or in the 
upper part of the middle lobe. Pneumothorax develops on the left side nearly 
twice as often as on the right. West, however, believes that the two sides are 
nearly equally affected. At times the opening through which the air escapes is 
so small that it cannot be found. Sometimes there is more than one perforation. 

Very much more rare as causes of pneumothorax are bronchiectasis, pulmonary 
abscess, and pulmonary gangrene. So rare are they that when cases of this kind 
occur they should be reported. This holds true as well of cases which develop 
from rupture of a vesicle in cases of emphysema of the lungs. Pneumothorax 
has arisen in the course of whooping-cough, diphtheria, and typhoid fever. 

Pneumothorax occurs three times as often in men as in women. 

Symptoms. — The onset of pneumothorax is often very sudden and severe, but 
at times it develops so insidiously that no signs of its presence are noted by the 
patient until he attempts to make some exertion, when dyspnea ensues. In cases 



430 DISEASES OF THE PLEURA 

of sudden onset there is not only urgent dyspnea, but sometimes syncope to the 
point of unconsciousness. These severe symptoms are much more prone to develop 
in a patient who has slight pulmonary disease than in one who has well-advanced 
lesions, because in the latter case, the lung being already partly useless, the other 
lung is ready to compensate for the inactivity of the diseased part. When the 
accident occurs on the comparatively healthy side death may speedily ensue. 
In some instances the pain may be so severe that angina pectoris is thought to be 
present. 

Physical Signs. — The physical signs in these cases of pneumothorax consist 
in bulging of the interspaces on the affected side, and at times the development 
of subcutaneous emphysema. There is also in many cases a distinct increase in 
the size of the chest on that side. If the air escapes on the right side the liver 
is markedly depressed and the heart is displaced to the left. In left-sided cases 
the heart may be pushed to the right of the median line. 

Percussion reveals hyperresonance unless there has been an old pleurisy with 
secondary pleural thickening. If the lung is adherent to the chest wall and col- 
lapsed by pressure, or consolidated by tuberculosis, a dull note may be present. 
In a case of this character under my care, in a patient whose general health seemed 
to negative the possibility of tuberculosis, this state was confirmed at autopsy; 
much relief was given before death by frequently permitting the air to escape from 
the chest, over part of the chest wall through a hollow needle. 

Auscultation reveals an absence of vesicular murmur over the area of hyper- 
resonance, and, perhaps loud amphoric breathing over the lung, particularly if it 
contain a cavity which freely communicates with the pleural space. 

Diagnosis. — In considering the possible presence of pneumothorax in the type 
which is insidious the following conditions must be included: A large cavity may 
give somewhat similar physical signs, but the limited area over which they are 
manifested or demonstrable separates the two states. Emphysema of the lungs 
is excluded by the universal presence of breath sounds and the fact that the con- 
dition is bilateral. Rupture of the diaphragm with diaphragmatic hernia should 
be considered if some injury has been suffered, and pyopneumothorax subphrenicus 
must be excluded by study of the pulmonary signs above the area involved and 
of the condition of the epihepatic and epigastric areas. 

Prognosis. — The prognosis of pneumothorax depends largely upon the cause of 
the condition and the associated states of effusion and empyema. Much depends 
upon the suddenness of onset. I have seen death occur in twelve hours in cases 
with sudden onset, and cases are on record of death in twenty minutes. On the 
other hand, if the dyspnea is not severe the pulmonary condition may be actually 
benefited by the temporary rest enforced by the collapse of the lung. West has 
placed the mortality at 70 per cent., and of these fatal cases 75 per cent, died within 
two weeks and 90 per cent, within a month. In those cases which do not die soon 
after the onset of this condition death may result either from empyema and exhaus- 
tion, or from the progress of the underlying disease. If the heart is feeble, if the 
other lung is far advanced in disease, and if the strength of the patient is badly 
impaired the prognosis is, of course, bad. Recovery takes place in about 10 per 
cent, of the cases of simple pneumothorax without fluid. 

Treatment. — The treatment of pneumothorax consists in the relief of pain, if 
it be very severe, by a small dose of morphine — say, J of a grain given hypodermi- 
cally. If the dyspnea is marked a large hollow needle, or aspirating cannula, should 
be introduced into the chest, but not attached to the aspirator. The pressure in 
the chest will cause more air to escape than will flow in, and as the lung is already 
collapsed any damage caused by its entrance is done. To prevent the air from 
entering, the finger may be temporarily used as a valve on each inspiring movement 
until a wash-bottle can be so arranged that the air will escape through the water 



DISEASES OF THE MEDIASTINUM 431 

it contains and then cannot return. If the air constantly reaccumulates the case 
should be treated by a drainage tube inserted as in the treatment of empyema. 
(See Empyema.) 

If edema of the other lung is threatened, dry cups should be applied over its 
base and atropine given freely hypodermically. 

When serous effusion is present, or when empyema is a complication, the con- 
ditions should be treated as described when discussing these conditions. 

A most exhaustive study of this subject has been made by West in London, 
and more recently by Emerson in Baltimore. 

When hydropneumothorax is present the lower part of the chest is flat on percus- 
sion as in ordinary pleural effusion, above this is an area of hyperresonance, and 
above this again is the Skodaic resonance due to the compressed lung. On shaking 
the patient a succussion sound is heard, and when the patient is erect auscultation 
may reveal "metallic tinkling," which is supposed to be due to the dropping of fluid 
into the liquid at the base of the chest. Succussion and metallic tinkling are the 
most important signs of hydropneumothorax. Another valuable sign is the so- 
called "coin sound" produced by striking a large coin, held against the chest wall, 
with another coin. The physician listens to the back of the chest as the percussion 
is done, by an assistant, on its anterior surface, and closes his unemployed ear with 
his finger-tip. If the coin be struck so that the sound has to be transmitted through 
the chest at the level of the fluid the sound is very indistinct. At the level of the 
air it is transmitted with startling clearness, and at the level of the lung the sound 
is- again impaired. 

DISEASES OF THE MEDIASTINUM. 

Under this heading are considered diseases of the mediastinum other than those 
of the heart and aorta. In my Fothergillian Prize Essay I collected 520 cases of 
mediastinal disease, and the facts there presented form the basis for the following 
views. The statistics on their face show that there were 134 cases recorded as 
carcinoma, 98 as sarcoma, 21 as lymphoma or lymphadenoma, and 115 as abscess. 
In other words, a large proportion of cases of disease in this area are due to malig- 
nant growths, for the remaining lesions are non-malignant or inflammatory. The 
statistics apparently indicate that cancer is by far the most frequent form of in- 
dividual growth. While we have no right to go "behind the returns," in the sense 
that cases reported as cancer may be regarded as sarcoma, it is nevertheless certain 
that sarcoma is really the most frequent growth in the mediastinum, because 
tissues favorable to its growth are found there in great abundance and tissues 
susceptible to carcinomatous growth are scanty. Again, it is well known that 
up to the middle of the last century, and later, little distinction was made between 
cancer and sarcoma, and so many cases of sarcoma were probably reported as 
cancer. Finally, lymphoma are so nearly allied to sarcoma that it is fair to add 
them to the so-called sarcomatous cases, making the total 119 reported as sarcoma. 

The non-malignant tumors of the mediastinum are fibroma, teratoma, dermoid 
cyst, and hydatid cyst. 

Notwithstanding the fact that the middle and posterior mediastinal spaces 
are more richly provided with lymphoid tissues than the anterior mediastinum, 
the statistics prove that malignant growth is more common in the latter space 
than in the other spaces. Thus, of the cases reported as sarcoma and cancer, 
in which the space affected was stated, 81 were in the anterior space as against 
28 in the posterior space, and only 5 in the middle space alone, although in many 
other instances the entire mediastinum was invaded. 

For this reason we should expect to find that sarcoma in a very large proportion 
of cases occurred as a secondary growth in the mediastinum; but an examination 
of the literature of the subject, both as regards general opinion and reports of cases, 



432 DISEASES OF THE PLEURA 

shows such a conclusion to be erroneous. Indeed, the mediastinum seems to rarely 
suffer from any form of this disease save the primary, and even in those cases in 
which the lesions were scattered all through the body from head to foot, this space 
seems to have escaped secondary contamination. Should the growth appear in 
the mediastinum, secondarily, it generally affects the posterior or middle spaces, 
owing to the large number of lymphatic glands and like tissues which are found 
in these cases. 

It is a curious fact that mediastinal growths are twice as common in men as in 
women, although women so much more frequently have malignant growths in 
nearby tissues, and in them, as already stated, malignant growth of the lung is 
said to be more common. 

The average age affected by mediastinal tumors is about thirty-seven years. 

Symptoms. — The symptomatology of mediastinal tumor is by no means clear 
and well defined, since so many other conditions may produce signs of the same 
character, and it has been stated very positively by certain writers before the 
days of the j-rays that such a growth cannot be diagnosticated during life. 

Although this assertion seems rather sweeping, there is, nevertheless, some 
truth in it, and in many cases, where we have no history to guide us and no evidence 
of a growth elsewhere, the diagnosis may be well-nigh impossible. 

Large tumors are found in the anterior mediastinum, which have not been diag- 
nosticated or suspected until a postmortem has been made, not from any lack of 
ability on the part of the physician, but because the symptoms of mediastinal 
disease have either been entirely absent or masked by others of more importance 
elsewhere. Thus, in a case reported by Bruen, an old woman, aged seventy years, 
entered the Philadelphia Hospital with decided symptoms of renal disorder, which 
in a few days caused her death. Although an examination was made of the chest, 
as a matter of routine duty, no special physical signs were discovered, and the 
disease, which was sarcoma in the anterior mediastinum, was not discovered until 
the body was placed on the postmortem table. The only symptoms of such a 
condition of affairs before death consisted in slight dyspnea and cough, both of 
which were supposed to arise from the renal lesions; and this is the more remarkable, 
since the growth weighed fourteen ounces, was six inches long by five inches broad 
and four inches in diameter, or, in other words, was about the size of a normal adult 
heart. No signs of sarcoma existed elsewhere in the body from which one might 
suspect any malignant disease. 

The first symptoms complained of by the patient vary quite as much as do the 
later ones, and depend, as do their successors, upon the parts most involved. By 
far the largest number of sufferers notice some interference with respiration, particu- 
larly on exertion, which soon increases, so that there may be constant dyspnea, 
and even attacks of partial suffocation. 

The dyspnea and other disturbances of respiration are, in many instances, due 
to several rather than any single cause, since, in addition to the mechanical pressure 
by the growth on the air-passages, we may also have such interference with the 
circulation of the blood, particularly in the thoracic veins, that pleural, pericardial, 
or mediastinal effusions of serum may occur. 

Effusions into the abdomen may occur, owing to involvement of the ascending 
vena cava, but such a condition is rather rare, probably owing to the fact that the 
ascending cava more frequently escapes than does the descending. Dropsy of the 
lower extremities, without abdominal effusion, sometimes comes on. 

In still another class of cases the pulmonary vein may be obstructed, and edema 
of the lung may develop. Hypostatic congestion is by no means rare, the patient 
often being forced, by cardiac weakness, pleural effusion, or pressure on the trachea, 
to lie in one position. In some cases loud venous murmurs can be heard in the 
jugular and other large superficial veins, and care has to be exercised as to the 



DISEASES OF THE MEDIASTINUM 433 

diagnosis of the true cause of the distress. The ribs and sternum may undergo 
gradual erosion and destruction from pressure, and the growth appear on the surface 
of the body. 

In a certain number of cases the nerves of the thorax seem to be more affected 
that the rest of its contents, and involvement of the vagi or the recurrent laryngeal 
nerves may bring on a long train of obscure and dangerous symptoms, both as 
regards the circulation, respiration, digestion, speech, and swallowing. 

Tumors of the mediastinum invading the lungs have frequently been mistaken 
for chronic and even acute pneumonia, growing, as they do, along the larger bron- 
chial tubes and bloodvessels. 

Without doubt, in a certain number of cases, either hypostatic pneumonia, 
or pneumonia due to pressure on the bronchial vessels, develops as the tumor 
invades the lung, and in such cases it is absolutely impossible to make a diagnosis 
unless there are symptoms of pressure in the mediastinum. Walsh has stated 
that if the lesion be due to a tumor, the affected side will increase in bulk rather 
than diminish, and that dyspnea out of proportion to the degree of consolidation 
points to a mediastinal disorder rather than one confined to the lungs. 

In a very large proportion of cases of mediastinal disease the condition is one 
of abscess. There were 115 cases in my collection of 520 of mediastinal disease. 
The proportion of acute and cold abscess in 79 cases in which the differentiation 
was made was 48 to 31. 

The most constant and severe symptom is, in nearly all cases, the deep-seated 
pain, which increases in severity from first to last, seldom remitting until suppura- 
tion has taken place and the pus has found some outlet. If the case be one of 
cold abscess, these painful symptoms may be masked by other more pressing ones, 
such as dyspnea and edema from pressure; although it should not be forgotten that 
such symptoms may appear with equal severity in both varieties of the disease. 
In the acute variety all the symptoms of ordinary inflammation appear, such as 
rigors and periodical or constant fever. 

As recovery took place in about 40 per cent, of the cases of mediastinal abscess 
according to the statistics of preantiseptic days, it ought to occur much more 
frequently now. 

Mediastinal growths are usually of such a nature as to be beyond either medicinal 
or surgical treatment, but abscess, dermoid cysts, and teratomata are sometimes 
operable. 



28 



DISEASES OF THE CIRCULATORY SYSTEM. 



DISEASES OF THE PERICARDIUM. 

PERICARDITIS. 

Acute Pericarditis. — Definition. — Acute pericarditis, sometimes called acute 
fibrinous or acute serofibrinous pericarditis, is, as its name implies, an acute inflam- 
mation of the pericardium, the serous membrane which envelops the heart. 

Etiology. — Acute pericarditis is practically always due to the presence of some 
infecting micro-organism, although certain conditions existing simultaneously 
may predispose to the infection by lowering vital resistance. In the great majority 
of cases it is due to acute articular rheumatism, in comparatively few it develops 
as a complication of croupous pneumonia, the pneumococcus being its cause, and 
it also develops as a complication of scarlet fever, in which disease the streptococcus 
associated with this malady is probably the provoking factor. Acute pericarditis 
is also frequently associated with renal disease, and is often, under these circum- 
stances, a form of terminal infection. So, too, it may develop in the course of 
various infectious diseases, such as smallpox, erysipelas, typhoid fever, and even in 
measles. Septic infections, such as general septicemia and ulcerative endocarditis, 
may cause it. In diabetes it occurs as a terminal infection. Of course, tuberculosis 
and syphilis, diseases which affect every tissue, may also affect this one. 

Acute pericarditis also develops by direct extension from inflammation in neigh- 
boring parts, in distinction from infection which takes place through the blood. 
Thus, inflammation of the mediastinal tissues may produce it, as in diseases of the 
bronchial glands, of the sternum, or of the vertebrae. So, too, pneumonia and 
pleurisy affecting nearby portions of the lung may cause inflammation of the 
pericardium. In infections involving the myocardium the overlying serosa — 
that is, the visceral layer of the pericardium — rarely escapes. So, too, pericarditis 
may be the first indication of impending rupture of that part of the aorta covered 
by pericardium. 

Pericarditis may also be due to injury to the chest wall or to the membrane 
itself. 

It is evident, therefore, that acute pericarditis is nearly always a condition 
secondary to some other affection, and that it is very rarely primary. When it is 
primary it is usually due to tuberculosis. (See articles on Croupous Pneumonia, 
Acute Rheumatic Fever, and Typhoid Fever.) 

Frequency. — The frequency of pericarditis as a primary disease is very limited, 
but as a secondary affection it is great. Very many cases present no sign of it 
during life, yet the condition is found at autopsy. It occurs almost as frequently 
in children as in adults, although at one time this class of patients was supposed 
to be not so commonly attacked as older persons. Sturges found it present in 
94 out of 100 cases of fatal heart disease in children. Of these cases 54 were of 
rheumatic origin. Indeed, it is probable that the disease is less prevalent after 
than before puberty. It occurs far more frequently in males than in females, 
and this is particularly true after puberty, when the greater exposure and activity 

(435) 



436 



DISEASES OF THE PERICARDIUM 



of males become dominant factors in causing rheumatism and other infections. 
At this time the proportion is from 4 to 1 to 6 to 1. 

Pericarditis, as we would expect, develops more commonly in severe cases of 
acute rheumatism than in mild cases, but, on the other hand, it is to be borne in 
mind that even in those cases with very mild joint symptoms severe pericardial 
involvement may occur. Prior attacks of rheumatism seem to increase the fre- 
quency of pericarditis in subsequent attacks. The condition usually comes on 
during the first week of the disease. This is, however, by no means always the 
case, and it may appear as late as the sixtieth day of the illness or during a relapse. 

Pericarditis due to renal disease, the Pericardite Brightique of the French, is 
distinctly a state of advanced years, occurring most commonly after forty-five 
or fifty years of age. It is more commonly met with in patients suffering from 
contracted kidney than in those that present the parenchymatous form of renal 
disease. 

Fig. 80 




Heart and pericardium, acute serofibrinous (pneumococcal) pericarditis. Most of the anterior 
parietal layer of the pericardium has been cut away, showing the villous (shaggy) irregular projec- 
tions of the fibrin. To the left, where the parietal pericardium is reflected over the right auricle and 
great vessels, cohesion of the layers may be seen; later, had the patient recovered, such fusion of the 
layers would have consituted the basis from which organized fibrous adhesions would have formed. 



Pathology. — As in inflammation of the pleura, so in inflammation of the pericar- 
dium, it is well to recognize three forms of acute pericarditis, viz., the acute dry 
or fibrinous, the acute exudative (serofibrinous), and the purulent type. In the first 
stage of all these forms of pericarditis the lining surface of the pericardium is lustre- 
less, opaque, and somewhat roughened by a delicate fibrinous exudate. It is also 
hyperemic and may be dotted with petechia?. It is the rubbing together of the 
two layers of the pericardium at this stage that causes the characteristic friction 
sound of the disease. As the inflammation progresses the membrane becomes 
completely covered by the exudation of fibrin, which may assume a villous forma- 
tion. Adhesions between the layers of the pericardium also take place. 

In the serofibrinous form a considerable quantity of serum is poured out into 



PERICARDITIS 



437 



the sac, and particles of fibrin and leukocytes are found in it. The quantity may 
be so large as greatly to distend the sac, displace the heart, and interfere with its 
function, particularly by pressure upon the auricles and cavse. In many cases 
as much as three pints have been found in the sac. West quotes cases in which 
the pericardial sac contained no less than five pints (due to scurvy), yet recovery 
occurred after aspiration. 

In the purulent form (pyopericardium) the serum and fibrin are mixed with pus 
cells and erythrocytes. Pyopericardium may arise as a primary purulent pericar- 
ditis or be converted from the serous form by infection with the Streptococcus, 
Pneumococcus, or Staphylococcus pyogenes aureus. Sometimes the tubercle bacillus 
acts as a pyogenic organism in this space. 

There is some difference of opinion as to the frequency of pyopericardium. Two 
opinions which represent the two sides of this question are as follows: Samuel 
West speaks of it as "one of the 

rarest of clinical rarities," but Battin Fig. 81 

says " it is a disease seldom suspected, 
still more rarely diagnosed, and 
hardly ever treated, and yet it is 
one that is present in 3 per cent, of 
the deaths in the records of the 
Children's Hospital." 

That the latter view is correct is 
shown by the fact that Breitung in 
324 cases of pericarditis found that 
108 were serofibrinous, 30 hemor- 
rhagic, and 20 purulent, or 6.1 per 
cent. In 769 autopsies collected by 
Still 24 instances of pyopericardium 
were found, and 11 were due to in- 
fection by the pneumococcus. Scott 
found it in no less than 16 cases out 
of 40 (40 per cent.), and in 38 cases 
of croupous pneumonia the same 
reporter found pyopericardium in 17, 
or 44.7 per cent. 

Symptoms of Acute Fibrinous Peri- 
carditis. — The symptoms of acute 
fibrinous pericarditis are often not 
pronounced. Pain would supposedly 
be a well-marked symptom, but it is 
not present in all cases, although 
when it is present it may be severe. 

Fortunately pain from this cause is rare in children. When it occurs it is 
usually felt from the right edge of the sternum to the left nipple and is fairly 
constant, although it has sharp exacerbations. In other cases the pain is chiefly 
situated in the epigastrium, or a sense of precordial distress develops, and the breath- 
ing may be oppressed. The action of the heart is rapid, often reaching 100 or 120 
and even 160 beats per minute in severe cases. The temperature is usually in- 
creased, but seldom rises above 102° or 103°. In some cases it is not abnormal. 
Nervous symptoms are sometimes notable and great restlessness or even active 
delirium may ensue, resembling that of delirium tremens. Vomiting is a common 
symptom. 

Physical Signs. — The physical signs of acute fibrinous pericarditis are as 
follows: Palpation over the base of the heart at the third interspace may reveal 




Area in which pericardial friction sound is 
best heard. 



438 DISEASES OF THE PERICARDIUM 

friction fremitus in well-marked cases, and auscultation will show a distinct friction 
sound in the same area when the disease is established. This sound is creaking 
and dry and has been called the "saddle-leather sound/' in that it resembles the 
creaking of an ordinary English leather saddle when it is first used. It differs 
from the friction sound of pleurisy in that it is to and fro and does not occur with 
the respirations. At times it has a gallop rhythm with a triple sound as of a horse 
galloping. If the stethoscope be pressed against the chest the sound can usually 
be intensified. These sounds vary with the severity of the inflammation of the 
pericardium and the action of the heart, being more sharply defined when the action 
is violent than when it is depressed. Indeed, variation in the action of the heart 
may cause a loud friction sound at one visit and a lack of it at the next. As a 
rule the pericardial friction sound is limited to the area of the cardiac base about 
the third or fourth interspaces, but it may be heard at the apex or along the sternum. 

Diagnosis of Acute Fibrinous Pericarditis. — Acute dry pericarditis can scarcely 
be confused with any other state, but several conditions resemble it somewhat. 
Thus in cases of early phthisis there is occasionally heard, near the apex of the left 
lung, a cardiopulmonary murmur or puffing sound during inspiration, occurring 
with each beat of the heart, and persisting if the patient holds his breath on a full 
inspiration, but disappearing on expiration. Another similar condition is the so- 
called " pleuropericardial friction sound," which is apparently due to the beating 
of the heart against the margin of- the lung. Both of these sounds are, however, 
more in the nature of murmurs than friction sounds. 

Symptoms of Serofibrinous Pericarditis. — With the development of effusion, in cases 
which go on to that state, symptoms of cardiac embarrassment begin to show them- 
selves. The evidences of cardiac disturbance are not always, however, in direct 
proportion to the amount of fluid, for in some instances large accumulations of 
fluid cause so little inconvenience as to be overlooked, while in others in which the 
fluid is moderate in quantity they are severe. It is important that these variations 
in the severity of the symptoms be remembered, because it is humiliating in the 
extreme to find after some time that an unsuspected pericardial effusion is present. 
Probably the most constant symptoms are dyspnea, a dusky skin, an anxious fades, 
and a rapid pulse, which varies in volume and speed with the respirations. The 
voice is somewhat husky, and active delirium may be present as in the dry form. 

Diagnosis of Pericardial Effusion. — When the pericardium is well filled with 
fluid the sac presents a peculiar pear-shaped swelling which consists of two spheres 
superimposed, the smaller one above the larger one. It extends across the middle 
zone of the chest from a little to the left of the right nipple to a little to the left of 
the left nipple, and from the central tendon of the diaphragm nearly to the top 
of the sternum. The pressure of this fluid upon the heart and its great vessels 
may very markedly interfere with their proper movement, but it does not greatly 
change its position. 

Physical Signs. — The physical signs of pericardial effusion are as follows: 
On inspection the apex beat is absent and in many cases it cannot be found on 
palpation unless the patient is turned on his face. The chest over the heart may 
be slightly bulging, and palpation may reveal the fact that the first rib can be 
felt projecting more prominently from beneath the clavicle than in health. So, 
too, inspection may reveal some prominence of the epigastrium, and there may be 
unusual tenderness on palpation of this area. 

The heart sounds, on auscultation, are distant and feeble and the area of cardiac 
dulness is greatly enlarged. Thus it extends to the right of the sternum to a level 
below that which forms the base of the cardiac triangle, and to the left of the nipple. 
There is also enlargement of the area of cardiac dulness at the base toward the 
left. The presence of dulness in the fifth interspace, to the right of the sternum 
(Rotch's sign), of dulness as high as the second cartilage or second interspace 



PERICARDITIS 439 

(Sansom's sign), combined with dulness over the sternum between these points, 
are pretty sure signs of pericardial effusion, particularly if at the left infrascapular 
angle there is dulness on percussion (Ewart's sign). The area of dulness is that of 
a flattened cone, or, as Ewart has well said "it is that of a bag of fluid spreading 
out at the base." This view has been combated by Dr. Frederick Shattuck, 
but the distended sac does undoubtedly take this shape, although inability to 
demonstrate its outline does not exclude effusion by any means. 

In doubtful cases, resort to the x-rays may aid greatly in deciding the question 
of the presence of effusion. 

The most important states to be differentiated from pericardial effusion are 
cardiac dilatation and hypertrophy, and aneurysm of the aorta with some leakage 
into the pericardial sac. The first is the condition most apt to mislead the physi- 
cian. I have seen this occur several times and I have seen the heart punctured 
on two occasions in an endeavor to aspirate the pericardial sac in the belief that 
effusion was present when in reality the condition was one of great cardiac dilatation 
with pericardial adhesion. The presence of feeble and distant heart sounds, the 
absence of a definite apex beat, and the manifest cardiac embarrassment all aided 
in producing an erroneous view in these cases. In such a case the history of old 
valvular difficulty and the diffuse character of the apex beat should help us to a 
clear view of the condition. In cardiac hypertrophy the distinct apex beat, the 
strong action of the heart, and its clear sounds separate the two conditions. An 
aneurysm of the root of the aorta with some pericardial effusion may be most 
misleading. In a case of this kind, seen by me, aspiration of the pericardial sac 
caused rupture of the aorta and instant death. 

Very large pericardial effusions have been taken for left-sided pleural effusions, 
and an encapsulated pleural effusion has been taken for an effusion into the peri- 
cardium. 

Prognosis of Acute Pericarditis with and without Effusion. — This is good in cases 
in which the heart is not seriously crippled by the effusion or by associated endo- 
cardial changes. The outlook is favorable in proportion to the smallness of the 
effusion and the benignity of the disease causing it. In pneumonia and renal 
disease the prognosis is worse than it is in rheumatism, in which disease it is good. 

In the great majority of cases pericardial effusion undergoes absorption. This 
happens in this sac far more frequently than in the pleural sacs, perhaps because 
of the constant action of the heart. When the effusion persists it must be removed. 
(See Treatment.) Life is sometimes prolonged for many weeks even after pyoperi- 
cardium develops. Coutts has recently reported the case of a child of four years 
that lived seventeen weeks and died only after operation. Nevertheless; pyoperi- 
cardium is a very fatal condition. 

Treatment. — In the early stages of acute pericarditis, if the heart is overacting 
and irritated, tincture of aconite may be given with advantage to quiet its action 
and to diminish friction. An ice-bag may be placed over the precordium in cases 
of pneumonia with this complication, and in rheumatism several fly blisters may 
be used. Later if the heart becomes feeble the best stimulants are the aromatic 
spirit -of ammonia, Hoffmann's anodyne, and alcohol. Digitalis except in small 
doses is rarely of any value, and may be prevented from acting properly by reason 
of the fever or because there is not room in the pericardial sac for full diastole to 
take place under its influence. 

If the quantity of effusion be very great it must be removed by aspiration or 
incision. The latter operation is always essential if pus is present, and even if 
serum is present incision is safer because it is by no means easy to diagnosticate 
the presence of fluid beyond a doubt and more difficult still to be sure of the part 
of the sac farthest away from the heart. Aspiration may be therefore in the 
nature of a plunge in the dark. Incision carefully made is safer. The best spot 



440 DISEASES OF THE PERICARDIUM 

for operative interference depends upon the individual conditions and the position 
of the apex beat. The usual areas of election are in the fourth interspace at the 
left edge of the sternum and at the fifth right interspace at the edge of the sternum. 

When incision is practised for pyopericardium the mortality is high, but never- 
theless it must be performed if recovery is to occur. Out of 51 cases collected 
by Porter 20 recovered and 31 died. 

The use of purgatives, diuretics, and diaphoretics to cause the removal of the 
fluid is almost useless. 

Chronic Pericarditis (Adhesive Form).— Definition and Pathology. — By chronic ad- 
hesive pericarditis is meant a condition in which one or all of the following patho- 
logical conditions arise as a result of an inflammatory process, which involves the 
pericardium and often the tissues that surround it: 

(1) There may develop a state in which partial or localized adhesions take place 
between the visceral and parietal layers of the pericardium. Several such adhesions 
may be present in the pericardium at the same time. These adhesions may be 
immediate or consist in long strings of fibrous tissue stretching across the pericardial 
sac. They are commonly found near the base, but also occur at the apex. 

(2) In the second class of cases the two layers of the pericardium are closely 
adherent, and the walls of the sac in some cases are much thickened. Here again 
the adhesion may not be universal, but in patches, although at times the entire 
sac is obliterated so that the heart is surrounded by a thick and tough capsule 
composed of the two layers, which cannot be separated. 

(3) In still a third class the inner surfaces of the pericardium are not so much 
involved as the outer surface, and as a consequence we find adhesions to the chest 
wall or to the pleura. It is perhaps hardly fair to class this type with those already 
named, because the pericarditis in these instances is usually the result of a spread 
of inflammation from neighboring parts, as from the pleura or mediastinal tissues. 

(4) Another type, and the most serious of all, is that in which the internal and 
external layers are glued together, and the external layer is adherent to neighboring 
tissues so that the heart, its membranes, and adjacent parts are bound up in an 
inflammatory mass or mat. If the mediastinal tissues are not affected the con- 
dition is called "pericarditis externa et interna," but if the mediastinal tissues are 
included it is given the name of "indurative mediastinopericarditis." In some 
cases the tissues for nearly the whole length of the left edge of the sternum may be 
involved. 

(5) Finally, a form of chronic pericarditis occurs which affects the visceral 
layer of the pericardium almost solely, and encloses the heart in a thickened inner 
layer. 

Related to the latter condition is the so-called "multiple serositis" or the "peri- 
cardiac pseudocirrhosis of the liver" of Pick, to which the name "iced liver" has 
been given by Curschmann. In such cases the pericardium suffers from a chronic 
hyperplastic or fibroid inflammatory process, which likewise affects the serous 
membranes elsewhere, whence the name "multiple serositis." In other words, in 
this diseased state all serous membranes of the thoracic and upper abdominal zones 
are involved in a hyperplastic process which is prone to affect the pericardium in 
particular. In some instances the pericardial sac contains fluid, but in others it is 
closed by the adhesions between its walls, and which go on even to calcification. 
When the condition is well developed the pericardium and pleurae are adherent to 
one another and to all adjacent tissues, and the peritoneum is also thickened and 
adherent to nearby organs. The liver is adherent to the diaphragm and even to 
the stomach, colon, omentum, and belly wall. It is the profuse hyperplasia of 
the peritoneum which causes the organs it covers to look as does a cake which has 
been "iced." The two symptoms of this condition which are most constant and 
characteristic are large ascites and a gradually increasing failure of cardiac power. 



PERICARDITIS 



441 



The cause of the excessive ascites is the perihepatitis and the compression of the 
abdominal vessels by the newly formed connective tissue. Beyond these two symp- 
toms the manifestations of the process are practically identical with those of 
adherent pericardium, as will be described below. The malady is a very slow 
and chronic process, lasting, it may be, for years. 



Fig. 82 




Heart, left ventricle. Adherent pericardium, with lipomatosis of the adhesions and slight fatty 

infiltration of the myocardium. 



Symptoms of Adhesive Pericarditis. — The symptoms of the milder forms just 
described are so moderate that no thought of their existence is had till autopsy 
reveals them. It is in the well-developed types that the condition may cause 
symptoms which are definite. Indeed, in some cases it may be impossible to 
correctly diagnosticate even the most severe forms. The subjective symptoms 
are pain in the precordium or a sense of constriction. This pain may be dull and 
constant or paroxysmal, arousing the suspicion of true angina pectoris. Palpita- 
tion is another common symptom and in some instances the action of the heart 
is irregular and hobbling. Shortness of breath on exertion is also present and at 
times the right ventricle becomes engorged and secondary engorgement of the liver 
and lungs ensues. Finally, what is taken for ordinary cardiac dropsy due to valvu- 
lar disease develops. In other cases pleural effusion develops from this cause. 



442 DISEASES OF THE PERICARDIUM 

The result of these adhesions is enlargement or hypertrophy and dilatation 
of the heart. This change, however, does not occur in all cases and it is chiefly 
present in cases in which valvular lesions coexist. The pressure produced by the 
thickened membranes results in some obstruction to the flow of blood in the great 
veins at the cardiac base, and this causes jugular distention. 

Diagnosis of Adhesive Pericarditis. — The physical signs to be searched for in 
making a diagnosis are as follows : 

Inspection may reveal depression of the precordial area and a drawing together 
of the ribs so that the intercostal spaces are narrowed. In place of this condition 
in this part of the chest, there may be distinct bulging. Again, the apex beat is 
often much displaced and as the pericardium is adherent to the chest wall changes 
in posture do not alter its position. The usual displacement of the apex is upward 
and outward. In other instances the apex beat cannot be seen or felt in its usual 
place, but a transmitted impulse can be found in the epigastrium. Perhaps the 
most important diagnostic symptom is retraction of the chest wall at systole. 
This retraction may be at the apex or along the left edge of the sternum in the third, 
fourth, and fifth interspaces. Roberts states that if the right ventricle is greatly 
enlarged the impulse can be seen to the right of the sternum. Broadbent has called 
attention to the fact that in many of the well-marked cases of adherent pericardium 
marked systolic retraction of the lower ribs on the posterolateral aspect of the chest 
is visible, if the patient is in a good light and the physician regards his back and 
side from a distance. This retraction is in the nature of a tug at systole. It is 
emphasized by a deep inspiration. Again, if the physician will place his head 
directly against the chest in this area he may have transmitted to it a shock at the 
time of systole. In some cases the adhesions between the pericardium and the 
diaphragm may prevent the normal epigastric respiratory movements. 

Percussion may reveal in some cases an increase in the area of cardiac dulness, 
but it is not constant. Auscultation may show reduplication of the pulmonary 
second sound, and a rough and widely distributed friction sound, and a somewhat 
prolonged presystolic murmur at the apex which is not necessarily due to mitral 
stenosis. 

The pulse often presents irregularities, particularly at the time of the inspiratory 
movements, the so-called pulsus paradoxus. Sudden collapse of the cervical 
veins on diastole may also be present. 

It must be distinctly understood that these signs are often absent or are difficult 
to discover. There is perhaps no more difficult diagnosis than that of some cases 
of adherent pericardium. The history of a severe or repeated attacks of acute 
rheumatic fever is an important point in judging of the likelihood of its presence, 
particularly if there is also a history of pericarditis. Progressive cardiac weakness 
without valvular lesions in a young person should raise the suspicion of this state, 
particularly if an insidious ascites and dropsy of the lower extremities develop. 

Prognosis of Adhesive Pericarditis. — The prognosis is of course very grave if the 
symptoms are severe and if the occupation is strenuous. With adequate rest 
life may in some cases be prolonged for years if the inflammatory state is stationary. 

Treatment of Adhesive Pericarditis. — The treatment cannot be curative for obvious 
reasons. It can only be palliative, by rest, good food, and the relief of dropsy by 
purges and diuretics. A sufficient number of cases have been successfully treated 
by operation, to break up adhesions, to justify cardiolysis. 

HYDROPERICARDIUM. 

This is a state of fluid in the pericardium due to transudation from vessels which 
are pressed upon by growths, or it results from hemic or vascular changes due to 
renal disease. It is not an inflammatory effusion. 



PNE UMOPERICARDI UM 443 

Symptoms. — Symptoms and physical signs are absent except when the fluid 
becomes copious enough to cause cardiac embarrassment, when the condition 
of the patient is found to be like that produced by an ordinary serous pericardial 
effusion due to true pericarditis. 

Prognosis. — The prognosis depends upon the cardiac state and the underlying 
cause. It is usually grave, because of the underlying malady. 

Treatment. — The treatment consists in free purgation, if the patient is able 
to stand it, and the use of diuretics. Otherwise it is that of general dropsy. (See 
Chronic Parenchymatous Nephritis.) 



HEMOPERICARDIUM. 

Blood in the pericardial sac arises from stab and other wounds, and it is also 
present in cases of purpura and of profound diseases of the blood. In other cases 
it arises from aneurysm of the aorta early in its upward course, and finally it may 
be due to rupture of the heart or aneurysm of one of the coronary arteries. Even 
in these cases death may be postponed a number of days. If a large amount of 
blood escapes into the pericardium the heart is stopped by the pressure on its surface 
and on the great veins at its base, so death is not due to actual loss of blood. This 
result is what one would expect, and I proved its truth some years ago in an experi- 
mental research. 

When the condition is due to disease it usually is hopeless. When due to injury 
the pericardium should be opened, the blood removed, and if a wound in the heart 
exists it should be closed. There are many cases of this sort on record in which 
operation has been performed and in which life has been saved. 



PNEUMOPERICARDIUM. 

Air or gas in the pericardium appears as the result of injury, whereby air enters 
the sac, or again as the result of a cavity in the lung perforating, through adhesions, 
into this space. It also may develop in cases of cancer or other ulcerative lesions 
of the esophagus, with adhesions between this tube and the pericardium, followed 
by perforation of the growth. Again, it occurs rarely, as the result of perforation, 
in pneumopyothorax. Cases are on record in which a gastric ulcer has caused 
adhesions to the diaphragm followed by perforation, and so pneumopericardium 
has developed. In still other instances the gas which is present is due to the 
presence of the Bacillus aerogenes capsulatus or other gas-producing organisms. 

The mere presence of air, or gas, in this cavity is such an abnormal state that 
some serous effusion nearly always takes place within a few hours; so that all 
cases of pneumopericardium are really to be considered as hydropneumopericardium 
and as they speedily become purulent by infection they are usually instances 
of pyopneumopericardium. 

Symptoms. — The symptoms resemble those of pericarditis with effusion, except 
that a considerable part of the area of cardiac dulness may give a high-pitched 
resonant note on percussion. This area of resonance varies greatly with the posture 
of the patient, being larger when he is recumbent than when he is erect. Another 
symptom which is quite characteristic, if it can be discovered, is a peculiar crackling 
sound due to the action of the heart in stirring up the fluid and the air. Sometimes 
these sounds are gurgling or churning in character. They have been compared to 
the splashing of water on a mill-wheel. There is but one condition which can 
produce symptoms like these, and that is a large cavity in the lung near the heart 
in which the fluid contents are disturbed by the movements of the heart. 



444 DISEASES OF THE HEART 

Prognosis. — The prognosis is, of course, very grave, but recovery has occurred. 

Treatment. — The treatment depends largely upon the cause. If the case is 
one of perforated esophageal cancer it is of course hopeless; in an instance of trau- 
matism with perforation surgical interference may give good results. 

PYOPERICARDIUM. 

(See Pericarditis with Effusion.) 



DISEASES OF THE HEART. 

HYPERTROPHY AND DILATATION OF THE HEART. 

Definition. — Hypertrophy of the heart is a condition in which there is a growth 
above normal of its muscular fibers resulting in an increase in the size and particu- 
larly in the muscular power and weight of the viscus. 

In dilatation one or more of the cardiac cavities is more capacious than normal; 
the wall may be normal, increased or decreased in thickness, with a cardiac power 
less than its muscular development would indicate. 

These conditions, which at first glance seem diametrically opposed to one another, 
are in reality nearly always present simultaneously in varying degree. For this 
reason I consider them side by side. 

When the wall of the ventricle is increased in thickness without any alteration 
in the size of its cavity the condition is called simple hypertrophy. When the 
cavity is larger than normal it is called eccentric hypertrophy, or hypertrophy with 
dilatation, and when the cavity is decreased in size it is known as concentric hyper- 
trophy. 

When dilatation is combined with hypertrophy it is called active dilatation. 
When there is no hypertrophy, but thinning of the walls alone, it is called passive 
dilatation. 

Hypertrophy of the Heart. — The existence of concentric hypertrophy has been 
denied. It certainly is very rare. Simple hypertrophy is also rare, but eccentric 
hypertrophy is one of the most common of secondary pathological changes. 

A large number of causes produce cardiac hypertrophy with dilatation. Some- 
times they act singly, but not rarely several of them are associated. The most 
common cause is valvular disease, which by its resulting regurgitation of obstruc- 
tion increases the labor of the heart. The second cause of importance is a state 
of the bloodvessels which renders the propulsion of the blood more difficult than 
in health. This obstruction to the free flow of blood may be general, as in cases 
of arteriocapillary fibrosis; or localized, as when there is roughening or narrowing 
of the aorta, or when a tumor presses upon the aorta; or, again, in cases of aneurysm. 
Other localized causes of hypertrophy are emphysema of the lungs or chronic 
phthisis and adherent pericardium. 

The increase in the size of the heart in cases of hypertrophy is sometimes very 
great. Thus, this' organ, which in the healthy man weighs about nine ounces, 
or 270 grams, and in the healthy woman about eight ounces (240 grams), may weigh 
as much as 53 ounces (1590 grams). Usually, however, the increase does not go 
beyond fifteen ounces (450 grams). 

A heart which has undergone hypertrophy is broadened or widened at its apex, 
but the actual increase in the size of this organ at this point depends largely upon 
the part of the heart which is chiefly affected. Thus, in cases in which the right 



HYPERTROPHY AND DILATATION OF THE HEART 445 

ventricle is chiefly involved, this part of the heart is often far larger than that part 
formed by the left ventricle, which seems small by contrast. When a hypertrophied 
heart is incised, its walls are found to be much thickened and the columnar carnese 
and papillary muscles larger than normal. The enlargement is due to both an 
increase in the number and size of the muscle fibres. 

Symptoms and Physical Signs of Cardiac Hypertrophy. — The chief symptom of 
ordinary eccentric hypertrophy, when it is adequate to compensate for the valvular 
lesion, or to overcome resistance, may be said to be the maintenance of a comfortable 
life and a normal circulation. Many persons develop this state without any 
knowledge of there being present any valvular disease, and remain in perfect health 
for years. 

If the physician chances to examine such a case he may find a cardiac murmur 
and then on closer study, discover the following physical signs, provided the process 
is well developed. On inspection the precordium is bulging, but the impulse trans- 
mitted to the chest wall is regular and deliberate in distinction from the cardiac 
hurry and irregularity present when compensation is ruptured. The apex beat 
is more diffuse than is normal and is often in the sixth or seventh interspace instead 
of in the fifth, and it is farther toward the axilla than in health. On palpation 
the apex beat is found to be forcible and it may be heaving, but if the patient be a 
full-chested individual these local signs may not be present. If emphysema of the 
lungs causes these enlarged organs to overlap the heart they may hide much of the 
hypertrophy. Percussion may reveal increase of the area of cardiac dulness to 
the left, to the right, and downward. Auscultation, instead of revealing an exagger- 
ation of the first sound, reveals that it is more distant, perhaps because the thick- 
ness of the heart walls muffles the sound, but the aortic sound is accentuated unless 
the aortic valves are diseased. 

If the patient takes violent exercise he may complain of palpitation and the 
thumping of his heart. 

When hypertrophy begins to fail the patient complains of shortness of breath 
on exertion, of palpitation and oppression, and if he persists in keeping on his feet 
the symptoms of cardiac failure (see Valvular Disease) develop. The first physical 
signs of the failure will be some reduplication of the first sound and diminution in its 
clearness. This reduplication is best heard just inside the apex beat when it first 
develops, but later it can be heard over a large area. The period between the first 
and second sound is prolonged as if the ventricle was able, only with the greatest 
endeavor, to slowly expel its blood. This means diminution of the period in which 
the heart muscle can obtain nourishment through its coronary vessels. 

The causes for this failure are various. In some instances the degenerative 
changes in the myocardium and in the bloodvessels which are incident to old age 
are the determining factors. In others some acute illness — as typhoid fever, 
influenza, pneumonia, or renal disease — may be the cause; or, again, severe exercise 
may produce so much exhaustion of the heart muscle and acute dilatation that the 
cardiac power is impaired for all time. 

Diagnosis. — Cardiac hypertrophy must be separated from several important 
conditions which are by no means rare. From dilatation hypertrophy is differ- 
entiated by the facts that the impulse in the former is feeble, in the latter it is 
strong, and by the feeble heart sounds in the former as compared to the stronger 
ones in hypertrophy. So, too, palpation of the apex in dilatation reveals a diffuse 
and feeble impulse and in hypertrophy a forcible beat. 

From pericardial effusion it is differentiated by the fact that, though the area of 
cardiac dulness is increased in both states, the cardiac impulse and cardiac sounds 
are muffled in effusion and exaggerated in hypertrophy. From displacement of 
the heart it can be differentiated by the fact that though the apex beat is displaced 
the general area of cardiac dulness is not increased in cases of displacement. 



446 .DISEASES OF THE HEART 

Again, in certain cases in which the chest wall is thin and the lung is retracted 
so that it fails to cover the heart as in health, the heart may be so close to the chest 
wall that its area of dulness will be abnormally large and its apex beat unduly 
forcible and diffuse. In such a case the careful study of the state of the lung and 
pleura will make the condition clear. 

Of the functional disorders that produce overaction of the heart and so cause 
apparent but not real hypertrophy, "tobacco heart," the irritable heart of exoph- 
thalmic goitre, and that of neurotic individuals must be remembered. 

Prognosis. — As cardiac hypertrophy in its common form is compensatory in 
character, and as it very rarely becomes excessive, in the sense that it is beyond the 
needs of the patient, the prognosis in a case in which it is present deals not with the 
question of how much greater will hypertrophy become, but rather how much 
longer will hypertrophy enable the heart to supply the bloodvessels with blood in 
satisfactory quantities. Unlike most alterations from the normal as the result 
of disease, this change is distinctly advantageous to the patient. 

The question as to how long the hypertrophy will be maintained can only be 
answered after its provoking cause or causes have been determined. If the hyper- 
trophy following valvular disease of the heart is adequate, if the patient is a young 
and otherwise healthy adult, and if the valvular lesion is not progressive, the prog- 
nosis as to the maintenance of the condition is usually good, but will depend upon 
the good habits of the patient, particularly as to alcohol, hard work and exposure, 
and upon the particular valve which is diseased. (See Prognosis of Valvular 
Lesions.) If the hypertrophy is the result of arteriocapillary fibrosis with its 
associated renal changes, the duration of life except under the most favorable 
conditions is brief, because the arterial obstruction is constantly increasing and 
the heart is constantly exposed to increasing strain, increasing toxemia, and is 
poorly nourished by its own coronary arteries. 

Treatment. — There is no treatment for compensatory hypertrophy except to 
maintain it by care as to manner of life, and the use of digitalis and rest if its integ- 
rity or maintenance is threatened. I have seeu a few cases of aortic regurgitation 
with great hypertrophy in which rest in bed and moderate doses of tincture of 
aconite have given better results than rest and digitalis, but in these cases the patient 
had been accustomed to severe toil, and when he was put at rest seemed to have 
excessive cardiac power, as shown by throbbing and oppression. On the other 
hand, when hypertrophy seems excessive, it is not rarely in reality lacking, and 
the violence of the heart movements may be abortive efforts at circulation. Often 
the use of nitroglycerin at such times will be advantageous if the arterial pressure 
is high. 

Dilatation of the Heart. — Passive dilatation (without hypertrophy) may be 
caused by valvular lesions, as the result of which the cavities of the heart become 
distended, but hypertrophy does not develop. Of these the chief cause is sudden 
and prolonged strain, and the feebleness often due to myocardial disease. Obstruc- 
tion to the flow of blood in the pulmonary vessels may cause dilatation of the right 
side of the heart, as in cases of pneumonia, in cases of pleurisy with effusion, and 
in cases of acute pulmonary edema complicating uremia. 

A common cause in men over fifty years is sudden effort, as in lifting a heavy 
weight or climbing rapidly a steep flight of steps. In the young and vigorous 
sudden strain may be followed by rapid return of the dilated heart to its normal 
size, but in those further on in years, or who have valvular or myocardial disease, 
an acute strain often results in permanent dilatation. It is very common for old 
men to try to prove that they are "as young as they used to be," and to attempt 
athletic feats which are followed by acu'te dilatation and perhaps immediate death, 
or death in a few days or weeks. In other instances the heart suffers from a gradual 
dilatation from prolonged strain, as in soldiers on the march. Not rarely dilatation 



HYPERTROPHY AND DILATATION OF THE HEART 447 

develops during the course of one of the acute infectious diseases or during con- 
valescence. 

When the strain is very gradual, instead of meeting the increased demand by 
increased effort, the heart slowly dilates and is perhaps never able to empty its 
cavities of blood. 

The intrinsic causes of dilatation are myocarditis, fatty degeneration, fatty 
infiltration, and serous infiltration from pericarditis. In some cases, however, 
no adequate intrinsic cause can be found. 

Symptoms of Cardiac Dilatation. — The symptoms and physical signs of passive 
dilatation are usually such that a diagnosis is readily made. When it is sudden 
in onset an acute or partial syncope with labored respiration and thoracic oppression 
may be present. 

When the onset is more gradual the main symptoms are impaired circulation, 
a tendency to syncope on suddenly standing or sitting up, congestion of the kidneys 
causing albuminuria, and a poor capillary circulation which causes the skin of 
the hands to remain pallid long after pressure. Many persons so afflicted cannot 
lie down without urgent dyspnea and cardiac distress. The pulse is small and 
irregular, and the arterial tension low. In other cases the pulse wave may be vol- 
uminous, but feeble. 

An inspection of the precordium shows that the apex beat, if visible at all, is 
diffuse and displaced outward and downward. On placing the finger-tip on the 
spot where the apex beat seems most marked, the examiner is surprised to find no 
impulse or one which is very slight. There is often visible, but rarely palpable, 
pulsation near the ensiform cartilage or in the epigastrium. Care must be taken 
that the overlying lung does not lead to an erroneous belief as to the presence of 
cardiac feebleness. If the whole hand is placed over the disturbed surface of the 
precordium it is remarkable how little impulse is discernible. Percussion shows 
an increase in the area of cardiac dulness to the left, to the right, and downward. 
Often it is also increased upward. 

On auscultation the first sound of the heart may be short and small, valvular 
and flapping, though fairly loud, and if the heart is strong enough there may be a 
systolic murmur at the apex, due to mitral regurgitation arising from stretching 
of the mitral orifice. As in ruptured compensatory hypertrophy the sounds of the 
heart may be equalized and the space between them may be altered so that the 
sounds are like those of the fetal heart or like the ticking of a watch. In other 
cases the first and second sounds may occur close together and the diastolic pause 
be prolonged. Very often great arrhythmia is present. If in addition to these 
signs there is a history of acute strain near or remote, with symptoms of cardiac 
feebleness, and particularly if there has been an acute illness due to infection, 
such as influenza or pneumonia, the diagnosis of dilatation may be made. Some- 
times cardiac dilatation causes pleural effusion (see Hydrothorax) . 

Prognosis. — The prognosis depends upon the degree of the dilatation, the state 
of the vessels and of the heart muscle and of the kidneys, and last, but not least, 
the lungs. When the latter are filled with rales the state is alarming, and if the 
vessels and kidneys are diseased the outlook is hopeless for much betterment. 
If the state of the vessels and the general condition of the patient indicate fatty 
myocardial degeneration the prognosis is also bad. If these states are absent, 
and rest can be maintained, improvement can be hoped for, but a complete cure 
with old-time vigor is rarely reached. 

Treatment. — The treatment is, first of all, rest in bed, or in any easy chair if 
bed is impossible because of orthopnea. The second object to be gained is the 
removal of the cause of the dilatation, if that be possible, as the reduction of high 
arterial tension by the use of nitroglycerin. Third, the employment of digitalis 
and strychnine for effect, recalling the fact that once digitalis has produced its 



448 DISEASES OF THE HEART 

action smaller doses will maintain its influence, and also bearing in mind the addi- 
tional fact that when it is in full effect sudden changes of posture are dangerous. 
Digitalis may also cause so much ventricular stimulation as to overdistend the 
auricle, which is poorly protected by the relaxed mitral ring. 

When the lungs and kidneys are engorged, the application of several dry cups 
over them is useful, and if jugular distention and hepatic congestion is marked, 
the patient may be freely bled if he is plethoric. So, too, hydragogue cathartics, 
such as jalap and compound extract of colocynth, may be used to unload the bowels 
and liver, but care must be taken that the patient is not exhausted by purging. 
Blue mass in the dose of 8 grains once a week is useful, and the pill of calomel, 
squill, and digitalis mentioned under Endocarditis may be used. If ascites is a 
pressing symptom tapping is indicated, while for general anasarca the formula 
given under Endocarditis, or apocynum cannabinum may be used, or the digitalis 
given more liberally. 

The diet should be light and nutritious, and often it is well to give pancreatized 
foods or starches with taka-diastase. Great care must be taken that the stomach 
is not distended by food or drink, and if gas accumulates in the stomach it should 
be expelled by the use of Hoffmann's anodyne in drachm doses, and by the employ- 
ment of a turpentine stupe. When dyspnea is urgent morphine and strychnine 
are useful drugs. 

High altitudes should be carefully avoided and only gentle exercise on level 
ground be allowed. 

DISEASE OF THE MYOCARDIUM. 

Disease of the myocardium may be divided into two classes, viz., degenerative 
and inflammatory. 

Degenerative Changes. — Etiology and Pathology. — The degenerative conditions 
are as follows : In the granular form, sometimes called " parenchymatous degenera- 
tion," there develops in the protoplasm of the cardiac muscle fibres albuminous 
granules which differ in size and in number, and may be present in such an excess 
as to obscure the nuclei and striae. The affected muscle is cloudy, softened, and 
paler than in health, its strength decreased, and the circulation is proportionately 
depressed. In a later stage some degree of fatty degeneration may also be present. 

This type of degeneration is observed in the course of acute infectious diseases, 
as diphtheria, typhoid and typhus fever, the pyemias, and even as a result of 
severe burns, and in debilitating conditions associated with severe cardiac work 
or the presence of toxic bodies in the blood. 

In fatty degeneration of the heart the affected fibres contain fat-globules, which, 
in marked cases, replace the structural elements, both the nuclei and protoplasm. 
In some instances this degenerative process is restricted to a single focus, or it may 
be scattered about or diffuse; in others it is universal. When the heart is examined 
at autopsy it is seen to be mottled and the papillary muscles in particular will 
reveal the fatty areas, the so-called "Tiger Herz" of the Germans. 

Diffuse fatty degeneration is caused by prolonged nutritional disorders. Per- 
nicious anemia and leukemia may also cause it, as may poisoning by arsenic, 
phosphorus, and antimony. Less commonly it is a sequence of various acute 
infectious diseases like diphtheria and scarlet fever or typhoid fever, and by 
degenerative or atheromatous changes in the coronary arteries. The local or cir- 
cumstantial forms follow embolism or other types of rapidly developed coronary 
occlusions. 

It is important that fatty degeneration be clearly separated horn, fatty infiltration, 
in which state the muscle fibres are not altered, but have been separated by the 
projection of fatty masses between them. This may cause some wasting or atrophy 



DISEASE OF THE MYOCARDIUM 449 

of the muscle fibres. This state is most commonly met with in very fat persons 
and in those who are addicted to excessive beer-drinking. Occasionally forms of 
amyloid and hyaline degeneration of the heart fibres occur. 

Brown induration or atrophy of the heart is often seen in cases of chronic valvular 
disease and in old persons. The muscle is more dense than normal and reddish- 
brown in hue, and about its nuclei brown pigment is deposited. Calcareous degen- 
eration, in which the muscle fibres become infiltrated with lime salts, is rare. 

Under the name of fragmentation and segmentation there is seen a state of the 
heart muscle in which its fibres are broken across in fragments, or its cells are 
separated at the point of junction (segmented). These changes may occur in 
acute infectious diseases or in cases of central nervous disease. In some cases 
they are probably agonal, and it may be that similar appearances are of postmortem 
origin, but the frequency with which granular change is seen at autopsy strongly 
indicates that it may be present and unrecognized in life, not only in fatal cases, 
but in those who recover. 

Symptoms of Myocardial Degeneration. — The symptoms of degeneration of the 
heart of the albuminous type cannot be considered as pathognomonic. Indeed, 
there may be no evidence of cardiac failure until a sudden and perhaps fatal attack 
of syncope, after a slight exertion, reveals the alarming state of the heart muscle. 
In other instances the feeble cardiac sounds on auscultation indicate the real condition 
of the heart. 

When fatty degeneration is present the same absence of symptoms may exist 
until the fatal syncope, or the patient may suffer from repeated attacks of syncope, 
or of vertigo with anginoid seizures. (See Stokes-Adams Disease, page 450.) The 
frequency and severity of these attacks are, however, by no means in direct propor- 
tion to the extent of the lesion in the heart muscle. In one instance a fatal syncope 
occurs, yet the heart scarcely seems altered in its fibres. In another case the life 
of the patient persists and fairly good health is maintained for years, yet at autopsy 
the heart muscle is so fatty and soft that the fingers can be pushed through it 
as if it were wet paper. 

In some instances the symptoms complained of by the patient seem to be epi- 
gastric and due to disordered digestion. How often do we hear of a man of advanced 
years dying of acute indigestion, which is really cardiac failure with gastric symp- 
toms, or cardiac failure caused by an overdistended stomach. 

The heart sounds when the patient is in his average state of health are distant 
and feeble, and his slow pulse is small and of low tension. Not rarely his radial 
and temporal arteries are very calcareous, but in other cases they are soft and devoid 
of resistance on pressure. 

There still remain to be considered several notable facts in connection with 
this disease. Notwithstanding the great feebleness of the heart in some cases and 
the exceedingly weak circulation of blood, dropsy in any form is a very rare con- 
dition. Indeed, if dropsy occurs it is almost certainly due to some complicating state. 
A second fact is that in some cases in place of anginoid attacks an epileptiform or 
apoplectiform seizure occurs. The epileptiform seizure is not that of grand mal, 
but petit mal, with this difference, that while, as in petit mal, there are no convul- 
sions, there is a period of profound unconsciousness which is rather a syncope 
than a coma such as is seen in true epilepsy. 

The apoplectiform seizures may very closely resemble true cerebral hemorrhage, 
even to the stertorous breathing, the hemiplegia, the unconsciousness, and Cheyne- 
Stokes respirations. That the case is not one of apoplexy is usually proved by 
finding that the high-tension pulse of cerebral hemorrhage is absent and replaced 
by the low tension and slow pulse of fatty degeneration. 

Prognosis of Myocardial Degeneration. — The prognosis in all cases of cardiac 
degenerative change is, of course, very grave. When it is present in children 
29 



450 DISEASES OF THE HEART 

after acute infectious diseases recovery may ensue under a course of arsenic, phos- 
phorus, and nux vomica, with absolute rest, and fresh air and sunshine, but even 
in this class of cases sudden death often intervenes. In the fatty heart of advanced 
age, whether the years be great or the patient prematurely old, the outlook is 
bad; but as no one can tell the extent of the lesions in the heart, a statement as to a 
brief duration of life is very prone to bring the physician's opinion into discredit 
if he attempts to name the time of dissolution. The wise physician rarely expresses 
a positive opinion as to the probable time of death in any case, much less in fatty 
heart. 

Stokes-Adams' Disease. — Cases of extreme slow pulse with vertigo, or syncope, 
or apoplectiform or epileptiform seizure, have been given the name of the "Stokes- 
Adams syndrome. " The first case was described by Thomas Spens in 1793. (See 
Bradycardia.) (Plates VIII, IX, and X.) 

Associated with the slowness of the pulse there is marked pulsation in the veins 
of the neck, and to use Stokes' own words, written in the Dublin Quarterly Journal 
of Medical Science in 1846, the number of reflex pulsations is difficult to be estab- 
lished, but they are more than double the number of the manifest ventricular 
contractions. Experimental and clinical studies, indicate that the symptom- 
complex in most if not all cases of this condition is due to what is now denominated 
"heart-block." In this state the auricles beat two, three, or four times as rapidly 
as do the ventricles. (See Mitral Stenosis.) Most cases of Stokes-Adams disease 
appear to be primarily arteriosclerotic or syphilitic in nature though myocardial 
lesions of other origin may be the cause. Autopsy in some reported cases has shown 
no evident lesion and these have been pronounced neurotic in character. A point 
to be noted in autopsies upon cases of this disease is whether lesion of the mesial 
leaflet of the tricuspid valve has interfered with the integrity of the muscle bundle 
of His. 

Myocarditis. — Definition. — This term is an unfortunate one in that it is often 
loosely applied to the degenerative changes just described as well as to those 
about to be mentioned. It is also unfortunate because it seems to indicate that 
there is a primary inflammatory state of the cardiac muscle fibres, whereas the 
changes in the fibres are secondary to inflammatory affections of the interstitial 
tissues of the heart and of its bloodvessels, which thereby cause atrophic and 
degenerative changes in the muscle. 

There are several forms of so-called myocarditis, of which the most common 
is a slow, low-grade inflammatory change called chronic interstitial myocarditis, 
manifested by a wasting of the muscle fibres and the intercalation of fibrous or 
fibro-elastic tissues. There is also an acute process, acute interstitial myocarditis, 
of which there are suppurative and non-suppurative varieties, the former being a 
manifestation of pyogenic infection of the heart wall. 

In the great majority of cases the chronic form is the result of pathological 
changes in the coronary arteries. These vessels suffer from an obliterative arteritis 
in their finer branches, undergo atheromatous change, or become plugged by an 
embolus or thrombus. The lesions which result from these changes differ widely 
in character, but all greatly impair the usefulness of the heart. In all conditions 
lessening the vascular lumen and so decreasing the nutrition of the heart, there 
develops an overgrowth of interstitial tissue with atrophy of the muscle fibres. 
It is probable that the process is at no time a true inflammation, but rather one 
in which diminished blood supply causes atrophy of the muscle, followed by a 
substitutive fibrosis. 

When a branch of a coronary artery is plugged the affected area may manifest 
the changes seen in an infarct, or when enough nourishment is available to prevent 
actual necrosis the deficient nutrition gives rise to fatty degeneration. In either 
case the affected area may become softened, and give way, causing rupture, or 



DISEASE OF THE MYOCARDIUM 451 

fibrous tissue gradually takes the place of the degenerated fibres. Later the scar 
tissue yields to pressure and a cardiac aneurysm ensues. 

Hypertrophied hearts may show a slight increase in the fibrous tissue, and in 
failing compensation and progressing dilatation this increase in interstitial tissue 
may be conspicuous. 

In some instances chronic myocarditis is not the result of vascular change, but 
of inflammatory processes in the pericardium and endocardium; and in syphilis 
there is often seen a marked increase in the interstitial tissues of the heart, which is 
not surprising in view of the serious changes produced by this disease in the small 
bloodvessels everywhere. Chronic myocarditis is more common in males than in 
females. 

Symptoms of Myocarditis. — The immediate effects upon the patient produced 
by the lesions just named vary to an extraordinary degree. Plugging of one of the 
large branches of a coronary artery usually results in sudden death. 

In some instances, however, the patient survives a severe attack of cardiac 
disturbance, but under these circumstances the plugging is usually in a small 
vessel, and a gradual substitution circulation is established, not by anastomosis, 
for these vessels are end-arteries, but by the so-called vessels of Thebesius, which 
in some cases are able to supply the heart with an adequate quantity of blood. 

When the closure of the vessel is gradual it not rarely happens that necrosis 
of the area deprived of blood is prevented by a blood supply through the vessels 
of Thebesius, so that the death of the patient is postponed until a very extraordinary 
degree of atheroma and narrowing in both coronary arteries is developed. The 
coronary arteries of a well-known member of the medical profession in Philadelphia, 
who died a few years since, were so diseased that only a thread-like passageway 
existed in these vessels, yet he led an active life to the end. Such patients may 
have no marked cardiac symptoms, but, as a rule, repeated attacks of angina pectoris 
of increasing intensity give warning of the sudden death to come. The other 
symptoms are the same as those described under fatty degeneration of the heart. 

The physical signs of myocardial degeneration are feebleness of the apex beat, 
equalization of the first and second sounds of the heart, and evidences of feeble circula- 
tion in the lungs and in the peripheral systemic vessels. 

The prognosis depends entirely upon the situation and the degree of the cardio- 
vascular change. So far as recovery is concerned, that is impossible. The 
probable duration of life is also difficult to determine. Many cases with all the 
symptoms of severe myocarditis live a long period, while others die with unex- 
pected suddenness. 

Treatment. — We cannot expect very much from treatment in patients suffering 
from chronic myocarditis. It must be evident from what has been said, under 
the discussion of the pathological conditions which cause these states, that the 
harm is done before the physician has an opportunity to place the patient under 
treatment. The only hope is that by regulating the manner of life, by increasing 
the action of the kidneys, if they are sluggish, by attending to the digestive appa- 
ratus, and by preventing undue cardiac strain through excessive muscular or mental 
exercise, we may be able materially to prolong the patient's life. In instances 
in which the bloodvessels are distinctly atheromatous or fibroid, the use of the 
iodide of strontium or sodium, in doses varying from 10 to 40 grains three times 
a day, is usually advantageous. This treatment may be continued for several 
weeks, and then the patient may receive a course of Donovan's solution as a general 
tonic, with perhaps a small quantity of nux vomica or strychnine added to it. 

If arterial tension is high, he should be given nitrite of sodium in doses varying 
from 1 to 2 grains three or four times a day, in order that the resistance which is 
offered by tense vessels to the action of the heart may be lessened. Under these 
circumstances, too, small doses of digitalis sometimes act advantageously, particu- 



452 DISEASES OF THE HEART 

larly if nitroglycerin is given at the same time. To give digitalis to a failing heart 
and yet to permit the arterial tension to remain high is of little ultimate advantage 
to the patient, since it increases the labor of the heart. It is much more important 
to diminish the labor by the use of rest and baths than to stimulate this viscus to 
increased endeavor by large doses of foxglove. 

Strophanthus may do better than digitalis in some cases. It must be remem- 
bered that if the heart has undergone distinct degenerative changes there is little 
muscular fiber upon which the digitalis may exert its stimulating influence, and 
there may be danger by increasing intracardiac pressure of causing rupture of 
some area of white necrosis, thereby causing cardiac aneurysm. 

It is hardly necessary to add that these patients should be warned against exces- 
sive muscular exercise or any severe cardiac strain, and they should be advised 
to lie down and rest several times a day, in order that the heart may at each period 
of rest recover as much strength as possible. 

Digestive disturbances, which by accumulation of gas may disturb the action 
of the heart, must be prevented by the institution of an easily digested and simple 
diet, small quantities of food being taken often so as to avoid overloading the 
stomach. If there is a tendency to an accumulation of gas in the bowel salol 
may be given as an intestinal antiseptic, or in its place a capsule of taka-diastase, 
pancreatin, mix vomica, and capsicum, which is recommended in the article on 
Angina Pectoris, may be administered. Some of these patients seem to be greatly 
benefited by the use of gentle massage every day or every other day, with the 
object of aiding in the circulation of the juices of the body. Great care should be 
taken that the massage is not so vigorous that the patient is fatigued by it. Strych- 
nine in the dose of ^V °f a grain three or four times a day is often exceedingly 
beneficial to these patients, particularly if there is any tendency to shortness of 
breath on lying down. 

In many instances when the heart is feeble as the result of fibroid changes in its 
muscle, or when the patient is convalescing from some disease like influenza, which 
seriously impairs the functional activity of this organ, excellent results are some- 
times obtained by the institution of what is known as the Nauheim baths, which 
were originally brought before the profession by Schott, of Nauheim in Germany. 
These baths are composed of water which is charged by nature with large quantities 
of carbonic acid gas. The water is also naturally warm. The patient is immersed 
in a bathtub, and immediately there is attached to the surface of his skin myriads 
of tiny bubbles of carbonic acid gas, which as they break produce a slight tingling 
sensation and exercise a stimulant influence upon the peripheral capillaries, as the 
result of which these capillaries are dilated and dermal hyperemia is induced. 
In this manner the circulation is equalized, internal congestions are overcome, and 
the heart finds it easier to pump blood through the dilated superficial capillaries 
than under ordinary conditions. Not infrequently when the patient first enters 
the bath a primary contraction of the peripheral capillaries ensues, and this results 
in a momentary increase in the work of the heart, so that the patient for a time 
feels somewhat oppressed. Usually he remains in the tub for ten or fifteen minutes, 
but this period is governed by the physician who superintends the use of the baths. 
On his removal from the bath the patient is carefully dried by an attendant and 
has absolute rest, for one or two hours. After the baths have been used for some 
time additional salt is added to the bath, and water containing larger quantities 
of gas is employed. In addition to these baths the patients are subjected to gentle 
resistance movements and massage so as to improve the circulation of blood and 
lymph in the muscles. Great care must be taken that these movements are not 
sufficient to tire the heart. When valvular disease is very marked, these baths 
are contra-indicated. 

The Nauheim baths are also contra-indicated in cases of advanced arteriosclerosis, 



CARDIAC ANEURYSM 



453 



and in chronic Blight's disease if it is well developed, although if the renal difficulty 
is largely due to congestion this plan of treatment is advantageous. Aneurysm 
also contra-indicates them, and bronchial asthma and chronic bronchitis contra- 
indicate them, or at least require great caution in their use. Cases of pulmonary 
tuberculosis with cardiac disease also should not be subjected to this method, nor 
should patients who are suffering from far-advanced degeneration of the heart 
muscle receive it. These baths should never be taken except under the care of a" 
local physician. 

It is important to note that the resistance exercises, which are carried out in 
connection with this plan of treatment, are probably equally beneficial, if not 
more beneficial, than the baths themselves. They consist in having the patient 
extend and flex his joints against the resistance offered by the attendant. 



CARDIAC ANEURYSM. 



Fig. 83 



Aneurysm of the heart may occur in one of three forms, viz., aneurysm of the 
heart walls, aneurysm of the valves, and aneurysm of the coronary arteries. An- 
eurysm of the cardiac walls consists in a localized 
dilatation or pouching of the wall, and is to be 
separated from dilatation of the heart, to which 
the term aneurysm is sometimes applied by French 
writers. The aneurysm usually affects the ventric- 
ular wall. Hall has collected 112 cases, in which 
the site of the aneurysm was as follows : left ven- 
tricle, 92 cases; right ventricle, 1 case; left auricle, 
2 cases; ventricular septum — (a) muscular part, 
8 cases; (6) membranous part, 7 cases; auricular 
septum, 2 cases. 

The left ventricle is therefore affected more 
commonly than all of the other chambers com- 
bined. The aneurysm is usually near the apex 
of the ventricle or in the anterior wall, just above 
the apex; 67 of Hall's cases were so situated. 

The condition, as one would naturally expect, is 
found more frequently in males. In the relative 
frequency in the two sexes, Thurnam's, Legg's, 
and Hall's and my own statistics show a remark- 
able resemblance. Of Thurnam's 40 cases, 30 
were males, 10 females; of Legg's 88 cases, 64 
were males, 24 females; and of 80 cases collected 
by me, 59 males, 21 females. In a total of 208 
cases, 74 per cent, were males, and 26 per cent, 
females. 

Aneurysm of the heart is a sequel of the sec- 
ondary myocardial changes already described. 
Thus the fibrous tissue which replaces the tissues 
which have undergone necrotic change may grad- 
ually yield before the blood pressure in the ventri- 
cle and form a sac, which is a true aneurysmal dilatation. This sac may communi- 
cate with the ventricle by a small opening. In other cases the ventricular wall at this 
point yields, so that the opening may be the full width of the sac. As in aneurysm 
of the bloodvessels, the wall of the sac is composed of several layers made up of 
the visceral layer of the pericardium, and perhaps of the parietal layer as well, 




Front view of heart, showing aneu- 
rysm of left apex of ventricle, which 
has perforated into the pericardium. 
The swelling of the aneurysm is visible 
externally, and the heart wall at the 
apex is no thicker than brown paper. 
No pericardial adhesion. The inter- 
ventricular branch of the left coro- 
nary artery is dissected out, and is 
very atheromatous, and at the upper 
end of the groove is completely 
blocked by a thrombus, which extends 
downward for two and one-half inches. 
(From a specimen in Dr. Littlejohn's 
Museum.) 



454 DISEASES OF THE HEART 

if it has become adherent. Under this is the fibrous tissue, and beneath this again 
forming the inner layer is the endocardium. Rarely several sacs are present. 

Three conditions may develop in such sacs. They may give way under pressure, 
causing sudden death, they may become filled with a clot, or their walls may be 
calcified.' Sometimes an aneurysm of this sort forms in the septum and ruptures 
into the right ventricle. 

In some cases the aneurysm may be due to fatty degeneration, without primary 
vascular disease. A softened spot in the heart muscle may bulge under strain, 
and rupture may occur before any real sac is formed. This is commonly called 
rupture of the heart, and usually involves the anterior wall of the left ventricle 
near the septum; but it may affect any part of the walls of the cardiac cavities. 

Death by rupture of the sac does not occur as frequently as would be imagined, 
and in this respect cardiac aneurysm resembles aortic aneurysm. Out of 60 cases 
collected by Legg, only 6 died by rupture. 

Aneurysms of the cardiac septa are so rare as to be curiosities. Hall states that 
only 2 cases have been reported in twenty years. 

An aneurysm of a valve is sometimes formed as a result of endocarditis. This 
condition usually affects the aortic and mitral leaflets with about equal frequency. 
One leaflet is contracted or destroyed and another leaflet then yields or sags, partly 
because of deficient support, forming a pocket or sac which projects into the left 
ventricle. Sometimes this sac ruptures, and so the valve becomes perforated. 
In other instances the entire valve becomes sacculated. 

Although atheroma of the coronary arteries is a very frequent lesion, aneurysm 
of these vessels is exceedingly rare. Hall could find only 25 recorded cases, of 
which 17 were in males. 

Symptoms. — The symptoms of cardiac aneurysm are not definite at any time, 
and, unless the sac is large, there may be none. Hall tells us that out of 76 cases 
an antemortem diagnosis was made only once. When the sac is large it may cause 
a marked increase in the area of cardiac dulness near the apex, and produce distinct 
pressure symptoms. A skiagraph may give valuable information of the lesion. 

WOUNDS OF THE HEART. 

Wounds of the heart are by no means uncommon, as the result of shooting or 
stabbing. Cases of recovery after both of these forms of trauma are recorded in 
considerable number. The stab wounds probably recover in greater number than 
those which suffer from bullet wounds. Death is usually due not to the direct 
injury of the heart, but to the fact that the pericardial sac soon becomes filled 
with blood, and the heart is unable to expand. In other words, even severe injury 
to the heart is not fatal unless the hemorrhage be free, or the organ is damaged 
in some vital spot, as in His's atrioventricular bundle. I proved these facts in a 
research carried out on dogs many years ago, and a number of surgeons have now 
reported cases in which a stab wound of the heart has been exposed and sutured, and 
recovery has ensued. Further than this, I have seen the heart punctured and blood 
aspirated from its cavities without injury to the patient. 

Gibbon and Stewart, of the Jefferson College Hospital staff and others, have 
reported interesting cases in which cardiac wounds were stitched with success. 

ENDOCARDITIS. 

Definition. — Endocarditis in an inflammation of the lining membrane of the 
heart, the endocardium. In the great majority of instances it chiefly affects the 
endocardium where it covers the valves (valvular endocarditis), and rarely it 
involves that part which covers the walls of the cavities (mural endocarditis). 



ENDOCARDITIS 455 

A distinction should also be drawn between the acute and chronic form of the 
disease and between the acute simple, or benign, form, and the so-called acute 
malignant, or ulcerative type. It is proper to state, however, that many persons 
deny the correctness of this division, and regard the two conditions as different 
stages or degrees of the same process. Finally, it is to be recalled that there are 
two types of chronic endocarditis, namely, that which is the result of the acute 
variety due to bacterial infection and that which arises in association with chronic 
arteriocapillary fibrosis and atheroma, which is a slow, retractile form of the disease. 

Acute Endocarditis. — Synonyms: Simple Endocarditis, Benign Endocarditis, Papil- 
lary Endocarditis. 

Etiology. — Virchow in 1855 advanced the view that the vegetations on the cardiac 
valves in septicemia were the result of this state and 1869 Freiberg isolated organ- 
isms in vegetations. The bacterial origin of endocarditis is now generally admitted, 
but all efforts to identify any particular organism as the specific cause have proved 
fruitless. Many organisms have been identified in the vegetations. Of these 
should be mentioned those found in acute rheumatism, pneumococci, streptococci, 
gonococci, and staphylococci, and, less frequently, the colon bacillus, typhoid 
bacillus, influenza bacillus, tubercle bacillus, and a number of other bacteria. The 
greater number are due to cocci. 

In the article on Acute Articular Rheumatism attention has already been called 
to the frequency with which this condition complicates that malady. So constant 
is this lesion during the course of acute articular rheumatism that it may be regarded 
as the condition next in constancy to the inflammation about the joints. It is 
probable that in all cases of acute rheumatism a slight endocarditis is present, 
but it may be so slight that no physical signs of its existence can be elicited. 

In children suffering from acute rheumatism the involvement of the endocardium 
is far more frequent than it is in adults. Thus, it is generally considered that from 
60 to 80 per cent, of children who have acute rheumatism develop endocarditis; 
whereas, the percentage usually accepted for adults is about 21 per cent. Eighty 
per cent, is possibly too high, and 21 per cent, is certainly too low an estimate. 
It is especially important to bear in mind that mild articular symptoms are not 
rarely accompanied by severe cardiac lesions, although, as a rule, the severity of 
the articular symptoms and the severity of the heart lesions go hand in hand. The 
first attack of rheumatic fever is more frequently the cause of cardiac lesions than 
subsequent attacks, and the signs of endocardial inflammation usually develop 
during the first ten days of the illness, although in rare cases a murmur may be 
heard before any arthritic signs develop. 

When acute rheumatism causes endocarditis, it commonly affects the mitral 
valve. The aortic leaflets are comparatively rarely affected, and the valves on 
the right side of the heart only in very rare instances. 

Next to acute rheumatism as a cause of acute endocarditis must be noted its 
association with chorea, in which disease, in its well-developed and typical forms, 
lesions of the lining membrane of the heart are very often present. The occurrence 
of endocardial disease in chorea is in direct proportion to the severity of the disease, 
but it is difficult to decide how frequently true endocarditis is actually present, 
because many choreic patients present on auscultation functional murmurs in the 
heart which disappear so rapidly that it is inconceivable that they could have 
been organic in origin. Again, so few cases of chorea come to autopsy during or 
immediately after the attack that it is impossible to study the exact state of the 
endocardium. If the various statistics of frequency of heart murmurs are added 
together, we find that these sounds occur in about 31 per cent, of cases of chorea. 

In a very considerable proportion of cases endocardial infection takes place 
during acute tonsillitis. Another cause of endocarditis is gonorrhea, which causes 
the ulcerative type of the disease more commonly than the benign form. Scarlet 



456 



DISEASES OF THE HEART 



fever may also be a causative factor, but whether this is due to direct infection of 
the endocardium by the micro-organism which causes scarlet fever or by its toxins, 
or results from the mixed infection so frequent in this disease, is not known. Rarely 
endocarditis is apparently due to tuberculosis, for this bacillus has been found in 
the valve lesions. Traumatic forms and endocarditis due to syphilis have been 
described. Occasionally acute endocarditis develops as a result of an exacerbation 
of the chronic form of the disease. 

Endocarditis has been reported as present in the fetus as a result of the infection 
of the blood through the placenta. In this period of existence the pulmonary 
valves are the parts affected. 

Fig. 84 




2 cm., 



Heart, acute endocarditis. The lesion on the aortic leaflets is verrucose and at points ulcerating. On 
the lateral ventricular aspect of the mitral valves are a number of vegetations, although the contact 
line and auricular surfaces of this valve were not involved. The vegetations on the ventricular surface 
probably resulted from inoculation by projecting vegetations situated on the aortic leaflet. It is to be 
remembered that endocarditis affects the mitral valves more commonly than the aortic valves. 



Pathology and Morbid Anatomy. — The degree of inflammation in the endocardium 
covering the cardiac valves varies greatly in different cases. Its frequency on 
the left side, particularly in the mitral valves, is due principally to the greater 
stress to which these leaflets are subjected and also to the higher oxygen content 
of the arterial blood. The lesions develop in the auricular aspect of the mitral 
leaflets and the ventricular side of the aortic valves; this distribution depends upon 
the friction and impact of the blood, and the same factors determine the distribution 
of the vegetations -along the lines of greatest pressure, where the leaflets impinge 
one upon another when closed. 

The earliest lesions are rarely seen, because death seldom occurs at this time. 
The affected area is clouded and the valves slightly swollen, due to cellular infiltra- 
tion and edema. In this softened condition the impact of one valve upon another 
roughens the surface along the line of contact, and there is deposited at this point 
blood platelets, leukocytes, and fibrin, the quantity of each varying at different 



ENDOCARDITIS 457 

stages and in different cases. This deposit on the leaflet, tendon, or muscle is at 
first microscopic, but by accretion may attain relatively massive proportions, and 
constitutes what is called a vegetation; essentially it is a thrombus. Often a row 
of these wart-like bodies is festooned along the line of contact or projects into the 
blood stream. Their disturbance of the blood current by obstruction and by 
rendering accurate coaptation of the opposed leaflets impossible, and thereby 
permitting regurgitation, causes a murmur the recognition of which is necessary 
for accurate diagnosis during life. 

Once formed, these vegetations are subject to important changes. They may 
be detached and swept off into the circulation, or they may soften and possibly 
be absorbed. (See Complications of Ulcerative Endocarditis.) Adhesions between 
leaflets may occur, but commonly the vegetations organize and permanently 
alter the contour, flexibility, and elasticity of the valves, thereby interfering with 
their proper functions. Finally, calcifying deposits may further add rigidity to the 
already damaged leaflets. In favorable cases the valve surface becomes smooth, 
but little thickening results, and function is more or less fully restored. 

Acute endocarditis ends in one of three ways: 1. The acute inflammation may 
subside and leave little or no alteration behind it. 2. The vegetations may persist 
and form large masses of an almost nodular character upon valves. 3. The valves 
become eroded or adherent, or cicatricial contractions may lead to distortions and 
consequent immediate insufficiency or obstruction. 

Symptoms. — In distinction from physical signs, there are no symptoms of ordinary 
acute endocarditis of the benign form. It is true that the pulse may be a little 
quicker than before the endocardium was affected and the fever a little higher, but 
neither of these symptoms is constant or characteristic. Some palpitation may 
be present, but so frequently are all symptoms absent that all too frequently the 
physician who is not careful fails to discover endocardial disease until the patient 
begins to move about and complains of cardiac weakness or dyspnea, and then the 
damage is done and is almost irreparable. Even the presence, on physical examina- 
tion, of a murmur over the mitral or aortic area does not prove the presence of 
endocarditis, because it not infrequently happens that a murmur due to anemia 
or to relaxation of the orifice is present. The presence of the murmur, while not 
pathognomonic of acute endocarditis, is, however, sufficient ground for the physician 
to treat his patient as a case with this lesion. 

Complications. — These consist most commonly of pericarditis and embolism 
of one of the cerebral or pulmonary arteries. Rarely acute cardiac dilatation 
ensues, and sometimes in infectious cases pneumonia and pleuritis develop. 

Diagnosis. — Care must be taken, as just stated, that anemic murmurs, murmurs 
due to relaxation of the orifices, and pericardial friction sounds are not mistaken 
for those due to endocardial disease. (See Valvular Disease.) 

Prognosis. — Death is very rarely due to acute simple endocarditis in the sense 
that death comes during the acute stage of the disease. All too frequently it 
follows as a consequence of the changes produced in the valves and heart muscle 
months or years after the acute stage has passed. A bad prognosis can always 
be given if the physician does not strenuously insist upon the patient resting in 
bed for several weeks after all articular and valvular signs have ceased. The 
process may affect not only the valves but the heart muscle to such an extent 
as to cause death during the acute illness. In children the mortality is about 
20 per cent. Ill-health and death may not come until years afterward, as time 
and chronic disease weakens the valves and heart muscle. Fifty per cent, of 
children who develop acute endocarditis and survive the acute attack succumb 
in the next ten years, but if they survive puberty the mortality, according to 
Dunn is about 7 per cent. In other words, such a patient has far better chances 
than an adult who develops acute endocarditis, because the growth and reparative 



458 DISEASES OF THE HEART 

power of the surviving child compensates thoroughly for the lesion. Indeed 
many of these patients lead long and active lives. 

Treatment. — To prevent endocarditis in the course of all infectious diseases, 
and particularly in acute rheumatism, the physician must insist on absolute rest 
in bed all through the illness and for some time after the attack has passed. The 
diet should be light and easily digested, and at no time should the digestive appar- 
atus be overburdened, for active and prolonged digestion tires the heart. If 
acute rheumatism is present, the salicylates should be used freely at once, not that 
they protect the valves directly, but they shorten the illness and so diminish the 
chance of involvement of the endocardium. Over the precordium, as a preventive 
of endocarditis and pericarditis, should be placed six or eight flying blisters, and 
alkaline diuretics, like citrate of potassium, should be freely used. An ice-bag 
may be placed over the heart if it is very irritable, and tincture of aconite may be 
given for the same purpose. After the endocardial symptoms have developed, 
rest of the most absolute character is the only useful plan of treatment. During 
convalescence weeks of rest is again the sine qua non. For the anemia often present 
iron and arsenic are useful, as is also cod-liver oil. Subsequent cardiac feebleness 
is to be treated by small doses of digitalis, as 3 to 5 drops of the tincture with 10 
drops of tincture of mix vomica three times a day and 2 drops of Fowler's solution. 

Ulcerative Endocarditis. — Definition. — Ulcerative endocarditis is a state in which 
the endocardium is ulcerated, vegetations are present, and there is an actual loss 
of substance in the valvular tissues, so that a valve or even a septum may be per- 
forated. A French physician, Bouillaud, first recognized this cardiac state with its 
associated signs of pyemia, but Kirkes, of England, first emphasized the fact that 
the heart was the seat of the difficulty, and that the symptoms arose from its 
condition. Since this time a host of pathologists, including Virchow, Wilks, 
Murchison, Charcot, Vulpian, and Birch-Hirschfeld in Europe, and Osier while 
in this country, have studied this malady. It is important to remember that 
ulcerative endocarditis occurs in an acute and chronic form. 

Etiology. — The disease is always due to microbic infection of the endocardium. 
It may be due to a secondary infection, during the course of one of the acute infec- 
tious diseases like typhoid fever, scarlet fever, pneumonia, or tonsillitis, or it more 
rarely arises as a primary lesion. The organisms are usually the Staphylococcus 
pyogenes aureus, the Streptococcus pyogenes, and the Pneumococcus, the Bacillus 
typhosus, the Gonococcus, the Bacillus coli communis. Acute endocarditis due 
to the meningococcus of Weichselbaum is very rare. A number of cases have been 
reported in which the meningococcus has been found in the circulating blood: one 
by Gwyn in 1889, another by Salomon in 1902, and a third by Warfield and Walker 
in 1903. The last of these is the only one in which the meningococcus was demon- 
strated to be the cause of the endocarditis. Any damage, new or old, to the surface 
of a valve predisposes that part to infection. In its subacute form this type of 
endocarditis has been proved by Schottmiiller, Libman and others to be very 
often due to the Streptococcus viridans which receives its name because in culture 
it produces a distinct green pigment. (See below.) 

Pathology and Morbid Anatomy. — Anatomically, the ulcerative form may be 
but a later stage of the acute simple type, and many cases occur in which no sharp 
line of demarcation can be drawn. Not infrequently it is engrafted upon an old 
or chronic valvular lesion, and patients having such lesions should be watched 
closely during an attack of any infectious disease associated with the constant or 
frequent occurrence of bacteremia. The infective process in the ulcerative type 
leads to necrosis of the already formed or forming vegetations, and even of the 
affected leaflet or adjacent myocardium. The fragments thrown into the circula- 
tion cause infarction and metastatic lesions in many tissues, especially in the spleen, 
kidneys, and brain. Marrow lesions, joint complications, and other manifestations 



ENDOCARDITIS 459 

of septicopyemia are often conspicuous. Whether the secondary processes be 
suppurative or not depends upon the character of the infecting organism. When 
involving the valves of the right heart (as it does more commonly than the acute 
simple form), pulmonary complications may be conspicuous, which, taken with 
the fact that it may be a sequence or complication of pneumonia, further tends to 
obscure the seat of the primary lesion. Occasionally the almost symptomless 
progress of the malady is due to the low virulence of the infecting organism, while 
intensely toxicogenic bacteria reverse the picture and cause evidences of severe 
infection and toxemia to be manifest. 

Symptoms. — The objective symptoms of ulcerative endocarditis may be no 
more marked than those of the simple form. Fever may not occur. If the disease 
develops during the course of one of the acute infectious diseases or as a result of 
septicemia, its existence may not be suspected. If it develops primarily the 
physician who does not carefully study the heart may believe that the fever in 
its acute period of rise and fall is the manifestation of one of the ordinary acute 
infectious diseases or he may suspect sepsis, typhoid fever, or malaria. Because 
of these symptoms, the disease may be divided into the septic form, the typhoid 
form, and the malarial form. A cerebral form also exists. 

In the septic form the patient presents the ordinary signs of septicemia. Chill 
after chill develops, and between the chills high fever and sweats are present. 
The patient looks profoundly septic, the tongue is dry, the eyes sunken, and petechia? 
may be present in the skin. The marked anemia is very noteworthy, and its 
severity is diagnostic. Leukocytosis is present if the infection is not exceedingly 
severe. Multiple metastatic abscesses may be found. The heart may or may 
not produce a murmur, but its action is hurried and feeble. 

The typhoid type is closely allied to that just described. The dry tongue, the 
subsultus, the tympanites, the diarrhea, the mental stupor, the swollen spleen, 
and the remitting fever may all present so typical a picture of a case of typhoid 
fever that only the constant recollection that such symptoms may be due to ulcera- 
tive endocarditis will save the physician from an error in diagnosis. Even epistaxis 
may develop. 

In the malarial type the constant recurrence of moderate chills, moderate fever, 
anemia, and some sweating may be very misleading. 

In the cerebral form there is severe headache, unconsciousness, and convulsions 
due to an associated meningitis. In some instances the simultaneous development 
of septic arthritis makes the case resemble acute rheumatism. Burrows has 
reported a case in which vomiting and purging were so severe that he believed the 
patient to be suffering from homicidal poisoning. 

Cases are recorded in which the splenic enlargement was so great that the patient 
was thought to be suffering from splenomedullary leukemia. In other cases the 
diagnosis of acute tuberculosis has been made. 

Albuminuria and hematuria are common symptoms, but renal infarction may 
take place without either albumin or blood being found in the urine. 

Endocardial murmurs are not always present. They are shifting in time and 
in character and may be found one day and be lost the next. Further, it sometimes 
happens that the murmurs change in character from day to day, owing to the 
progressive character of the lesions. When murmurs exist they are more frequently 
due to old lesions than to the new ones produced by the acute infection. 

In that type due to streptococcus viridans the symptoms are insidious in onset 
with joint pains and aches, like those of influenza, with albuminuria, and sometimes 
vomiting and diarrhea. Because of its slow course it is called endocarditis lenta. 
It is nearly always fatal in from a few weeks to several months. The kidneys 
suffer gravely from small septic emboli. Although the spleen is enlarged and 
petechia? may appear blood cultures are usually sterile. 



460 DISEASES OF THE HEART 

Complications. — The complications of ulcerative endocarditis are many and 
serious. It not infrequently happens that a septic embolus not only plugs an 
important vessel, and so causes an infarct in such organs as the kidney, the lung, 
and the spleen, but it acts as a focus of septic development. Such embolic closure 
frequently occurs in the branches of the left middle cerebral artery, and causes 
temporary or permanent aphasia or hemiplegia. Lesions of the cranial nerves occur. 
Peripheral vessels, such as the popliteal or brachial or lingual arteries, may also 
be affected. Occasionally violent abdominal pain, followed by -bloody stools and 
signs of collapse, indicates that embolism of the mesenteric vessels has taken place. 
Sometimes uremia, due to the septic nephritis which is present, ends the patient's 
life. Septic foci in the skin and lymph nodes may develop. 

Diagnosis. — The points of value in diagnosis are the suddenness of onset in some 
cases, the up-and-down temperature waves, which form steep curves on the charts, 
the repeated rigors, the presence of distinct leukocytosis, the presence of pyogenic 
organisms in the blood, the absence of the malarial organism and of the Widal 
reaction, and, finally, the presence of great feebleness and irregularity of the heart's 
action. In some cases, however, the diagnosis from physical signs may be practi- 
cally impossible. 

Prognosis. — It is hardly necessary to state that the prognosis is most grave. 
Recovery rarely occurs, and death may take place in the first two weeks or earlier. 
Sometimes life is preserved for weeks. The duration depends largely upon the 
character of the infection, the condition of the heart and of its valves, and the 
occurrence of complications. Some cases extend over a period of several months, 
and most of them last for several weeks. That healing may take place and recovery 
occur in cases of true ulcerative endocarditis is proved by a large number of cases 
now on record, in which the condition has been proved by subsequent autopsies 
to have existed, the patient dying of another malady. 

Treatment. — The treatment of ulcerative endocarditis is not very satisfactory. 
Antistreptococcic serum may be of benefit in a few cases, provided that the strep- 
tococcus is the cause of the disease, and provided that the variety of streptococcus 
used in the preparation of the serum is the same as that present in the heart. Aside 
from this specific treatment, the only thing to do is to support the system by the 
wise use of tonics, such as tincture of the chloride of iron and the tonic bitters. 
Full doses of quinine may be used. The most important function of the physician 
is to maintain nutrition by the use of good food and to order no drugs which, by 
disordering digestion, will interfere with the digestive and assimilative functions. 

Chronic Endocarditis. — As already stated, chronic endocarditis is frequently 
a sequence of one of the acute forms just described, and, therefore, as a rule, it 
affects the left side of the heart and the mitral leaflets oftener than the aortic 
valves. In some instances, however, it depends upon alcoholism, gout, and syphilis, 
in which case associated changes in the heart muscle and bloodvessels are also 
found. Libman has now studied 125 cases of what he designates subacute bacterial 
endocarditis, 21 of them in the bacteria-free stage. The iive clinical features of 
this stage are: (1) Marked progressive anemia; (2) brown pigmentation of the 
face; (3) marked evidence of renal disease; (4) marked enlargement of the spleen; 
(5) endocarditic symptoms, as periodic elevation of temperature, petechia?, occa- 
sional joint symptoms, and embolisms. A slowly progressing valvulitis or sclerosis 
of the valves, which comes on insidiously, is frequently associated with arterio- 
sclerosis (arteriosclerotic endocarditis) , with chronic renal disease, chronic metallic 
poisoning, especially that due to lead, and other conditions associated with high 
arterial tension, with or without the presence in the blood of some specific irritant 
to which the changes may be ascribed. As the acute inflammatory process merges 
into the chronic form, one or two changes appear in the endocardium. There is 
an overproduction of connective tissue in the endocardium, with thickening, stiffen- 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 461 

ing, and lessened elasticity, which chiefly affects the valvular leaflets. Following 
this condition, as a result of further degenerative changes, we find contractions 
or localized yieldings of the valves which produce an unevenness of their surfaces, 
so that their edges can no longer be accurately approximated; nor do they permit 
the free flow of blood through the orifice which they guard, since they are unable 
to yield during the period at which a free flow of blood should normally take place. 
Even when the valves are thickened and distorted they may still be adequately 
covered by endothelium, but in some instances the endothelium may be absent, 
thereby exposing calcareous and roughened surfaces upon which fibrin is sometimes 
deposited. The chief factors in producing cardiac failure in chronic endocarditis 
are irregular contractions which distort the valves, causing their edges to become 
everted, inverted, or curled up. In addition the chordae tendinese which control 
the valves guarding the auriculoventricular orifices become shortened and thickened 
so that they interfere with the free movement of the valves. (See Diseases of the 
Myocardium.) 

In that form of the disease in which mural endocarditis is present, patches of 
sclerosis or cicatrices may be seen over the walls of the ventricles. (See Chronic 
Valvular Disease.) 

CHRONIC VALVULAR DISEASE AS A RESULT OF CHRONIC 

ENDOCARDITIS. 

Chronic valvular disease of the heart is very constantly met with in medical 
practice, and its frequency is, as a rule, in direct proportion to the age of the patient 
examined. This is due to the sclerotic changes which are prone to take place in 
the valves as age advances, and to the fact that in those who have passed the period 
of middle life the heart in all its parts is unable to withstand the strains, which 
may come to it, as well as in earlier periods. The chief causes of valvular lesions 
may be placed in three divisions, namely: (1) those due to infectious diseases, 
particularly rheumatism, which may leave behind damage which only becomes 
apparent when age or some unusual strain weakens the heart muscle; (2) fibroid 
or sclerotic changes ensuing as a result of age, gout, syphilis, and alcoholism; .(3) 
definite myocardial degeneration and dilatation which does not cause direct but 
indirect valvular failure in function, as described elsewhere. (See Relative In- 
sufficiency.) 

Experience in the larger London hospitals, some twenty-five years ago, led me 
to believe that cardiac valvular disease was much more common in England than 
in America. It is interesting to note, however, that this view was incorrect, for out 
of 59,762 medical cases which are recorded in hospitals in London, there were 
3059 cases of valvular heart disease, or a percentage of 5.1 ; and out of 91,985 medical 
cases in hospitals in different cities in the United States, there were 4108 cases of 
valvular disease, or a percentage of 4.4. The actual difference in frequency in 
England and America is, therefore, not very marked, not only as regards endocar- 
ditis, but acute rheumatism as well. (See Acute Rheumatism.) 

Valves Affected. — Series of statistics differ somewhat as to the relative fre- 
quency with which different valves are affected. One difficulty is that there has 
never been a sufficiently large collection of statistics to give results free from error. 
Another difficulty lies in the differentiation of true and false aortic stenosis; for 
it is evident that certain statistics which give a large percentage of this lesion 
include cases in which there is not true simple stenosis (which is quite rare without 
regurgitation) but cases in which atheroma and aortic roughening cause a systolic 
aortic murmur. 

All clinicians and pathologists are in accord in stating that mitral regurgitation 
is the most common lesion by long odds. Jiirgensen has analyzed 2470 cases of 



462 DISEASES OF THE HEART 

valvular cardiac disease, with the following results as to the relative frequency 
with which valvular disease occurs: mitral disease, 1616; aortic disease, 457; 
pulmonary valvular disease, 56; tricuspid disease, 10; associated aortic and mitral 
disease, 224; associated mitral and tricuspid disease, 45; lesions at the mitral, 
aortic, and tricuspid valves, 24; and at the aortic and tricuspid valves, 2. Unfor- 
tunately he does not state what the lesions are — i. e., regurgitant or stenotic. 
It is an open question, too, how many of the cases of so-called mitral disease and 
tricuspid disease were secondary murmurs due to dilatation of those orifices and 
not to true valvular defects. 

Some years ago, T. G. Ashton, my then chief of clinic at the Jefferson Hospital, 
made an analysis of 1024 cases of valvular disease met with in life insurance exami- 
nations. His results showed that of these 557 were cases of mitral regurgitation, 
136 were aortic stenosis, 47 were aortic regurgitation, 32 were mitral stenosis, and 
11 tricuspid regurgitation. I believe that these statistics, while accurate in them- 
selves, are to some extent misleading, and that the proportion of cases of aortic 
stenosis is too high and mitral stenosis too low. (See article on Aortic Stenosis.) 
The figures obtained by the analysis of 908 cases of valvular heart disease treated 
in Westminster Hospital, London, show that the most common single lesions are 
mitral regurgitation, mitral stenosis, aortic regurgitation, and aortic stenosis, 1 in 
order of arrangement, and that of double lesions at one orifice the relative fre- 
quency is double aortic, double mitral, double pulmonary, and double aortic with 
double mitral. Mitral regurgitation quite frequently occurs as the result of aortic 
regurgitation, through dilatation of the mitral orifice. 

Mitral disease affects more women than men; aortic disease more men than 
women. 

Aortic regurgitation is the most fatal lesion. Mitral stenosis ranks second in 
fatality, aortic stenosis third, and mitral regurgitation fourth. The mortality 
of double aortic lesions is greater than that of double mitral. 

The statistics of A. Lockhart Gillespie, based on a study of 1914 cases treated 
in the Edinburgh Royal Infirmary, are especially interesting in that they show 
the mortality of valvular lesions in the two sexes according to age. Gillespie 
found that the maximum mortality in males with aortic incompetence or stenosis 
occurs between the age of fifty and sixty-nine, but in those with double lesions 
the years from twenty-nine are those with the highest mortality. The female 
maximum mortality in aortic incompetence and aortic stenosis falls between the 
years of forty-nine and fifty. Mitral stenosis proves most fatal at from thirty 
to thirty-nine years in males, and from forty to forty-nine in females. The death 
rate in females between twenty and twenty-nine, forty and forty-nine, and sixty and 
sixty-nine is higher than in males at similar periods. The death rate in mitral 
incompetence in both sexes rises progressively with the age. In cases of double 
mitral lesion, the male maximum mortality falls between thirty and forty-nine, 
and in the female between fifty and sixty-nine. 

Before proceeding to a consideration of the various valvular lesions it is essential 
that the mechanism of the valves in health and disease be clearly understood (Fig. 
85). The cardiac valves are arranged in such a way that they prevent a reflux 
of blood into that cavity which the blood has just left in the progress of the normal 
circulation. As a rule, these valves are capable of fitting together so tightly that 
they completely arid effectively close the orifice which they guard, but even without 
the presence of any condition of disease they may at times give way, and permit 
some reflux. The moderate reflux occurring during great muscular strain may be 
regarded as a physiological attempt to relieve the blood pressure in the cardiac 
cavities, and if it is not maintained for too great a length of time it does no harm. 

1 This probably refers to true stenosis and not to cases in which only the aortic systolic murmur was 
present. (See Aortic Stenosis.) 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 463 



Fig 



It must also be recalled that there are at least two ways in which the cardiac 
valves may become incompetent to prevent reflux of blood. In the first, and by 
far the most common type, the valves are diseased, as already described in the 
article on Endocarditis, so that they cannot become closely approximated, or they 
are glued together in such a way that the same result is achieved, and so they 
also obstruct the flow of blood. In the second type the rings, which form the bases 
of the valves and the margins of the orifices, yield, and as they relax the orifice 
becomes too large to be closed by the valves, which may still be practically normal 
in themselves. This condition exists for a brief space of time in acute cardiac 
strain, as just stated. It persists for a long time or becomes permanent in instances 
where the heart is feeble and the strain is 
very severe or prolonged, and it is frequently 
found in cases of dilatation and feebleness of 
the heart muscle. 

Those forms of valvular incompetence 
which occur in athletes or others after 
severe exertion can therefore be put aside 
as beyond the scope of these particular 
pages, although they will again be discussed 
under the head of Functional Disorders of 
the heart. 

In those cases in which the valve becomes 
incompetent to close an orifice, and so per- 
mits regurgitation to take place, the failure 
of the valve is so gradual, as a rule, that 
there develops simultaneously an increase in 
the size and strength of the heart muscle, so 
that it may by increased power and activity 
compensate for the leakage which occurs. 
As a result it very frequently happens that 
this compensatory hypertrophy is fully equal 
to the increased demands made on the heart 
muscle, and not until the occurrence of a 
severe illness, or until advancing years im- 
pairs the power of its fibres, are any mani- 
festations of valvular lesions to be found in 
the patient, save the physical signs of 
hypertrophy and the murmur caused by 
the regurgitating blood. Sometimes even 
the murmur may disappear for a time. 

In cases in which a valve is ruptured or 
severely damaged by disease so that it fails in its function before the heart can 
undergo compensatory hypertrophy, we often see signs of great circulatory em- 
barrassment from the very first part of the illness. 

In all cases of valvular disease in their early stages much depends upon the 
inherent strength of the heart muscle and its ability to increase in power, and there- 
fore it is evident that it is of vital importance for the patient to rest at this period 
in order that the strength of the heart may be conserved, and in order that it may 
not be subjected to a severe strain with associated dilatation at the most critical 
period of its existence. This is the more important because diseases which second- 
arily infect the valves usually impair, to some extent at least, the myocardium as 
well. 

In health, when the valves are intact, the heart always possesses a considerable 
degree of reserve energy and power, using only a small part of its store of energy 




Diagram modified from Page to show the 
relation of the various valves. A study of 
this diagram will render clear the time of 
the various cardiac murmurs. Thus in 
mitral regurgitation the blood passes back 
from the left ventricle to the left auricle dur- 
ing systole, and is dammed up in the pulmo- 
nary veins, the openings of which are seen in 
the auricular wall, producing pressure on 
the pulmonary valves, the sounds of which 
are thereby accentuated. 



464 



DISEASES OF THE HEART 



in a day's work. As a consequence a healthy man can run a considerable distance, 
or leave his desk and go hunting, without engendering anything more than fatigue 
of his voluntary muscles and some healthy cardiac tire. This reserve energy is 
kept for just such purposes. On the other hand, if a man who is a sufferer from 
valvular or myocardial disease, even if he is seemingly in perfect health, attempts 
to follow the first one, he soon begins to suffer from cardiac embarrassment, and 
if he persists may become very gravely ill from acute cardiac failure, and rupture 
his compensation by excessive exercise to such an extent that he may be bedridden 
for the rest of his days. In the latter instance nearly all his reserve energy is 
being used daily in the maintenance of a normal circulation and, having little 
reserve, he cannot undertake feats that demand great calls upon his reserve. This 
is illustrated in the following squares: 





All Energy 

In Constant 

Use. 



In health, large reserve. 



In disease, small reserve. 



Far-advanced disease, 
no reserve. 



In the last square it is seen that all the reserve is in constant use, and, therefore, 
if any extra exertion is made, the heart promptly fails and death may occur. Even 
in those cases in which sufficient hypertrophy develops to adequately compensate 
for the leak in the valve, the heart is never as capable for work as in health because 
the reserve is never restored completely and the degree of leakage may increase 
at any moment of strain. 

A consideration of these facts makes one therapeutic fact stand pre-eminent 
above all others, namely, that rest is the chief measure to be instituted whenever 
compensation is failing, as by rest alone can we expect to restore reserve energy. 

These remarks have so far dealt with regurgitant conditions. In stenosis of 
the cardiac orifices the same facts hold true, for in such cases the question is whether 
the heart muscle possesses enough strength to drive the blood through the obstructed 
area. 

Given a case of valvular disease the prospects of survival depend almost entirely 
upon the ability of the heart to undergo compensatory hypertrophy, and therefore 
the prognosis depends largely upon the state of the muscle, the absence of arterio- 
capillary fibrosis, which, if present, strains the heart and wearies it, the ability 
of the patient to pursue an easy occupation and his willingness to avoid habits 
of life which strain the heart. 

With these preliminary remarks we may pass on to a discussion of the individual 
valvular lesions, taking up first of all the most common of them, namely: 

Mitral Regurgitation. — Mitral regurgitation, often called " mitral incompetency" 
or "mitral insufficiency," depends in the great majority of cases upon thickening, 
shortening, or distortion of the mitral leaflets, those bicuspid valves which in 
health guard the left auriculoventricular orifice, in such a way that the blood when 
pressed upon by the contracting walls of the ventricle cannot regurgitate into the 
left auricle. 

Associated with this valvular defect there are usually vegetations on the edges 
of the valves which prevent proper approximation of their edges. The chordae 
tendinese, which extend from the ventricular wall to the leaflets for the purpose of 
giving them support, are shortened so that they will not permit the full movement 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 465 

of the valves. In some instances the valves, their fibrous bases, the chordae tend- 
inese, and even the endocardium are so completely calcareous that the ordinary 
physiological functions of the part are impossible. It is evident that it is almost 
impossible for such advanced changes to be present without at the same time causing 
some obstruction to the flow of blood from the auricle to the ventricle, and therefore 
we find that in nearly all cases of well-developed mitral regurgitation some mitral 
stenosis also exists. 

Fig. 86 




A large vegetation on the mitral leaflet. (Kast and Rumpler.) It can be readily seen that this 
would cause both a mitral obstructive and a mitral regurgitant murmur. 



Pathology. — The morbid anatomy has already been discussed under the heading 
of Endocarditis. The morbid physiology or pathology of mitral regurgitation is 
as follows: 

During systole the blood from the left ventricle in cases of mitral regurgitation 
flows in two directions. A larger part escapes into the aorta, as in health, and a 
smaller part of it regurgitates through the imperfectly guarded mitral, or left 
auriculo ventricular orifice, into the left auricle. The results of this regurgitation 
are multiple. In the first place the auricle not only receives blood during diastole 
from the pulmonary veins, but it also receives the blood which regurgitates from 
the left ventricle. This excess of blood requires the auricle to dilate beyond its 
ordinary capacity, and if the excess of blood is great this dilatation of necessity 
means distention. If the regurgitation progresses gradually there is developed a 
certain amount of hypertrophy in the auricular walls which enables the auricle 
when it contracts to empty itself completely and to prevent continuous overdisten- 
tion, but the muscular fibres in the auricle are never well developed as compared to 
30 



466 DISEASES OF THE HEART 

those of the ventricle, and therefore compensatory hypertrophy can never be so 
complete. 

The second result of this lesion is dilatation and hypertrophy of the left ventricle, 
which is due to several causes, namely, the fact that when the left auricle empties 
itself it delivers to the ventricle an excess of blood over the normal quantity, for 
the reasons just given. To hold this excess of blood the ventricle must dilate, 
and, to expel it on contraction, the ventricle must undergo hypertrophy. The 
general system still requires as much blood as before, and in order to provide it 
with that quantity the ventricle must increase its activity in order that the amount 
lost by regurgitation may be compensated for by increased cardiac action. 

The third result is found in dilatation and hypertrophy of the right ventricle, 
the labors of which are increased by the fact that the engorgement of the left 
auricle renders it difficult for the pulmonary veins to empty themselves into it. 
As a consequence they, and their tributary branches, become engorged, raising 
the resistance in the pulmonary vessels, and so the right ventricle finds it less easy 
to pump blood through the lungs. If the pulmonary engorgement is very marked, 
and dilatation develops in the right ventricle more rapidly than does compensatory 
hypertrophy, there is produced an insufficiency of the tricuspid valves guarding 
the right auriculoventricular orifice. 

Fourth, the right auricle now feels the same stress as was felt primarily by the 
left auricle, and it undergoes dilatation and hypertrophy, but this hypertrophy 
is rarely, if ever, adequate to the task set before it, and as it fails to properly empty 
itself, evidence of engorgement of the jugular veins becomes manifest in that 
they become swollen, the liver and kidneys are congested, and edema develops 
in the lower extremities. 

Fifth, certain definite changes take place in the lungs. As a result of their 
being constantly engorged with blood, they suffer from brown induration and 
atheromatous changes appear in the pulmonary arteries and veins as years go by. 
Finally, we find in addition serious congestion at the bases of the lungs as a result 
of impotence of the right ventricle and obstruction to the flow of blood from the 
pulmonary veins. 

Lastly, we find, at autopsy, in these cases red atrophy of the liver and congested, 
cyanotic kidneys. 

In those cases in which there is no primary disease of the mitral leaflets, but 
in which they fail because of acute dilatation of the ventricle so that the auriculo- 
ventricular orifice is widened and the valves cannot close it, there is developed the 
same train of symptoms save that they are more rapid in onset and more severe. 
This condition develops after great cardiac strain, in which the aortic valves are 
ruptured or the left ventricle and its auriculoventricular orifice greatly dilated. 
The resulting engorgement of the lungs may be so severe that their bloodvessels 
may rupture and profuse hemoptysis ensue. These patients nearly always succumb 
shortly, or remain chronic invalids, because the stress develops so suddenly that 
compensatory hypertrophy cannot take place. We have, therefore, an apparent 
paradox, namely, that actual disease of the mitral valves is rarely so serious in its 
consequences as is sudden incompetency of these valves due to other causes. 

In those cases in which the relaxation of the mitral orifice takes place because 
of cardiac feebleness after an acute illness, or after severe exercise in healthy youth, 
there are frequently no subjective symptoms, and perfect recovery usually 
occurs. 

Still another cause of mitral incompetence, aside from actual primary valvular 
disease, is Bright's disease, which increases arterial tension and thereby throws an 
increased strain on the left ventricle and the mitral valves when the blood is to be 
thrown out into the aorta. Usually in these cases the renal condition indirectly 
impairs the power of the ventricle, rendering its nutrition faulty through impoverish- 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 467 



Fig. 87 



ment of the blood and toxemia, and valvular failure then arises as a result of gradual 
widening of the auriculoventricular orifice. 

Symptoms. — It must be evident from what has just been said that many cases 
of mitral regurgitation may present no symptoms for years after the lesion is 
established, for as it develops so does a compensatory hypertrophy develop. It 
is only upon extra exertion, which the heart is not prepared to meet, that symptoms 
of cardiac embarrassment ensue, and if the exertion is not very severe and not 
repeated, the dyspnea and palpitation from which the patient suffers may be con- 
sidered by him as due to indigestion. If no illness impairs the heart muscle and 
no laborious pursuit causes it too great stress, the patient advances in comfort 
to old age, when symptoms develop as a result of the fact that his arterial tension 
gradually increases, thereby giving 
his heart more work to do at each 
beat, and at the same time his heart 
muscle undergoes the changes inci- 
dent to advancing years. When 
compensation "ruptures," to use the 
ordinary term applied to this unfor- 
tunate state, subjective and object- 
ive signs appear. 

The subjective symptoms (that 
is, those felt by the patient) vary 
considerably in the early and mild 
degrees of failing compensation. In 
some instances shortness of breath on 
exertion brings the patient to the 
physician, in other instances digestive 
disturbances due to hepatic congestion 
and secondary gastric catarrh are 
complained of, and in others the 
patient may complain of a cough, 
which is due to a mild pulmonary 
congestion and bronchitis having 
its origin in the cardiac failure. In 
still another class they may suffer ex- 
cessively from cold in moderately cold 
weather, and perhaps become easily 
fatigued while walking in cold air 
because the cold contracts the per- 
ipheral capillaries and so increases 
the labor of the heart. When the 
failure of the heart is well marked, 
dyspnea, inability to lie down because 

of oppression, and pain in the epigastrium are perhaps the symptoms of which 
the patient will most complain. 

The objective symptoms (that is, those seen by the physician) are even more 
characteristic. The capillary circulation is sufficiently impaired to produce some 
stasis and consequent cyanosis of the lips and finger-tips or even of the face. The 
fingers, particularly in young persons in whom the disease has lasted for some time, 
are club-shaped — that is, they do not taper, but have thickened tips ; there is more 
or less edema of the feet and ankles, and perhaps blood-spitting as a result of intense 
pulmonary engorgement or infarction. 

Physical Signs. — The physical signs in such a case are usually well developed. 
Inspection of the precordium reveals a diffuse and perhaps forcible apex beat. 




Showing at x the apex beat, where the murmurs 
of mitral regurgitation and obstruction can be best 
heard. The arrow pointing to the axilla indicates 
the direction in which the regurgitant murmur is 
transmitted, and the arrow pointing to the ster- 
num the direction of transmission of the obstructive 
murmur. 



468 DISEASES OF THE HEART 

Palpation shows a distinct thrill in children, and in this class of patients this thrill 
can frequently be seen as well. The apex beat may be distinctly felt well outside 
and below the nipple line. If the compensating hypertrophy is well developed 
the apex beat may be forcible, but if compensatory hypertrophy is lacking it is 
feeble and diffuse. On percussing the precordium the normal area of cardiac 
dulness will be found to be enlarged. This enlargement is usually transverse or 
lateral, so that it may extend to the right edge of the sternum owing to enlargement 
of the right ventricle, and as far as the left of the nipple from dilatation and hyper- 
trophy of the left ventricle. 

Auscultation provides us with the signs that determine the exact nature of the 
lesions, for the signs so far described are not distinctive of mitral regurgitation. 
When the ear of the physician is applied over the apex of the heart there is heard a 
soft, and often quite loud, murmur, which occurs synchronously with the apex beat, 
or with systole, or contraction of the ventricle. This murmur is transmitted to the 
left axilla, and it may be to the angle of the left scapula. Sawtelle and Grey 
have done much to prove that the 'transmission of the murmur toward the apex 
takes place by way of the chordae tendinese and papillary muscles and they believe 
that the occurrence of the murmur in the left axilla is due to the proximity of the 
anterior papillary muscle to that area. If it is very loud it may be heard in any 
part of the chest. If the regurgitation is great enough to cause engorgement of 
the lung the pulmonary second sound, due to a quick shutting of the pulmonary 
valves guarding the orifice of the pulmonary artery, may be louder than normal. 
This is best heard at the third left costal cartilage. When the regurgitation is 
severe enough to have resulted in tricuspid regurgitation from engorgement of 
the right side of the heart, there may be heard at the fifth costal cartilage on 
the right side a comparatively soft systolic murmur due to this secondary leak, 
but in some instances the mitral murmur completely obscures the tricuspid 
murmur. In others the tricuspid murmur can be heard only at the ensiform 
cartilage. 

It is of vital importance for the physician to recall the fact that a murmur so 
slight as to be almost inaudible is not an indication of the presence of a small 
and unimportant lesion of the mitral valve. On the contrary, the presence of a 
faint murmur often, but not always, indicates that the heart is too feeble to drive 
the blood with sufficient force to make the murmur clearly audible. 

The pulse of mitral regurgitation varies, of course, with the extent of the lesion 
and the degree of compensation. It is usually nearly normal, though lacking 
somewhat in volume even when compensation is complete. It is irregular and 
small when compensation is insufficient. When compensation is ruptured, it is 
very small and hobbling. 

Diagnosis. — It is desirable to separate mitral regurgitation due to dilatation 
of the mitral orifice from mitral regurgitation due to true valvular disease. This 
is in many cases impossible if the action of the heart is already seriously impaired, 
the more so because in many instances the secondary dilatation produces some 
widening of the orifice. While the physical signs may not be distinctive the absence 
of any history of rheumatism or other infection which affects the valves, and the 
presence, or history of the presence, of any exhausting illness which weakens the 
heart muscle, or of any strain which has dilated the orifice, would indicate that 
dilatation rather than true valvular disease is present. This is particularly true 
if the strain, though moderate, has occurred during convalescence, while the heart 
is weak. This differentiation is important because in some cases with returning 
health and strength the leak may cease and perfect recovery ensue, whereas if the 
valve is actually diseased good health can come only from compensatory hyper- 
trophy and the murmur will probably always persist. 

The possibility of a murmur being due to anemia is also to be recalled, but 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 469 

hemic murmurs are usually very soft and are best heard near the base rather than 
at the apex. 

The diagnosis of mitral regurgitation is therefore chiefly based upon the presence 
of a murmur heard most clearly with systole at the apex and transmitted to the 
axilla. 

Prognosis. — The prognosis in a case of mitral regurgitation depends upon the 
age of the patient, his occupation, the general condition of his vitality, and the 
severity of the lesion. When a child develops mitral disease it often does not 
survive puberty, chiefly because dilatation in such a case is usually excessive and 
because the constantly increasing demands of its growth require of its heart more 
than it can provide. In young adults who will rest after damage to the valves 
during an attack of rheumatism until compensation is really established, the 
prognosis is good, provided that the subsequent occupation is not too strenuous, 
although with the onset of old age vascular changes will probably cause breakdown. 
In feeble persons, however, the prognosis may be unfavorable from the onset, 
particularly if hypertrophy is lacking and dilatation is marked. In old persons 
the prognosis is bad for obvious reasons, since the heart cannot, at this time of 
life, readily gather new strength to meet new demands. 

If syphilis or alcoholism are factors in the case the prognosis is grave, and if the 
kidneys are diseased the prognosis is, of course, very bad. So, too, the presence 
of arteriocapillary fibrosis with high arterial tension is a serious or grave factor, 
in that it gives the heart so much work to do. (For the relationship of this lesion 
to age and mortality, see page 462, in article on Chronic Valvular Disease.) 

Treatment. — (This is discussed at the end of the articles on Valvular Disease.) 

Mitral Stenosis. — Definition. — By mitral stenosis we mean a condition of the 
tissues composing the mitral valves or surrounding the left auriculo ventricular 
orifice whereby the blood is prevented from passing with normal ease from the left 
auricle to the left ventricle. It is sometimes called "mitral obstruction." 

Etiology and Pathology. — Mitral stenosis is more common in females than in 
males, although the reason for this is not clear. Cabot denies this but Sir Dyce 
Duckworth found that out of 264 cases of this disease 177 were females, and other 
statistics are practically in accord with Duckworth's. It is due to gluing together of 
the mitral valves as the result of acute endocarditis arising from acute rheumatism. 

With this adhesion of the valves there is often associated a growth of vegetations 
on their edges and not uncommonly thickening and sclerosis of the chordae tendinese, 
the papillary muscles and the leaflets themselves, so that the parts lose their elas- 
ticity and are so stiffened that they are unable to move out of the way of the blood 
stream when it seeks to pass into the ventricle. This sclerotic process is so marked 
in some cases that the tissues may seem almost cartilaginous in character, and in 
advanced life lime salts may be deposited to such an extent that the fibrous tissue 
is calcareous and even the walls of the ventricle are infiltrated by calcareous masses. 
In some instances the adhesions are so complete that the valves form a funnel- 
shaped tube through which the blood must find its way. In other instances the 
edges of the valves are adherent and their margins thickened, leaving only a small 
orifice between them, forming the so-called " button-hole" mitral orifice, and in 
still other cases the conjoined edges of the valves are so drawn or puckered that the 
orifice when the auricle is opened looks like the normal anus. 

The funnel-shaped opening is most commonly seen in children, but it is not 
always as some have thought, a congenital lesion; the button-hole orifice is much 
more common in adults. Sansom states that the proportion is one button-hole 
to eight funnels in children, and that as adult life is reached the proportion changes 
to twenty-five botton-holes to one funnel. 

There can also be no doubt that chronic contracted kidney with associated 
arteriocapillary fibrosis not only causes mitral stenosis, but that even the funnel- 



470 DISEASES OF THE HEART 

shaped opening just described may be developed in this type of cases. The studies 
of Duroziez and Huchard in France, and of Goodhart, Sansom, and Pitt in England 
prove this fact. In 542 autopsies in cases of interstitial nephritis, Pitt found mitral 
stenosis 33 times. 

The results of mitral obstruction are overdistention of the left auricle and scanty 
blood supply to the left ventricle. The engorgement of the left auricle results 
from its inability to empty itself, and leads to dilatation and to some degree of 
hypertrophy. In some instances the growth of muscle fibres is so scanty that no 
true hypertrophy ensues, in others they seem to become actually atrophied, but 
in other instances very complete compensatory hypertrophy develops, so that 
the auricular wall is distinctly thicker than normal. Indeed, it may appear as a 
firm muscular mass which does not collapse at autopsy as the ordinary auricle 
is wont to do. Whether hypertrophy exists or not, dilatation is always present. 
When such an auricle is opened the endocardium is often found to be thickened and 
a laminated clot may line its cavity. In other instances polypoid or globular 
coagula are attached to the auricular walls, and these globular thrombi may almost 
fill the auricle. At times the thrombus is free, acting as a ball valve in the auriculo- 
ventricular orifice. 

The accumulation of blood in the auricle leads to the engorgement of the lung, 
and the same changes occur in its vessels and tissues that have been described 
under "Pulmonary Congestion" and "Mitral Regurgitation." So, too, the right 
ventricle undergoes hypertrophy and dilatation from similar causes, and the tri- 
cuspid valves, even more frequently than in mitral regurgitation, give way, so 
that pulsation of the jugular veins, pulsation of the liver, and edema of the lower 
extremities finally develops. Embolism often occurs in mitral stenosis, and, as in 
all cases of embolism arising in the heart, the embolus usually lodges in the left 
hemisphere of the brain. 

If the narrowing of the auriculoventricular orifice is not progressive, and if the 
auricle and right ventricle undergo compensatory hypertrophy, the signs of ad- 
vanced disease may not ensue. It is only when auricular hypertrophy fails that 
the malady becomes manifest and induces the symptoms of cardiac failure which 
in all respects resemble those described under Mitral Regurgitation, save that the 
venous and hepatic pulsation just described are more frequently present. 

Symptoms. — These consist, when compensation fails, in dyspnea, orthopnea, 
scanty urine, pulmonary congestion, and occasionally hemoptysis from infection 
or engorgement of the lungs. 

Physical Signs. — The physical signs of mitral obstruction are as follows: 
Inspection of the chest reveals pulsation at the apex of the heart near the nipple, 
and also the base of the heart close to the sternum, in the second or third left 
intercostal spaces. Not rarely there may be, in addition, epigastric pulsation. 
If a straw, or piece of cardboard, be placed over the pulsating spots at the apex and 
base, it will be found that they do not move synchronously, but the lower one 
moves with the ventricle and the upper one with the auricle. It has been claimed 
that the auricle does not produce this upper pulsation, and that it is due to the 
movement of the conus arteriosus of the right ventricle, but this is seemingly 
disproved by the fact that the two movements are not synchronous with systole. 
If the patient be a child these pulsations are much more noticeable than if he be an 
adult, at which time of life pulsation may be absent. Retraction of the interspaces 
from the third to the fifth rib with each systole occurs in persons with a thin chest- 
wall and is due to the movement of the right auricle. In children bulging of the 
chest-wall close to the sternum and in the epigastrium may be quite marked, and 
if pulsation be well defined in this area and absent from the region of the nipple, 
indicating hypertrophy of the right ventricle, the diagnosis of mitral stenosis is 
strengthened, provided that adherent pericardium can be excluded. 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 471 



Palpation does not always give us much information, but sometimes it practically 
decides the diagnosis, for there are three signs on palpation which are noteworthy 
in this lesion. There is a thrill which is presystolic in point of time and is felt in 
the fourth or fifth interspace inside the nipple line. It is characterized by sudden 
arrest at the moment of systole. It is thought by some to be due to the impact 
of the blood squirted by the auricle in a narrow stream against the ventricular 
wall. This sign may be considered diagnostic of mitral stenosis provided we have 
excluded the possibility of aortic regurgitation; which sometimes causes a similar 
sign. This thrill may be present at one time and entirely absent at another, and 
it may be absent when the patient is in the dorsal decubitus and present when he 
is erect, or, again, it is present after exercise and absent after rest. The second 
sign of some importance in the diagnosis of this disease by palpation is the heaving 
impulse, felt just below the margin of 

the last costal cartilage on the left FlG - 88 

side without such impulse near the 
nipple. This has already been spoken 
of under inspection as indicative of 
hypertrophy of the right ventricle. 
Care must be taken, however, that 
signs of hypertrophy of the left ven- 
tricle are really absent, for it some- 
times happens that an overlapping 
of the lung covers the left side of the 
heart so that it does not transmit its 
impulse to the chest- wall. The third 
sign on palpation is the discovery of 
the edge of the enlarged liver, which 
pulsates, if there is back pressure due 
to tricuspid regurgitation, below the 
level of the floating ribs on the right 
side. Here, again, care is necessary, 
for it often happens that the liver 
is moved by a transmitted impulse 
from the heart muscle through the 
diaphragm. 

Percussion of the precordium may 
reveal, in cases of mitral stenosis, a 
distinct increase in the area of cardiac 
dulness to the right, with compara- 
tively little extension of dulness to 
the left. This is due to the enlarge- 
ment of the right ventricle. When, 

however, the disease is far advanced and the heart is greatly dilated or hyper- 
trophied the left margin of dulness is distinctly extended, and in such cases the 
area of cardiac dulness to the left of the nipple line may be very great. 

Auscultation is, of course, the most important aid in the diagnosis of mitral 
stenosis, since it presents no less than six points of interest. The first of these is 
the presence of a murmur which occurs during diastole, gradually increasing as 
the auricle contracts until it is loudest in presystole, or in a brief murmur which is 
immediately presystolic, and is best heard between the nipple and the sternum, 
on the nipple level (Figs. 87 and 88). In most cases the murmur can be heard only 
in this area, but in some instances it is so loud as to extend all over the chest. 
The murmur is usually harsher than that of mitral regurgitation, and is vibratory 
in character. It is due to the passage of the blood through the obstructed auriculo- 




MO shows area of greatest intensity of a mitral 
obstructive murmur; TR shows area of greatest 
intensity of a tricuspid regurgitant murmur. The 
fine lines indicate the area in which is felt the char- 
acteristic thrill of mitral stenosis. 



472 DISEASES OF THE HEART 

ventricular orifice, and it ceases with the close of auricular systole. At times it 
is so metallic as to be musical rather than purring. 

Another sign of importance is the accentuation of the pulmonary second sound, 
which is best heard at the third left interspace, and is due to the high pressure in 
the pulmonary artery, produced by back pressure on the column of blood in the 
lungs. This accentuation is, however, not so constant in stenosis as in regurgita- 
tion because of the greater irregularity of the heart in stenosis. 

A third sign is the reduplication of the second sound of the heart so that it appears 
as a "tap-tap," or resembles the "postman's knock." It is very characteristic 
of mitral stenosis and is heard at two places: at the apex and at the base of the 
heart. It is, however, supposed to be due to different causes at each spot. At the 
apex Sansom believes it is due to the sudden rush of the blood into the ventricle 
through the narrow orifice under the pressure of the hypertrophied auricle. 
When this reduplicated second sound is heard at the base, and this is where 
it is usually heard, it is most diagnostic, and is supposed to be due to an 
asynchronous closure of the aortic and pulmonary valves, but in all probability 
the cause is similar to the sound at the apex. This is sometimes called the "gallop 
rhythm." 

The fourth sign of importance is the loud and sudden snapping sound which is 
heard at the close of systole of the ventricle. It is supposed to be due to forcible 
snapping to of the bicuspid or mitral valves. 

The fifth sign is not only somewhat indicative of stenosis, but much more of 
cardiac breakdown, namely, absence of the first sound of the heart at- the apex. 

Still a sixth sign of mitral stenosis is sometimes of value, namely, great irregularity 
as to rhythm and force. In no form of valvular lesion with rupture of compensation 
is the heart so tumultuous as in this disease. In mitral stenosis more than in 
any other disease partial or complete heart block may develop, due to the fact 
that the inflammatory process in the valve goes deeply enough to partly or com- 
pletely cut off the fibres of His' bundle, so that the impulse which arises at the 
sino-auricular node passes with difficulty or fails to pass from the auricle to the 
ventricle. (See Plate VIII and Fig. 91.) This results in lack of co-ordination, 
the auricle and ventricle beating asynchronously each for itself. Usually in such 
cases there is a very rapid jugular pulse with an abnormally slow radial or carotid 
pulse. The ventricle takes up a beat of its own which is usually slow and the auricle 
beats very fast so that the ratio may be 140 to 40 beats per minute if the block 
is complete. The auricular beat is best seen in the jugulars. (See Arrhythmia.) 

As already stated, the absence of a murmur may be more indicative of grave 
valvular disease than its presence. 

When cardiac breakdown ensues it not infrequently happens that the presystolic 
murmur itself disappears because the auricle is too feeble to drive the blood through 
the auriculo ventricular orifice with enough force to make a murmur. Often this 
loss of power is due to auricular fibrillation, a condition in which the auricular 
wall does not contract but suffers from fibrillary thrills and is only a sac through 
which the blood passes to the ventricle. Sudden death may ensue or life may 
persist for several years in cases of fibrillation. (Plate VII.) 

Diagnosis. — Mitral stenosis is at times the most difficult of all the cardiac lesions 
to diagnosticate, chiefly because when compensation is ruptured no murmur may 
be present, and the action of the heart being exceedingly irregular its sounds are 
confused. Again, stenosis is so frequently associated with mitral regurgitation 
that the double murmur may cause confusion, the more so as only one murmur 
may be present at one time and both at another time, and also because the regurgi- 
tant murmur is often so loud that it covers the stenotic murmur, with the result 
that unless the physician is on the qui vive to discover the less noticeable sound it is 
overlooked. In cases which are manifestly ones of mitral stenosis the physician 



> 

a. 




l r2 0) 

.2 c3 += 

> 2 

m 

o -rH 






o 
'£ 



03 

£ 

a 

£ 
o 
u 

CD 

Sh 

'5 

a 



03 



c 



3 
o 

'3 

d 

a 
> 



fig 



fl tf 



O 

^ Til C, 

-p 

— I ^4-H 

3 o 

d, 03 
03 

a> ft 



S^ 



o 






o 

o . 
S 03 



o3 



- o 

rt 03 a 

a) a S 

« fi £ 

03 03 

§ S 2 
§ a'43 

£ * rt 

m'O o 

oS [3 o 

03 a <3 

g CO o 

2 £ 

MO £ 






2. 2^ 
-p '+3 t O 

O^ a; 

-£ ft a) 

fi — I r^H 



0) 



p3 

o 

o3 



bfl 

'o 

o3 



03 

03 

o 



PO 

bfi 
3 



o 

J-l 

bfi 

a 

•^H 
O 

<3 

03 
3 



03 

r— t 



03 S-i " Z 
^ 2 -+-2 c3 

<3 03 ^ ~^ 
p2 ^-, 03 

-^<2^ 

3 °^ o 

ifll 

omoS 

§ £^ 

O 0) « 5? 

03 ri 03 2 

pH to 

JT§e 

O u3.S 



•4P 

J-l 

03 



03 

S 
o 

^H 

«+h 

b£ 

'5 

Jh 

-P> 

03 

_2 

!-< 
03 

ft 

a 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 473 

need not hesitate to express an opinion, but in the obscure forms of the disease he 
should always reserve his statement until he has had an opportunity of examining 
the heart several times under conditions of rest and exercise, and, perhaps, after 
the use of digitalis or some other drug to strengthen the muscle. 

As the physical signs have already been thoroughly described, it is only necessary, 
at this point, to differentiate mitral stenosis from those conditions which resemble it. 

The most important of these is the so-called "Flint's murmur" first described 
in 1862 by Dr. Austin Flint, of New York. It occurs in some cases of aortic regurgi- 
tation, and is supposed to be due to the regurgitating blood striking upon the 
mitral valves and chordae tendinese in such a way that they vibrate and so cause a 
sound. This sound is diastolic in point of time because it occurs after the blood 
has been sent out into the aorta and while the ventricle is receiving more blood 
from the auricle. Its time of occurrence is, therefore, practically identical with 
the murmur of mitral stenosis. 

The following points make the differentiation between mitral stenosis and 
"Flint's murmur" in most cases, although in some cases the separation may be 
impossible. In cases with aortic regurgitation auscultation at the second right 
costal cartilage and along the sternum will reveal a diastolic murmur, which will 
not be well defined in these areas in mitral stenosis unless the mitral murmur is so 
loud as to be heard pretty much everywhere in the chest. The pulse in aortic 
regurgitation is characterized by a full wave followed by a sudden fall — the " Cor- 
rigan pulse" — whereas the pulse of mitral obstruction is a fine thread, irregular 
and feeble. Again, in cases of aortic regurgitation with "Flint's murmur" there 
are rarely, if ever, those well-developed signs of pulmonary, hepatic, and splenic 
engorgement which have been described as occurring in mitral stenosis, nor does 
the patient so frequently suffer from hemoptysis due to pulmonary congestion or 
infarction. Further than this, the sharp, snapping first sound of the heart char- 
acteristic of mitral obstruction is not present with "Flint's murmur." 

A second condition resembling mitral stenosis is tricuspid stenosis. On general 
principles, this latter lesion can be excluded on the rule of probabilities, for tri- 
cuspid stenosis is an exceedingly rare lesion. If it exists it is usually heard best 
in the tricuspid area (the area of the fourth right intercostal space), but it may be 
clearly heard in the mitral area, and as tricuspid stenosis and mitral stenosis exist 
together in some cases and occur simultaneously, they may not be separable and 
nothing be known of the lesion on the right side of the heart until autopsy. 

At times children suffering from adhesive pericarditis present a presystolic 
sound like that of stenosis. It is to be discovered by the signs of adhesive pericardi- 
tis (which see). In every case of valvulitis due to rheumatism we should bear in 
mind the possible if not the probable, presence of adherent pericardium. The 
presence of this condition is rendered likely if the liver is not only enlarged, but 
very firm, and if ascites develops in excess of that seen in cardiac dropsy. This 
point is of importance, because if the pericardium is adherent we cannot expect 
very good results from digitalis nor from any other method of treatment. 

When a patient presents himself with a disordered circulation and confused 
or irregular heart sounds, and no murmur, it must be recalled that while such a 
state may be due to tobacco heart, it may also be caused by mitral stenosis with 
no murmur or be due to excessive doses of digitalis. 

Prognosis. — The prognosis of mitral stenosis is not as favorable as is that of 
mitral regurgitation or aortic stenosis, and children nearly always succumb to it 
before they reach adult years. Adults who have a severe lesion also rarely survive 
for many years after it begins, but there are very marked exceptions to this rule. 
Thus, I have under observation at present a case of mitral stenosis which I examined 
twenty-two years ago, and who was told thirty years ago that the lesion existed. 
During all these years (he is now sixty-nine years of age) he has led a very active 



474 DISEASES OF THE HEART 

life, both physical and mental, with no cardiac embarrassment, although he had 
an attack of hematuria when I first saw him, which was due to an infarction of the 
kidney. During this time he has taken no treatment, except at rare intervals, 
his compensation being complete. 

In young women with mitral stenosis, marriage and consequent child-bearing 
often cause rupture of compensation and death. 

The average age at death in cases of this disease is stated by Sansom to be about 
thirty-two and seven-tenth years. (See General Discussion of Valvular Lesions 
and Their Effect on Mortality, page 462.) (For treatment see close of these 
articles.) 

Aortic Stenosis. — Definition. — Aortic stenosis, often called "aortic obstruction," 
is a condition in which the left ventricle finds it more difficult than normal to 
expel the blood through the aortic orifice, because this orifice is narrowed by disease. 
The murmur which is produced by the blood under these circumstances is systolic 
in point of time, for it occurs as the left ventricle expels its contents. It is best 
heard at the second right costal cartilage or under the sternum, at its upper portion. 
It is of vital importance, however, to recall the fact that the presence of a systolic 
murmur at this point is not necessarily indicative of actual obstruction of the aortic 
orifice. An aortic systolic murmur does not necessarily mean an aortic valvular 
lesion. The murmur is usually due to roughening of the lining of the aorta by 
atheromatous plaques. Aneurysm may also be provocative of such a sound. 
So rare is true simple aortic obstruction that it may be said that the presence of a 
systolic aortic murmur is in most cases probably not due to this lesion, unless it is 
associated with aortic regurgitation. Some clinicians of repute assert that they 
have never seen pure aortic stenosis without regurgitation. Cabot states that 
in 252 autopsies made at the Massachusetts General Hospital on persons with 
valvular disease, there was not a single instance of uncomplicated aortic stenosis. 

Etiology. — The causes of aortic obstruction are multiple. In the first place, 
it may be the result of rheumatic endocarditis of so severe a type that not only 
the mitral but the aortic valves are involved, for it is only in rare cases that rheu- 
matism attacks the aortic valves and leaves the mitral valves untouched. In such 
a case the endocardium covering the valves is roughened in patches, and upon 
these patches is deposited fibrin from the blood stream, which, with proliferated 
cells, form granulations and vegetations, fibrous thickening, and, finally, the 
deposition of lime salts. If the inflammation is severe the edge of the valves may 
become glued together, and so a funnel-shaped opening is formed, which is much 
narrower than the normal aortic orifice. In rare instances, instead of the valves 
being adherent and thickened, they are adherent and thinned, so that they appear 
atrophied. Such a condition is found at times in children and is thought to be 
congenital, but even in young children the cause may be rheumatism, and Sansom 
asserts that the condition may be due to rheumatic endocarditis in intra-uterine 
life. Rheumatism may be considered the usual cause of aortic obstruction in 
children or in those who have not as yet reached advanced years. 

The cause of aortic obstruction is often not acute in character, as in the types 
just described, but chronic, being due to a gradual atheromatous change, which, 
having involved the aorta itself, spreads to the aortic valves, and causes a slowly 
progressive thickening and calcification of their tissues. This is the form of stenosis 
which is often of a- very advanced type, so that the orifice may be but a small 
slit or chink through which the blood escapes. 

From what has just been said, it is easy to understand how it is that obstruction 
to the flow of blood in the area of the aortic valve is exceedingly rare as a single 
lesion. The very nature of the morbid changes which take place in the tissues 
at this point renders the simultaneous existence of aortic obstruction and regurgita- 
tion probable, for the valves at the aortic orifice are either glued together as a 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 475 



Fig. 89 




result of rheumatic endocarditis, or, more commonly, are thickened by chronic 
endocarditis and calcareous deposits. In either instance they are not only in the 
way of the blood as it passes out of the ventricle, but they are incapable of prevent- 
ing its regurgitation, since they are too thick and too stiff to approximate their 
edges. In other instances the presence of vegetations on the valves, in addition 
to these changes, adds to the impairment of their functional activity. 

The secondary changes produced by aortic obstruction are chiefly connected 
with the left ventricle. Under favorable conditions this portion of the heart 
usually develops a satisfactory compensatory hypertrophy, the muscle fibres 
gaining in strength and size as the process of narrowing in the aortic area gradually 
progresses. As a consequence, it not rarely occurs that even an extreme degree 
of aortic obstruction is accompanied by such a complete compensatory hypertrophy 
that the presence of the lesion is 
only discovered at autopsy. It is 
interesting to note that the hyper- 
trophy of aortic obstruction differs 
somewhat from that of aortic regur- 
gitation in the fact that the ven- 
tricular walls increase in thickness 
without undergoing any great dilata- 
tion, whereas, in aortic regurgitation 
they both dilate and hypertrophy, 
causing eccentric hypertrophy. 

So long as the compensatory hy- 
pertrophy of the left ventricle in 
aortic obstruction is adequate, prac- 
tically no changes occur in the other 
parts of the heart. It is only when 
compensation ruptures that symp- 
toms of impaired circulation ensue, 
as the mitral valves give way under 
the strain, and congestion of the left 
auricle and of the lungs develops. 
This may in time increase the labor of 
the right ventricle and lead to its hy- 
pertrophy. 

Symptoms and Physical Signs. — Pa- 
tients suffering from aortic obstruc- 
tion rarely present or complain of 
any symptoms which are in any way 
characteristic of the lesion. At 
times a sense of constriction or oppression is felt over the aortic area, as it is in 
cases of aortitis or atheroma of the aorta, and as it is felt in some cases of true 
angina pectoris. When there is an associated aortic regurgitation, the symp- 
toms are of that lesion. (See Aortic Regurgitation.) 

The physical signs vary considerably with the type of patient examined and 
with the stage of the disease. In old men whose chest walls are thickened and 
rigid and whose lungs are often emphysematous, so that the edge of the left Jung 
projects between the heart and the chest wall, it may not be possible to either 
see or feel an apex beat, even though the heart be considerably hypertrophied. 
On the other hand, if the patient be young, or the chest wall pliable, the apex beat 
may be seen and felt distinctly and forcibly, and it is usually a little below and a 
little outside the nipple because of the hypertrophy. If the action of the heart is 
forcible and the fingers are placed over the second right intercostal space, a distinct 



^i) 



Showing area of greatest intensity and the direc- 
tion of transmission into subclavian and carotid 
arteries of the aortic obstructive murmur. 



476 DISEASES OF THE HEART 

thrill can be felt. This thrill is in the nature of a vibration and is often transmitted 
down the sternum and even up into the carotids. This thrill felt in the area 
described is very characteristic of aortic obstruction, but it is also felt in aortic 
aneurysm. 

The area of cardiac dulness on percussion is not materially enlarged, unless 
associated regurgitation has caused its well-known secondary cardiac changes. 

Auscultation reveals a murmur which is loudest at the second right costal carti- 
lage near the sternum. 

This sound is transmitted in most cases into the vessels of the neck, and not 
infrequently it is heard over the sternum as low as the ensiform cartilage. It 
occurs with systole of the heart, and it is usually loud if compensation is preserved. 
Not only is it loud, but it is apt to be harsh and even musical, and it is long and 
blowing in character. The aortic second sound is usually absent. 

When rupture of an aortic valve takes place the murmur is usually widely diffused, 
very loud and musical. I showed a patient to the College of Physicians of Phila- 
delphia in 1902 that possessed a murmur capable of being heard when the ear was 
eighteen inches from the chest. It could be heard on top of his head, in his radial 
arteries, and if the stethoscope was placed so that his lips encircled it the murmur 
could be heard in his mouth. There was also a loud aortic regurgitant murmur 
in his case. The patient was a brakeman who suffered from sudden and severe 
dyspnea and syncope on lifting a heavy weight, and who had a history of syphilis. 

The pulse in aortic obstruction is small (pulsus parvus) because the heart cannot 
expel a large wave of blood through the narrow aortic opening. The wave rises 
gradually and then falls gradually, unlike the sharp upward jerk felt in aortic 
regurgitation. 

Diagnosis. — Sufficient emphasis has already been placed on the fact that a 
systolic murmur at the second right costal cartilage does not mean, necessarily, 
aortic obstruction, but if the time of the murmur, the thrill, the peculiar pulse and 
atheromatous vessels are present in an old person the diagnosis is fairly certain. 
When the murmur is due to atheroma of the aorta alone the aortic second sound 
is usually sharp and clear instead of being impaired as it is in true obstruction. 
Aneurysm is excluded by the absence of the characteristic signs of that state. 
(See Aortic Aneurysm.) 

Sewall asserts that an aortic stenotic murmur heard at the apex disappears 
on pressure of the stethoscope, and so separates itself from the systolic murmur of 
mitral regurgitation. 

Prognosis.— The prognosis in a case of aortic stenosis is generally considered 
as more favorable than in any other valvular lesion, but in each individual case 
the physician must base his prophecy as to life upon the age of the patient, the 
state of his arteries, and the condition of the kidneys. The mere presence of 
far-advanced atheroma in aged persons who have an aortic stenotic lesion is not 
necessarily of evil import. As Sir Clifford Allbutt well says, " We see well-to-do old 
ladies leading tranquil lives up to four-score years or more with systolic aortic 
murmurs of a quarter of a century's standing." On the other hand, in somewhat 
younger persons, who have more fibrous and less calcareous arterial changes, the 
prognosis is not so good, either because they are at a period of life when they are 
prone to resort to exercise and so strain the heart, or because there is a tendency 
to fibroid heart as well. Allbutt's view that "a person who in young or middle 
life begins to suffer overtly from the symptoms of aortic stenosis has but a few 
years to live" is certainly correct. (For treatment see end of article on Valvular 
Disease.) 

Aortic Regurgitation. — Definition. — Aortic regurgitation is often called "aortic 
insufficiency" or " aortic incompetency," and consists, as its names indicate, in a 
condition of the aortic leaflets, or of the aortic orifice, whereby the blood after 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 477 

being expelled by the contraction of the left ventricle into the aorta is permitted 
to return. 

Etiology and Pathology. — By far the most common cause of this lesion is acute 
rheumatism, which causes the same changes in the valves at the aortic orifice as 
have already been described as taking place in the mitral leaflets, namely, distortion, 
retraction, stiffening, and the development of vegetations. As a rule, when rheu- 
matism is the cause the mitral valves also suffer seriously, so that the aortic and 
mitral lesions coexist. A second common cause is aortitis, or atheroma of the 
aorta, which extends to the valves and causes sclerotic and degenerative changes 
which alter the position and functional ability of the aortic cusps. This atheroma 
may be due to mere senility, or to syphilis, gout, or even malarial infection. It is 
remarkable how many of these cases have a history of excessive toil, excessive 
venery, and excessive drinking, with the result that the bloodvessels and heart 
have had to stand strain, toxemia, and infection. The cases of aortic regurgitation 
which are due to these causes suffer the greatest destruction of the valves, for their 
surfaces may ulcerate or the deposition of an excess of lime salts causes necrosis 
to such an extent that only stumps of the valves exist. 

A third cause, which is much more rare, does not primarily involve the valves, 
but the aortic orifice. The aortic ring undergoes dilatation and as a result the 
valves cannot become approximated. In other words, the opening is too large 
for them to close it. This condition is met with in cases of aneurysm of the aorta. 
It is not by any means as frequent as dilatation of the mitral orifice, because the 
ring around the opening of the aorta is largely made up of fibrous and fibro-elastic 
tissues, that which supports the mitral orifice is largely muscular. 

The question as to whether a diastolic aortic murmur can be present without 
disease of the aortic valves has been much discussed, particularly of late, by Cabot 
and Locke, of Boston, and Gibson, of Edinburgh. As is well known, the aortic 
ring is so firm that it seems impossible that it can yield as do the rings of the pul- 
monary and mitral orifices. Cabot and Locke believe that diastolic aortic murmurs 
are not uncommon in connection with diffuse or localized dilatation of the aorta, 
but in view of the evidence presented by Gibson, we must, I think, agree with him 
that diastolic murmurs, without valvular lesions, are rare at the aortic orifices, 
and that when they occur they are due to defective approximation of the different 
aortic cusps rather than to yielding of the aortic ring. 

A fourth cause is rupture of an aortic leaflet as the result of violent strain. This 
accident rarely, if ever, occurs unless the valve has already been weakened by disease. 

A fifth cause is the presence of vegetations on the aortic valves, developing in 
the course of the acute infections or chorea. Some of these lesions differ from those 
due to ordinary endocarditis in that they are not always permanent, but may 
entirely disappear. 

A sixth cause is ulcerative endocarditis, in which great destruction of the valves 
may take place or abundant vegetations develop. This is usually due to the 
pneumococcus. (See Croupous Pneumonia.) 

A seventh cause is congenital malformation, which is exceedingly rare. Indeed, 
aortic regurgitation due to this cause is more rare than are congenital defects 
themselves, for congenital defects in the valves may not be severe enough to permit 
leakage. 

Finally (eighth) a functional relaxation of the aortic orifice occasionally is met 
with in which temporary regurgitation takes place for the same reasons as have 
been described elsewhere. I saw a case of this character while on duty at St. 
Clement's Hospital some twenty-five years ago, in a young girl who had a loud, 
aortic regurgitant murmur and apparently a fusiform aneurysm of the innominate 
artery. At the autopsy the vessels seemed perfectly normal in size, but on testing 
them they were found to be unusually yielding and elastic. 



478 DISEASES OF THE HEART 

The secondary effects of aortic regurgitation upon the left ventricle are most 
important and interesting. The left ventricle no sooner expels its contents into 
the aorta and begins to dilate in order to receive the blood from the auricle, than 
it also receives part of the blood it has just sent into the aorta by reason of the 
fact that the aortic valves permit regurgitation. The ventricle, therefore, contains 
not only the normal amount of blood from the auricle, but an additional quantity 
from the aorta, and so it becomes dilated to contain this excess and also undergoes 
hypertrophy in order to expel this excess into the aorta and empty itself. Any 
strain upon the heart increases the dilatation, and as a result we often see, particu- 
larly in those who live by manual labor, an extraordinary increase in the size of 
the heart, which is both greatly dilated and greatly hypertrophied, the so-called ec- 
centric hypertrophy of aortic regurgitation resulting in the " ox heart" or corbovinum. 

The rapidity and degree of the hypertrophy is extraordinary in some cases. 
Sansom speaks of a case in which the heart was thought to have gained an ounce 
each week for four or five weeks, and Dulles has recorded a case in which the heart 
weighed forty-eight ounces. When the ventricle is much dilated the ring guarding 
the mitral orifice may yield and insufficiency of the mitral valves ensue and thus 
cause dilatation of the left auricle, congestion of the lungs, and hypertrophy of 
the right side of the heart. In some cases of aortic insufficiency, when the cause 
is atheroma, the pathological process of fibrosis and calcification gradually extends 
to the tissues around the opening of the coronary arteries, which are then unable 
to properly supply the heart with blood, or the coronary arteries themselves become 
atheromatous. Under such conditions compensatory hypertrophy may never 
be established, or if established rapidly fails and death ensues. 

Symptoms and Physical Signs. — The symptoms of aortic regurgitation are more 
characteristic than are those of any other form of valvular disease, and are more 
constantly met with in such cases, although compensation may be adequate in 
many cases for a time at least. Dizziness and partial syncope often appear or 
suddenly sitting up or on standing up, and at times are present even when the 
patient lies down. Palpitation and dyspnea on exertion are pressing symptoms 
if the heart is feeble, and even when compensation is adequate pain in the region 
of the heart is often a severe symptom, being radiated into the arms or into the 
neck. At this time the attacks may be identical with those of true angina pectoris. 
Sudden death occurs more frequently in this form of valvular disease than in any 
other. 

When compensatory hypertrophy is lost the patient is forced to sleep sitting 
erect or nearly erect in an easy chair; he is usually very pallid, but at times cyanotic. 
Cough and pulmonary complications do not ensue until the mitral valves give way. 

When the cardiac failure is well marked, and it is evident that death cannot be 
many days away, distressing mental symptoms often appear. Hallucinations are 
pressing and even an active delirium may develop. At times the patient becomes 
suicidal. In some cases these mental disturbances are due to disordered and 
inadequate cerebral blood supply, and at times they are due to a complicating 
nephritis arising as a late lesion of the general breakdown. 

Physical Signs. — The physical signs are characteristic when well developed. 
On inspection the carotid arteries are seen to pulsate markedly, and even the head 
may be moved by the impulse transmitted to it by the heart. The thorax, in 
the precordium and neighboring parts, heaves with each pulsation of the heart 
and is often bulging, owing to the cardiac hypertrophy and dilatation. An ocular 
examination of all the superficial arteries will show a characteristic throbbing or 
jerking, and if a glass slide be lightly pressed against the lower lip capillary pulsation 
is readily seen, in that the color of the mucous membrane rises and falls with the 
movements of the heart. Such capillary pulsation, often called "Quincke's pulse/' 
can be seen under the thumb-nail when it is gently pressed upon, and in the red 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 479 



Fig. 90 



line produced on the skin of the forehead by drawing the end of a pencil over this 
part. As the arteries are often elongated, and therefore more tortuous than in 
health, the impulse of the wave of blood which tends to straighten the curves makes 
the vessels move laterally as they beat, and this increases the pumping effect which 
is produced by the so-called "Corrigan pulse." 

The apex beat is always far below and far outside the nipple because of the 
dilatation and hypertrophy of the left ventricle, and also because of the elongation 
of the aortic arch. On palpating the heart the impulse on systole is powerful and 
diffuse except when compensation is ruptured, when it is feeble. 

The pulse when felt by the finger-tips feels as it looks on inspecting the arteries. 
With each systole of the heart the almost empty artery suddenly gives to the 
finger a short, sharp impulse, which equally suddenly disappears, the vessel being 
in an instant apparently as empty as 
before. The hypertrophied and dila- 
ted heart expels a large wave of blood 
into the aorta, of which a part at 
once falls back into the ventricle, so 
that what might be called the tail of 
the pulse is lost. This is the so-called 
"Corrigan pulse," sometimes called 
the "water-hammer pulse," or "trip- 
hammer pulse." It can be empha- 
sized in the radial arteries by raising 
the hand above the head. This pulse 
is usually regular as to rhythm and 
force, and the blood pressure is high. 
If it becomes constantly irregular, it 
is a sign of grave cardiac failure. 
Aside from high blood pressure, which 
is usually above 160 in the arm, there 
is an additional sign of diagnostic 
value. If the patient is recumbent 
so as to be relatively free from hy- 
drostatic variations in his arterial 
tree it will be found that the systolic 
pressure in the leg is always 40 to 100 
points higher than in the arm. This 
difference is not found in any other 
valvular lesion, but it is often absent 
in children. If the auscultatory 
method of estimating blood pressure 
the mercury is practically at zero. 

On percussion the area of cardiac dulness is found to be greatly enlarged, so 
that it extends far over to the anterior axillary line in some instances, and three 
inches below the nipple. Dulness due to the enlarged heart is also found even as 
far as the right edge of the sternum. 

Auscultation. — Auscultation reveals a diastolic murmur, due to the return of the 
blood from the aorta after the systole has expelled it into the vessel, and while 
the ventricle is once more opening for a new supply from the auricle. This murmur 
is heard in its greatest intensity at the fourth left intercostal space, or at the second 
right costal cartilage in the so-called aortic area. It is heard at the fourth left 
intercostal space because the reflux of blood carries the murmur back into the ven- 
tricle, and because the aortic opening as a matter of fact is nearer this area than 
the second right intercostal space (Fig. 90). In still other cases the diastolic 




Showing the area in which the murmur of aortic 
regurgitation can be most clearly heard. 

is used the tapping sound persists until 



480 DISEASES OF THE HEART 

murmur may be very clearly heard at the cardiac apex as well as at the second 
right intercostal area, although between the two no murmur at all, or only a very 
faint sound, can be discovered. The explanation of this is that the right ventricle 
occupies the anterior surface of the heart, except at the extreme left edge, where the 
left ventricle protrudes and where the apex comes closely in contact with the chest 
wall. 

The murmur of aortic regurgitation is not widely transmitted, but is limited, 
as a rule, to the area described, although when it is very loud it may be heard 
everywhere in the chest. The quality of this murmur is blowing or purring. There 
is no accentuation of the pulmonary second sound at the third left costal cartilage, 
unless there is an associated mitral regurgitation or stenosis. The first sound of 
the heart is loud or prolonged owing to the large amount of blood which has to be 
expelled at systole. In some cases a diastolic sound near the apex may mislead 
the physician into a diagnosis of mitral obstruction, but it is in reality the so-called 
"Flint's murmur." (See Mitral Stenosis.) 

If the stethoscope is placed over any one of the large superficial arteries there is 
sometimes heard, in cases of aortic regurgitation, a sharp systolic, "pistol-shot" 
sound, which is said to be due to sudden filling of the vessel. This sound is not 
transmitted from the heart, but is local in origin. It is a modification of the arterial 
sound which can be elicited in most persons with a strong pulse, if the artery is 
occluded by pressure with a stethoscope. Very rarely a diastolic arterial sound 
can be heard, the so-called "Duroziez sign," which is thought to be due to a trans- 
mitted cardiac sound. 

Diagnosis. — The symptoms and physical signs of aortic regurgitation having 
been described, it remains to separate them from those conditions which possess a 
resemblance. Occasionally in some persons a diastolic cardiopulmonary murmur 
is heard, but it disappears with change in posture and is dissipated or is accentuated 
by forced expiration and inspiration. At the level of the second and third left rib 
there is heard at times a hemic murmur or hum due to anemia, but this is systolic 
in time. Cabot has, however, reported cases in which diastolic murmurs were 
hemic and due to anemia. 

Finally, it is to be recalled that the aortic regurgitation murmur is often incon- 
stant, and if not heard at one examination may be at another, or when the patient 
exercises or changes his posture. 

Prognosis. — Facts in regard to the relative fatality of aortic regurgitation have 
already been given. Allbutt says ten years constitute a long time of life in any 
case of aortic regurgitation. It is not only a serious lesion, but it is the valvular 
lesion above all others which produces sudden death; but death in aortic regurgita- 
tion is not always sudden. A majority of cases gradually " play out" with dyspnea, 
dropsy, and cardiac distress. Much depends on the age of the patient, his previous 
habits, and the cause of the disease. In a young adult with a good history, and 
in whom the lesion has followed rheumatism without great injury to other parts, 
compensatory hypertrophy may carry him along for many years unless he ruptures 
it by severe strain, or it is dissipated by illness. When the lesion comes on as the 
result of atheroma it is more serious because it is evidence of general cardiovascular 
degeneration, and the coronary arteries, through which the heart is chiefly nour- 
ished, no sooner share in the degenerative change than feebleness of the heart 
ensues. If perchance the kidneys share in the cardiocapillary fibrosis, the outlook 
is all the more grave. When fast living and debauchery are factors in the case, and 
an old syphilitic infection is impairing the myocardium, the outlook is worse still. 
(For treatment see end of article on Valvular Disease.) 

Tricuspid Regurgitation. — Definition. — Tricuspid regurgitation, or insufficiency, 
is a condition in which the blood flows backward into the right auricle from the 
right ventricle, upon the contraction of the latter. 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 481 

Etiology and Pathology. — This is a rare lesion and is due to two chief causes. 
It occurs most commonly as a result of disease on the left side of the heart, whereby 
the blood is dammed back into the lung and so, by preventing free pulmonary 
circulation, an undue strain is thrown on the tricuspid leaflets. In other instances 
the primary obstruction exists in the lungs, as in pulmonary emphysema, fibroid 
phthisis, and bronchiectasis. 

As indicating the relative frequency of these causes, Newton Pitt reports from 
Guy's Hospital that out of 405 cases of tricuspid regurgitation examined at autopsy, 
in a period of twenty-five years, 200 cases were due to left-sided failure with valvular 
disease. Of this number 64 were cases of mitral regurgitation with mitral endo- 
carditis or adherent pericardium, 66 were due to mitral stenosis, 61 to mitral with 
associated aortic disease, and 9 had valvular lesions not named. In 71 cases the 
tricuspid condition was due to left-sided failure without valvular disease, in 56 
cases the cause lay in muscular failure of the whole heart, and in 55 the lesion was 
not left-sided, but was right-sided alone. Seven cases were due to disease of the 
pulmonary valves, of which 5 were stenosis and 2 pulmonary regurgitation. In 
4 cases no cause could be found, and in 12 the reports as to the exact state of the 
heart were too imperfect for analysis. 

The valves in these cases are usually healthy and fail to close the right auriculo- 
ventricular opening because the orifice is enlarged as a result of dilatation of the 
ventricle. 

The second cause of this lesion lies in the heart itself, that is, an endocarditis 
involving the right side of the heart. This is generally stated to be very rare, 
although in fetal life endocarditis is more commonly on the right side of the heart 
than the left. Bramwell, however, combats the statement that acute endocarditis 
rarely affects the tricuspid valves, and believes that endocarditis of the right 
heart often exists and is overlooked. Out of 28 cases of recent simple endocarditis 
he found disease of the tricuspid valves in 14, or 50 per cent. Nevertheless, the 
lesions are not so pronounced as those due to this cause on the left side of the heart. 
In ulcerative endocarditis Osier found the tricuspid valves affected in 19 cases out 
of 238 instances of that disease. 

A case in which tricuspid disease was discovered during intra-uterine life is 
reported by Peter, of Paris! ! 

Symptoms and Physical Signs. — When the cause exists in the left side of the 
heart the symptoms are those naturally arising in cases of pulmonary congestion 
and engorgement. A low-grade bronchitis, with some dulness at the bases of the 
lungs posteriorly from hypostatic congestion, with cough and occasionally blood- 
stained sputum, is discoverable. The jugular veins become distended and pulsate, 
the liver becomes enlarged and may pulsate, and there is marked cyanosis. It is a 
noteworthy fact that the presence of jugular pulsation, while a sign of well-developed 
regurgitation, is not by any means as grave a sign as is its absence in the presence 
of other evidences of cardiac embarrassment, because if the right ventricle is 
strong it may drive the regurgitating blood with sufficient force to cause jugular 
pulsation, whereas if it be weak no jugular pulsation can ensue. On the other 
hand, the presence of jugular pulsation shows that the regurgitation is a grave one, 
because it does not occur until a considerable quantity of blood flows into the 
auricle and distends the veins sufficiently to interfere with the valves, so that they 
cannot prevent auricular regurgitation as they do in health. 

A distinct impulse in the upper epigastrium is often present. 

The pulsation of the liver is best discovered, if not seen, by placing the finger-tips 
or hand against the floating, ribs at the side, and the other hand near the ensiform 
cartilage, and then exerting gentle pressure upon the liver from both directions. 
Care must be taken that a directly transmitted impulse from a hypertrophied 
heart is not taken for true expansile pulsation of the liver. 
31 



482 DISEASES OF THE HEART 

On percussion, increase in the area of cardiac dulness to the right of the sternum 
is demonstrable. 

On auscultation at the apex a soft systolic murmur, or purr, can be heard, which 
is found to be loudest at about the fifth interspace, to the right of the sternum 
or at the base of the ensiform cartilage, and which may be in a few cases transmitted 
to the right axillary area. The murmur of tricuspid regurgitation has been said 
to resemble the sounds made by a small jet of escaping steam, and it may be singing 
or musical. Duroziez says that venous blood "sings" more than arterial blood. 

Diagnosis. — True tricuspid regurgitation must be differentiated from regurgita- 
tion at this orifice, which is temporary and not constant. These valves not rarely 
give way from severe strain, as in athletes during exertion. They act in this way 
as a "safety-valve" to relieve undue pressure, and as soon as the strain ceases the 
heart gradually returns to its normal size and the murmur disappears. So, too, 
a similar murmur may develop in cases of profound asthenia resulting from pro- 
longed fevers, particularly if the heart is strained by the patient attempting to do 
too much. Such a murmur may or may not pass away with rest. 

Prognosis. — The prognosis depends entirely upon the exciting cause, the age 
of the patient, and his general state and manner of life. In those who have to do 
manual labor the prognosis is usually bad. 

Tricuspid Stenosis. — This condition sometimes arises as the result of an attack 
of endocarditis involving both sides of the heart, and is usually associated with 
mitral stenosis. In other instances it is congenital. In the large majority of 
cases it is found as an associated lesion, and it is exceedingly rare. 

In 1899 Newton Pitt collected 87 cases of tricuspid stenosis from the postmortem 
records of Guy's Hospital extending over a period of twenty-six years, and compris- 
ing a total of 12,000 autopsies. Leudet, in his Paris thesis on tricuspid stenosis, 
gives the following figures, based on 114 postmortem examinations which were 
collected from various sources, and which include the cases collected by Fenwick: 

Stenosis of the tricuspid valve alone . . . 11 

Stenosis of the tricuspid and of the orifice of the pulmonary artery .... 3 

Stenosis of the tricuspid, mitral, and pulmonary 1 

Stenosis of the tricuspid, mitral, and aortic 21 

Stenosis of the tricuspid and mitral 78 

F. W. Griffith, of Leeds, has examined Leudet's tabulation of cases and has 
shown that probably only two of them were unassociated with lesions of the other 
valves. These figures show the rarity of uncomplicated tricuspid stenosis. 

Diagnosis. — The diagnosis of the lesion during life is usually very difficult, but 
it can be made. The murmur, if present, is presystolic in time and has its greatest 
intensity at the fifth right interspace near the sternum. As already stated, this 
murmur is usually associated with that of mitral stenosis, and its existence may be 
completely masked by the presystolic murmur at the mitral orifice. Additional 
physical signs of tricuspid stenosis are distention of the jugular veins without 
pulsation, or with very slight pulsation due to the feeble auricular regurgitant 
impulse. 

As dropsy is a late symptom of severe mitral stenosis, the early development of 
dropsy in a case with a presystolic murmur which is not aortic strongly indicates 
tricuspid obstruction. 

Disease of the Pulmonary Valves. — Lesions of the pulmonary valves are so 
rarely met with that many practitioners of large experience have never seen a 
case presenting them. When actual lesions occur they are nearly always congenital, 
and the usual lesion is that of pulmonary stenosis or obstruction, for pulmonary 
regurgitation is the rarest of cardiac lesions. On the other hand, there is no area 
at which we listen for the purpose of determining the state of the heart valves, 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 483 

in which murmurs are so constantly found as the so-called pulmonary area, at 
the second and third left intercostal space. These murmurs are not due to actual 
disease of the pulmonary valves or of the pulmonary artery, but they arise from 
causes of a non-organic character and are usually systolic in point of time. These 
functional murmurs may be due to one of several causes, as, for example, anemia 
and chlorosis, producing the so-called hemic murmur. They also occur in pregnant 
women and in women after childbirth. In other instances they are present as a 
sign of Graves' disease or of nervous tachycardia, and in still others they arise 
from some abnormal position of the heart, caused by conditions which alter the 
relationship of the heart muscle to its great vessels. These conditions all produce 
a pulmonary murmur which may be considered as within the area of the pulmonary 
artery or near its valves. In addition we sometimes hear at this point a so-called, 
cardiopulmonary murmur, which is supposed to be due to the effect of the blood- 
vessel upon the lung, or vice versa, in that the murmur occurs during forced 
inspiration, or expiration. This murmur is not rarely seen at this point in early 
tuberculosis of the apex of the left lung. 

Pulmonary Stenosis. — The systolic murmur which is due to actual organic 
disease at the pulmonary valve is due to stenosis, as already stated, and is commonly 
due to gluing together of the cusps of the pulmonary valves in antenatal life. This 
murmur is more harsh than the soft purring murmurs of the functional type just 
described. The patient usually has a history of having been cyanotic all his life, 
with dyspnea on the slightest exertion. Percussion and palpation will usually 
reveal a distinct increase of cardiac dulness to the right from hypertrophy of the 
right ventricle. Palpation also will reveal a distinct systolic thrill over the area 
of the pulmonary valves. 

The points by which the true systolic murmur is to be separated from the func- 
tional murmurs already described are the absence of systolic thrill in the case of the 
functional murmurs, the harshness of the true murmur, and the hypertrophy of 
the right ventricle in cases of actual pulmonary disease. From aneurysm of the 
descending portion of the aortic arch the true pulmonary murmur is separated by 
the fact that in such a case the hypertrophy chiefly involves the left side of the 
heart, by the additional fact that there is a bruit, not a murmur, and by the presence 
of a bruit posteriorly on the left side between the vertebras and scapula. There 
are also pressure symptoms in aneurysm in many cases. Finally, if it be aneurysm, 
percussion of the third left costal cartilage will reveal dulness, which is absent in 
pulmonary stenosis. The murmur of aortic stenosis is heard louder at the second 
right costal cartilage than at the second or third left cartilage, and is transmitted 
into the carotids, but the pulmonary murmur is not. 

Pulmonaey regurgitation, the rarest of all valvular lesions, is usually fetal 
in origin, but cases have been recorded in which it has arisen as a result of ulcerative 
endocarditis. The murmur due to this cause is, of course, diastolic, and is produced 
by the blood falling back from the pulmonary artery into the right ventricle. 
It is to be separated from aortic regurgitation by the fact that it is heard best to 
the left of the sternum instead of to the right, and by the absence of the Corrigan 
pulse of aortic disease. There are signs of dilatation and hypertrophy of the right 
ventricle, and the pulmonary second sound may be accentuated. It is by no 
means uncommon for the existence of pulmonary regurgitation to be unsuspected 
until autopsy. 

Treatment of Chronic Valvular Disease. — It is of vital importance that the physician 
remember the fact that the mere presence of a valvular lesion in the heart does not 
indicate drug treatment. On the contrary, much harm is frequently done by the 
administration of cardiac stimulants to patients who are found to possess a valvular 
lesion, with the result that natural compensation is disturbed and cardiac symptoms 



484 DISEASES OF THE HEART 

may be noted by the patient for the first time in his history. It is only when the 
patient presents symptoms which indicate failure of cardiac function that the 
physician should think of administering remedies which have a direct influence upon 
the heart. In other words, when compensation is complete, no cardiac treatment 
is indicated, but when it is ruptured therapeutic measures should be instituted. 
I have again and again seen patients who have presented some ailment involving 
other organs in the body than the heart, in whom the physician, on examination, 
found a mitral regurgitant murmur, and immediately proceeded to administer 
digitalis, forgetting that the presence of a murmur in the absence of evidences of 
circulatory failure is not an indication for the use of the drug. 

Another important point to be borne in mind when the physician is called upon 
to treat a case in which compensation is failing is that, far and above all drugs in 
value, is rest for the patient; not only rest of the body, but rest of the mind. The 
heart is an organ which, of course, cannot have complete rest at any time; but its 
work can be diminished one-half if the patient can be made to take no exercise, 
and if he will carefully abstain from business worries and cares. It is a remarkable 
fact that disease of the coronary arteries and of the heart muscle is more common 
in brain-workers than in those who gain their living by manual toil, and this is 
an indication of the fact that mental labor throws a severe strain upon the heart. 
Careful observation will promptly prove that patients who are not benefited by 
digitalis and other cardiac stimulants, when suffering from ruptured compensation, 
will at once improve if rest is insisted upon; for, manifestly, the rupture of com- 
pensation is largely the result of cardiac fatigue, and this fatigue cannot be put 
aside by the mere administration of stimulants. In order that the juices of the 
body may be kept moving, it is useful in these cases, when they are made to rest 
in bed, to use more or less vigorous massage daily, its vigor depending upon the 
strength of the individual. If the massage is too vigorous, it may produce very 
considerable fatigue, and it should not be employed to this extent. 

In all cases of ruptured compensation the patient should be warned of the danger 
of sudden, severe effort, since, even if death does not ensue under these circum- 
stances, the heart may be so dilated or fatigued that irreparable damage is done 
to it. 

Digitalis is without doubt facile princeps the best of cardiac stimulants. I 
have proved that it actually increases the muscular development of the heart, and 
the manner in which it acts results in an increased nerve and blood supply to this 
viscus which is not equalled by the results obtained from the administration of 
any other remedy. Digitalis is, in a large number of cases, given in too large 
doses. Not infrequently as much as 10, or even 20 minims of the tincture are 
given three times a day, with the result, that in the course of a few days the heart 
is overstimulated by the drug; its cumulative effect is produced, and instead of 
doing good it may do serious harm. I have known of cases in which the use of 
full doses of digitalis, persisted in for a considerable period of time, have resulted 
in the sudden death of the individual. 

When digitalis is given in overdoses it produces a curious irregularity of force 
and rhythm in the heart, with imperfect systole, followed by wide diastole, and 
this causes a hobbling pulse. The urine may also be reduced in amount instead 
of increased, as it should be, under the influence of the remedy. 

It has been my experience that if the patient is made to rest, small doses of 
digitalis produce satisfactory results, not more than 5 drops of the tincture being 
given three times a day. The only conditions in which I think that the use of 
large doses is justified are when the condition of the heart is found to be exceedingly 
feeble, and the patient's condition so critical that immediate stimulation is neces- 
sary; and again, when because of idiosyncrasy or other cause the heart is found not 
to respond to smaller doses. In the first class of cases it has been my experience 



CHRONIC VALVULAR DISEASE AS A RESULT OF ENDOCARDITIS 485 

that it is better to overcome pressing cardiac weakness by more rapidly acting and 
diffusible stimulants such as Hoffmann's anodyne, strychnine, and caffeine for 
the first twenty-four or forty-eight hours until the digitalis has a chance to act; 
for it must always be remembered that digitalis is a drug which produces its effects 
very slowly, and maintains these effects for some time after its use has been stopped. 
When large doses are given, it has been my experience that they may be decreased 
to about one-half or one-quarter the original quantity at the end of a few days, and 
their effects maintained by the use of smaller quantities. I do not think that I 
am exaggerating the case when I state that digitalis through its abuse, does almost 
as much harm as it does good. (See my Text-book of Therapeutics, 15th ed., article 
"Digitalis.") 

The fluid extract of digitalis may be given in the dose of from J to 5 minims, 
according to the needs of the case. One-half to 1 minim every eight hours is 
usually sufficient. A physiologically tested preparation should always be employed. 

When dropsy is present it has been held that the infusion of digitalis is the best 
preparation, on the ground that it is more diuretic. But any slight increase in 
diuretic power is, I think, counterbalanced by the fact that it is much more apt 
to disorder the stomach, which is in a disturbed condition in any case of grave 
disease, and particularly so in heart disease. 

When digitalis has been given in full doses to a patient suffering from ruptured 
compensation, he should be warned against getting up suddenly, and particularly 
against evacuating the bladder when in a standing position, as dangerous syncope 
may occur under these circumstances. 

Before deciding upon the administration of any cardiac stimulant in a case with 
ruptured compensation, the physician should make a careful study of the state 
of the bloodvessels, and if the arterial tension is higher than normal he should 
remember that the use of nitroglycerin to reduce this tension, and thereby diminish 
the work of the heart, is a more important therapeutic procedure than the adminis- 
tration of a stimulant which simply urges the heart to do more work in the face of 
vascular obstruction. In such a case the fact that digitalis stimulates the vasomotor 
system and raises arterial tension should also be remembered. Nitroglycerin 
can often be given to advantage to prevent this arterial effect of the drug. Stro- 
phanthus, which is a much less powerful stimulant than digitalis, possesses the 
advantage that it does not raise arterial pressure by stimulating the vasomotor 
system, and can often be given in the dose of 5 to 10 minims of the tincture every 
eight hours with advantage. Large doses of strophanthus are prone to produce 
an irritative diarrhea. 

There is a host of drugs which have been recommended for ruptured compensa- 
tion, but none of them approach these three in value, and often when these fail 
the failure is due to a mistake in the dose rather than to a fault of the drug. Should 
there be any tendency to hypostatic congestion of the lungs or pulmonary edema, 
digitalis may be freely given, and strychnine and atropine administered as vaso- 
motor stimulants. Two or three dry cups over the base of each lung are also useful 
under these circumstances, and sometimes a sharp purgative may do good if dropsy 
is present; but the possibility of the purge weakening the patient must always be 
borne in mind. 

Attacks of acute cardiac failure are to be combated by Hoffmann's anodyne 
in the dose of 1 to 2 drachms every hour or two, or aromatic spirit of ammonia 
in the dose of J to 1 drachm. If, associated with the cardiac failure, there is high 
arterial tension, the nitroglycerin should be used hypodermically in the dose of 
5"V to liro °f a grain, and repeated every half-hour until the tension is lowered, but 
sometimes high tension is needful. 

When marked dropsy is present, the use of magnesium sulphate in concentrated 
solution, a heaping teaspoonful to one-half glass of water taken before breakfast, 



486 DISEASES OF THE HEART 

will often do good by removing large quantities of fluid from the patient's body. 
A very useful remedy in cardiac dropsy, both by reason of its action on the heart 
and because of its diuretic effect, is apocynum cannabinum given in the dose of 
from 5 to 30 minims of the tincture twice or thrice a day until it produces slight 
purgation. Care should be taken that a tincture of real apocynum cannabinum 
is obtained. Much of that on the market is apocynum androsimefolium, which 
has no such therapeutic properties, but which so closely resembles apocynum 
cannabinum that its leaves are often unintentionally substituted for the true drug. 
Another very useful prescription in cardiac dropsy is a tablet composed of 

Extract of sourwood leaves .2 grains. 

Extract of elder flowers 2 grains. 

Extract of squill \ grain. 

Take one or two tablets three times a day. 

For generations physicians have been in the habit of employing a pill composed 
of— 

Powdered squill 1 grain. 

Powdered digitalis leaves 1 grain. 

Calomel . - 1 grain. 

three times a day in the treatment of cardiac dropsy, for its stimulant and diuretic 
effect. If free diuresis is not produced by this pill at the end of the third day 
it should be stopped, and a saline purgative administered to sweep out the calomel 
from the alimentary canal. 

In many cases of cardiac disease, particularly if the presence of anemia is marked, 
iron and arsenic are indicated, both on general principles and because we cannot 
expect to improve the nutrition of the heart when it is supplied by impoverished 
blood. 

It is important to remember that in nearly every case of failing compensation 
there is a certain amount of hepatic congestion. This is best relieved by the use 
of 5 or 10 grains of blue mass given every week or ten days. Frequently digitalis 
and other stimulants will act much better after the liver has been unloaded by the 
mercury than they will when this gland is congested. 

When the rupture of compensation has resulted in dyspnea and anxiety, morphine 
proves itself a most valubale remedy. It should not be given except in cases in 
which there is dire need of rest, since if used too frequently it loses its good effects, 
and frequently causes constipation and disorder of digestion. On the other hand, 
the quiet and rest produced by J to J of a grain of morphine will often cause mar- 
vellous improvement. It has seemed to me that it is most satisfactory in mitral 
lesions. If dropsy is present, it cannot be given hypodermically in the lower parts 
of the body because it will not be absorbed. 

When there is great engorgement of the jugular veins, and manifest distention 
of the right side of the heart with pulmonary congestion, venesection to the extent 
of about 8 ounces to a pint, according to the size of the individual, is often very 
valuable as a means of relief. It also is a remedy which is to be reserved for some- 
what desperate conditions, as manifestly it is not proper to bleed frequently. 

It is generally considered that digitalis does less good in cases of aortic regurgita- 
tion than in other valvular lesions, and I believe this opinion is correct. Some 
have taught that it is contra-indicated in aortic regurgitation. While this may 
be the general rule, every now and then we meet with cases in which cautious 
use of the drug in this state produces excellent results, provided compensation is 
ruptured. 

In some instances when the heart's action is very irregular and excitable an 
ice-bag applied over the precordium is advantageous. 

When the patient has had syphilis, chronic rheumatism, or gout, or manifests 



DISORDERS OF CARDIAC ACTION NOT DUE TO VALVULAR LESIONS 487 

evidences of arterial capillary fibrosis, iodide of sodium or iodide of potassium in 
the dose of 10 or 15 grains three or four times a day is advantageous. 

The diet in cases of valvular disease should be simple, but nutritious. The 
patient had better eat four or five small meals a day than two or three hearty 
ones, and the greatest possible care should be taken that foods which are prone to 
produce gaseous distention of the stomach and bowels are avoided. Fatty sub- 
stances are very apt to produce such symptoms, as are also the starches, when they 
remain in the stomach undigested for a considerable period of time. This, however, 
can be put aside in the case of the starches by the use of taka-diastase or pancreatin 
and by the use of powdered capsicum, either in pill or upon the food, for the purpose 
of stimulating the gastric mucous membrane, which is often atonic or catarrhal 
as a result of the impaired hepatic circulation. 



DISORDERS OF CARDIAC ACTION NOT DUE TO VALVULAR LESIONS. 

Neuroses. — Definition. — By neuroses of the heart it is meant to include a 
number of conditions widely separated in their actual causes, but depending upon 
a disorder of the nerve supply of this organ, so that, without there being necessarily 
present any grave lesions, its functional activity is impaired or perverted. 

Palpitation. — Palpitation of the heart may be due to any of the valvular or other 
lesions that cause the heart to beat rapidly or irregularly when the individual takes 
exercise. In other cases it arises from the accumulation of gas in the stomach or 
colon, which by its pressure causes cardiac disturbance. In other instances it is 
due to intense nervous erethism, and in still others it arises from the excessive use 
of tobacco, or of coffee or tea. So, too, sudden nervous shock may cause repeated 
attacks of this character. Probably the most frequent cause of cardiac palpitation 
is not connected with the nerves supplying the heart, but is due to irregularities 
in the nervous control of the vasomotor system, whereby the tension of the vessels 
is relaxed and as a result the heart beats rapidly because the ordinary pressure 
in the arteries is suddenly removed. It is remarkable how cases of palpitation 
get well if attention is paid to the state of the bloodvessels rather than the heart. 
The so-called "irritable heart of soldiers," first described by J. M. Da Costa, is due 
in all probability to this cause as well as to the imperfect action of the vagus. 
Associated with the disordered cardiac action it will often be found that the periph- 
eral capillaries suddenly become dilated, so that the blood can flow more rapidly 
than normal into them. Profuse diuresis, in which the urine is found to be pale 
and clear, shows that a similar relaxation of the renal vessels has ensued. These 
symptoms often cause the patient great alarm and bring him at once to the physician 
with the statement that heart disease is feared. It is usually the case that a patient 
who says he has heart disease has only a neurosis, unless some physician has found 
a real lesion and told him of its existence. 

Tachycardia. — Many cases of neurosis are closely allied, if not identical, with 
that condition of rapid heart called tachycardia. This may be due to vasomotor 
palsy, to a deficient action of the vagus nerves, or to some central nervous lesion. 
(The tachycardia of exophthalmic goitre is not considered here.) 

Such attacks occur in young hysterical women and are called "pseudo-angina," 
because a sense of cardiac expansion is often present with the rapid beating of 
the heart. They also appear in women near the menopause, and in men who 
have been guilty of excessive sexual abuse. A few cases in men are apparently 
due to some organic nervous lesion. The pulse may rise as high as 220. The 
tachycardia may be paroxysmal or continuous. In a case under my care in 1890, 
a woman who had seen her husband and sons drowned in the great Johnstown 
flood, and had been swept from the roof of her floating cottage, presented a pulse 



488 DISEASES OF THE HEART 

rate which was uncountable, it was so fast. This persisted for months and was 
present two years after the catastrophe. 

Rapid, feeble heart sounds, in which the first and second sounds appear alike, 
are met with in prolonged exhausting fevers such as severe typhoid fever, and to 
this state is given the name "fetal heart sounds" or "embryocardia." 

Bradycardia. — Great slowness of the heart's action (bradycardia) is caused, to 
some extent at least, by conditions which are the antithesis of those that cause 
tachycardia. A sudden or persistent rise of arterial pressure may cause a very 
slow pulse, as the heart endeavors to force blood through tightly contracted vessels. 
This may be called vascular bradycardia. Again, it occurs as the result of irritation 
of the vagus nerves, by poisons such as digitalis and opium, or in chronic lead 
poisoning, or again in cases of jaundice when the slowing is due to the biliary salts 
in the blood. It is also met with in cases of cerebral hemorrhage, cerebral tumor, 
and in the coma following epilepsy. 

A pulse below 60, or even as low as 40, is sometimes felt after a woman has given 
birth to a child. (Plates VIII, IX, and X.) 

Occasionally cases are met with in which the bradycardia becomes extraordinary. 
The late D. W. Prentiss reported to the Association of American Physicians in 
1889, 1890, and 1891 the case of a man whose pulse at times fell to 11 per minute 
and rarely rose over 40 per minute for two years. In this case no very distinct 
morbid lesions were found at autopsy, although the patient died suddenly in an 
attack. (See Stokes-Adams Disease and Arrhythmia.) 

Arrhythmia. — This is very commonly met with in persons who have taken ex- 
cessive doses of digitalis, and it is also a common symptom in mitral stenosis with 
ruptured compensation. The so-called gallop rhythm may appear in these cases. 
(See Mitral Stenosis.) 

Modern studies of the physiology of the heart must be understood when cases 
of arrhythmia are observed. It is to be remembered that the contractility of the 
heart muscle is inherent, that is to say, the muscle contracts by virtue of its own 
properties and not as the result of a direct nervous impulse, as do other muscles. 
It must also be recalled that the contraction wave starts in the sino-auricular node 
which exists near the orifice of the coronary sinus in the right auricle, passes over 
the auricular wall to Tawara's node, and thence by the bundle of His, which mus- 
cular band or bundle crosses the auriculoventricular junction, splitting into two 
bands, one for each ventricle. By this means the impulse passes to the muscle 
cells of the ventricles and the musculi papillares (Fig. 91). Although this con- 
traction wave is myogenic in origin it is of course influenced by extraneous causes, 
chiefly nervous, and by the contents and heat of the blood passing through the 
cavities of the heart. The auricles and ventricles can, however, originate con- 
traction waves independent of one another and such inco-ordination is one of the 
chief causes of arrhythmia. During systole the conductivity, contractility, and 
irritability of the heart are abolished, but they are restored during diastole. 

In some cases of arrhythmia auscultation will reveal a normal first and second 
sound followed closely by another first sound less well marked and by a second 
sound which is very feeble, or it may be inaudible. This is called an extrasystole. 
The beat is a feeble one because the heart muscle has not had time to have its 
vital properties restored. After this abortive extrasystole there is a longer pause 
than is common and then the heart, having had a long period of recuperation, gives 
a very forcible beat which often alarms the patient. The delay in the development 
of this powerful systole is not due to exhaustion of the ventricle by reason of the 
first systole but because of the extrasystole which renders the muscle refractory to 
stimulation, and as a result the ordinary contraction wave passing over the auricu- 
loventricular bundle is unable to cause contraction of the ventricle. The response 
to one normal sino-auricular impulse is therefore entirely missed and the long 



DISORDERS OF CARDIAC ACTION NOT DUE TO VALVULAR LESIONS 489 

pause permits the ventricle to recover its contractility and to accumulate a 
large amount of blood. The sequence is therefore a forcible systole, an extrasy stole 
arising in the node of Tawara or in the wall of the ventricle, a sino-auricular 
impulse at the time for the next regular systole, which accomplishes nothing, and 
then a regular systole normal as to time, but more forcible than usual, because of 
long recuperation (Fig. 91). This regular systole may occur slightly before it 



Fig. 91 



Right 
vagus 




Tawara's node 
His' bundle 



f \ : i ■ 



Centres of ventricular 
contraction 




Centres of ventricular contraction 



Right side of the heart showing diagrammatically the distribution of the two vagus nerves to different 
parts of the viscus. The impulse to contraction originates at the sino-auricular node and passes over 
the wall of the auricle to Tawara's node, and thence over His' bundle across the auriculoventricular 
septum to be distributed throughout the ventricular wall. If the upper, sino-auricular, node is dam- 
aged, or if its impulses fail to get across the wall of the auricle, Tawara's node acts in its place to 
start off the ventricle. If a lesion at the base of the mesial segment of the tricuspid valve damages 
His' bundle, so that Tawara's node is cut off from the ventricle, then the ventricle may originate its 
own impulses to contraction. 



would have taken place in a perfect rhythm, because the irritability of the muscle 
has been increased by the missing of its normal rhythmic contraction. Extra- 
systole may arise from a number of causes widely different in origin. In one case 
the condition is apparently a purely functional disorder which lasts for years, the 
patient seeming to be in perfect health and the contractions of the heart being 
irregular because the vagus is irritable. Another case depends upon the absorption 



490 DISEASES OF THE HEART 

from the alimentary canal of certain toxic matters which entering the blood affects 
the heart as do certain drugs. A third case is more grave, in that the irregularity 
arises from a toxemia due to one of the infectious diseases which may result in purely 
functional disorder or give rise to morbid changes in the bundle of His or elsewhere 
in the heart muscle. In the aged there may be irregularity due to organic disease 
or irritable vagus. Lastly, arrhythmia may be due to myocardial degeneration 
often associated with syphilis, nephritis or arteriocapillary fibrosis. (Plates VIII, 
IX, and X.) 

In still another type of cardiac disturbance the systoles are normal as to rhythm, 
but irregular as to force, each alternate systole being less forcible than the other. 
This gives rise to the so-called pulsus alternans. 

It. is notable that Tawara in examining 112 hearts postmortem in cases in which 
arrhythmia had been present during life found no lesions that could have been re- 
sponsible for the symptoms which had been present. 

Treatment of Cardiac Disorders. — In the treatment of the various cardiac neuroses 
it is essential that the physician shall first determine what portion of the circulatory 
system is chiefly affected by disordered innervation. Not infrequently, however, 
it will be found that both the heart and vasomotor system are out of order, and 
therefore the treatment will have to be devoted to regulating the nerve supply 
of the functions of both of these important vascular areas. 

When it is believed that attacks of tachycardia have their origin in a condition 
in which the pneumogastric nerves fail to control the action of the heart, digitalis 
is, of course, a valuable remedy in that it exercises a powerful stimulating influence 
upon the pneumogastric nerves. In some instances, however, the action of the 
heart is already sufficiently vigorous and the administration of digitalis, while 
stimulating the pneumogastric nerves, also stimulates the heart to such an excessive 
degree that its action becomes too violent. Under these circumstances it is well 
to combine with the digitalis a little aconite, which drug also stimulates the pneumo- k 
gastric nerves, and thereby aids the digitalis in controlling the heart, and at the 
same time combats the influence of the digitalis upon the heart muscle itself, 
thereby preventing overstimulation. A prescription made up as follows will often 
be of advantage, the quantities of the ingredients being varied to suit the needs of 
the individual case: 

1$ — Tinct. digitalis (physiologically tested) f 5j (4.0) 

Tinct. aconiti f 3j ( 4.0) 

Tinct. belladonnse f 5jij (12.0) 

Tinct. cardamom, comp q. s. ad f §iij. . 

A teaspoonful to a dessertspoonful three or four times a day. 

The efficiency of this prescription may be increased by the application of a bella- 
donna plaster over the heart. 

When by the use of the sphygmocardiograph it is found that there is obstruc- 
tion to the passage of the impulse over the bundle of His large doses of atropine 
are very useful. When extrasy stoles occur digitalis by diminishing the activity of 
Tawara's node and His's bundle may do good (Fig. 91). (Plate VII.) 

In those cases in which the cardiac irregularity depends chiefly upon alternate 
spasm and relaxation of the bloodvessels, so that they are at one moment offering 
too much resistance and at another too little resistance to the flow of blood, much 
benefit can be produced by hydrotherapeutic measures, such as directing that the 
patient shall take an alternate hot and cold sponging in the morning on getting 
up; first, drenching himself with a sponge dipped in as hot water as he can bear, 
and next drenching himself with a sponge dipped in cold water. In this way he 
does not become chilled, but the elasticity and tone of the bloodvessels is much 
improved. The prescription just recommended is also beneficial in many of these 
cases, and not infrequently moderate doses of tincture of mix vomica are advan- 



t3 J2 
PI'S 

P a 
o 

'3 ■+£ 

3 o3 

3 .8 

03 ^ 

-^ 

> 

v-ci 

m s 

° ft 



o3 o3 
> P 



> 

< 



.2 

CO 

o 

ffl 

CO 

& 
C 

"o 

o 



3 

cd 

CD 

X 

s 

«-> 

cd 



e^ 

o> 

• ~ o 

«'£ 

cd£ 
lO 0) 

^"ft 
„P 

1§ 

ft"o 

3 §5 

02 > 
03 

P3 ° 

CD 

• r'o 

O -r-l 

CO P 

3| 

_r ^ 

s.s 

ft- 1 - 5 

■p ^ 
s s 

rP 03 

co +_ 

CO-" 

„ ;-( 

CD c3 

*'E 

*"■ 03 

c3 ^ 

P^ 
•So 

-^ v -^ 

P fe o8 

• ~ P -^> 
<M ^ o3 

03 -h .(J 

-^ ^ Ph 

o8 -e o3 

^t^rP 

3 * 



sh 

CD 
nJ 
f-i 

c3 

!§ 
c3 

<u 

rP 

a 

o 
?-t 

ti 

03 

O 
03 

rP 
-*3 



- o3 >> 

fa « "fa 

^ If o 
P cc 
03X5 
> 03 



P 

X> 

b£ 
.£, 

0) 

,p 

£ 
o 

m 

b£ 

.S 
'o 
o3 

-t-3 
f-l 

CD 

ft 

ft 
p 

CD 
-P 
H 




CD" 
O 

d 

O 
Fh 

+3 
O 



I— I 
Oh 



co 

CO 

cd 

-1-3 

w 



u 

u 

cr 



o 
u 




o 



u 



O^ cd^ 3 
CD O g » 

^ 3 CD ~„ -^ k* 

2 > 22 h 

CO 03 02 M 

03 O^ 



o 

cp -t-3 



cc 



0,d 

-+3 CD 
CO .r-j 

* 2 

CD 



CO 

S3 03 



CO CD 

CD 

CD 

is 

8 ft 
r> co 
-+3 

-ci a 

ft 03 
CO 

CD -1-3 
Jh CO 

b CDC^ 

03 r-l 

fH , 4=i 



CD 
CO 
CD 

4C 



CD CD 

0+3«H 



CD-C1 

ci a 

CD B 
d 

^ CD C 






T5 
Cd 

o 
>> 

Cd 

m 



CD 5^ ^ O 



3^£ k 

^H 03 j?^ a; 



03 CD 
CD Fh 
_Q CD 



O 
CD 

CD 

d CD 



CD 



— CD 

o 3 

(11 M 



CD 



f-t I 1 

CD 
ft-S 



s-< CO 

CD 1> 

ft 



CD 



03 

CD . 

~ O M , 

CD CO^XJ 
CO 03 >£ CD 

ft^^g 

S o cj ^ 

CD* 






<K CO CD 



CD 



■^00 o O'-g d 

03$3 CD 03. CO 

^ co ^ £>-§ 
bD CD £;£ S 

M -8 3 « 

Cj co _^> 73 

F-l , — i 03 

fi 03 CD - 

o ci c p— i i2 r S 

o ?h 2 ™ rS -t- 3 
o o * - 

« u . 

- CD^ 2 
O^H Ci p 



d ft 

o£ 

03 

03 CO 
CD 

bfl-H? 

CI 



CD 



CO 



i>n3 
^ C 

03 



~ ^ 03 _i 

Ec.S C^ 



£ M '3)'ci 



CD'S 

3^ o 

^^ CD ® 

CD CO _£ c3 O •+= 



• CI o 

03 12 

% £ 

ft o 

ftt^ 

So 

^^ 

O cp 



CD 



IS 



C3 15 



co bfi^3 

S S Ci 

2 co ® 

„-, t-t o c 5 i_r cs 

3 CD^O 
3^C 03 

c ^-^ 

>i 03 >. 



03 S"^ 

"CJ -t-= 

Ci m 

<-» CD 






03 



«•*- fl 



r- ( CD 

CD 



CD ^ 

co 



co 

o 

CD CO O ."Ci 

^h 03 03^ 

CD -P- 



y.rt cd 

" co g 

CD .S 
g CD 

«+h Eh 
o 

£ "2 

.2 c 

03 03 

^ ^3 

CD 03 
" ft 



° 15 
-t-3 03 

C^ 



Ph O 



ft 
53 



If^bc-B^pl 
j a 



bfi 

c8 a 

O ^H 



CD . 

CO 03 .^j 






83 



CO 03 '" CD 

«^§^ 

,2 o 

c 



CD 



03 O 

a o 

gEH 



CD d d ^i 

>P^ o 



CD 

+2 bb 

° 2 

ft^ 
d +3 






X 







2^ 

S *" i..irt 02 
13 > 

<a c3 !> <o > 

3 3 G> o <u -•-= 



ANGINA PECTORIS 491 

tageous. When the disorder depends upon the excessive use of tobacco, this drug 
must, of course, be prohibited; and if the patient is overworked, and suffering from 
nervous strain, he must be sent away on a vacation; or, if his condition is grave, 
be given a "rest cure." When a disordered circulation is associated with pain 
in the neighborhood of the heart, small doses of antipyrin, 2 to 3 grains, are often 
useful; and if the tension is high, nitroglycerin should be given. 

ANGINA PECTORIS. 

Definition. — By angina pectoris is meant a condition in which a patient, usually 
in or past middle life, is seized by a severe, agonizing pain in the cardiac area, 
which extends in most cases down the left arm even to the wrist, and suffers from 
intense mental anxiety and a sense of impending dissolution. It is important 
that pseudo-angina be not confused with it. (See Aortitis.) 

Etiology and Pathology. — The cause of true angina pectoris is usually athero- 
matous change in the coronary arteries, although this is by no means always the 
case. Thus, Potain found stenosis of both coronary arteries in 20 out of 45 cases 
at autopsy, and Huchard in 38 out of 70 cases. It is distinctly a disease of the brain- 
worker rather than of the man who gains his bread by manual labor. The laborer 
and artisan present to us very commonly the most surprising degenerative changes 
in their arteries in the way of calcification of their radials and temporals, but they 
rarely have true angina. On the other hand, the man who is subjected to nervous 
strain rarely shows extraordinary calcareous changes, but he is the unfortunate 
victim of this terrible malady. Physicians are peculiarly prone to it. The number 
of deaths among the leaders of the profession in Philadelphia during the last two de- 
cades from this cause is extraordinary. Mental strain with a sedentary life are, there- 
fore, causes. Gout, syphilis, and renal disease are also causes. The disease affects 
men much oftener than women. Out of 65 cases collected by me only 4 occurred 
in women, and out of 290 cases collected by Forbes, Huchard, and Lartigue only 
47 occurred in women. Aside from the narrowed and thickened coronary arteries 
and the fibroid changes in the heart which result from their state, there are no 
characteristic lesions of true angina pectoris. Among the exciting causes of an 
attack are to be named nervous wear and tear, anger, or muscular exertion, par- 
ticularly if it be made in the face of a cold wind, which contracts the capillaries 
and so increases still more the labor of the heart. So, too, errors in diet, by causing 
gastric disorder, may reflexly cause an attack. 

Sir Douglas Powell and Merklen give the age incidence for true angina at twenty 
to forty years. This is probably too young. The actual age is forty to sixty years. 

Symptoms. — When angina pectoris is well developed there is no symptom-complex 
so characteristic and dramatic. Seized on a sudden or with but a few moments' 
warning, the patient stands or sits transfixed with pain and fear. It is difficult 
to tell whether his arrested respiration is controlled by the disease or his own will- 
power. The sense of dissolution or of impending death is so real that the patient 
expresses the belief that death is at hand, if he can find breath to speak. The 
expression of the face is one of intense anxiety or horror, the skin is pallid to the 
degree of cadaveric hue, and the brow is marble white and perhaps bedewed with 
sweat as the attack advances. The pulse during an attack is usually slow, small, 
and very tense, becoming feebler and more relaxed as the paroxysm passes away. 
The pain is often beyond the patient's power of description after his recovery, 
both as to severity and character. Some patients say that the heart feels as if it 
were being crushed in a vise; others that a huge stone is crushing the chest wall; 
others that a heavy bar of steel is laid across the thorax. At times the pain not 
only extends down the left arm to the fingers, but to the right arm as well. As 
the attack passes off the patient's expression of keen suffering is modified. A flush 



492 DISEASES OF THE HEART 

may supplant the pallor and a sigh reveals that the seizure has passed. At this 
time the patient not rarely belches up large volumes of gas, and this seems to give 
much relief. It is this which gives rise to the euphemistic diagnosis of "acute 
indigestion" in some of these cases. Sometimes more than one attack may occur 
in an hour, but this is rare. 

Modified forms of severe angina are constantly met with in which the pain 
is not so severe as in the cases just described. The degree of modification may be 
so great that little or no pain is felt, this form being called angina pectoris sine dolor e. 

Diagnosis. — When angina pectoris presents itself in its well-developed form, 
there cannot be much doubt as to its true character. The question of the character 
of an attack is, however, often in doubt when the symptoms are not all present. 
While it is a rule that valvular disease of the heart rarely causes pain, it is a fact 
that attacks of anginoid pain are occasionally met with in cases of aortic regurgita- 
tion, particularly if dilatation of the heart is marked. This state can be determined 
by the diastolic murmur and the "Corrigan pulse." Again, aortitis may cause 
symptoms practically identical with those of true angina, and it may be impossible 
to separate the disease of the aorta from that of the coronary arteries because the 
lesion spreads from the aorta to the openings of these vessels. That is the angina 
may be due to aortitis. 

It is of some importance to differentiate the angina pectoris due to ordinary 
coronary sclerosis and secondary myocardial change from that due to syphilis. 
This is probably impossible by the physical signs in the circulation, but can be 
made if a history of late syphilis can be obtained, or if the patient is prematurely 
aged or if he gives a Wassermann or Ruelin reaction. While these changes, when 
due to syphilis, cannot be treated as successfully as can secondary syphilis, for they 
are of the nature of late syphilitic affections, more aid can be given by the use of the 
iodides of mercury and salvarsan than in those cases which present changes in the 
coronary arteries from other causes. 

A form of pseudo-angina is occasionally seen in nervous women and in men 
who resort to wine, tobacco, and women to excess. It differs from true angina 
pectoris in the facts that the man is usually under thirty years rather than over 
forty years of age; his vessels are usually in fair condition; there is a history of. 
neurosis or excessive venery and of the excessive use of tobacco, and the sensation 
about the heart is that of distention instead of constriction. 

Prognosis. — From what has been said as to the state of the vessels and the heart 
muscle in true angina pectoris it must be evident that the prognosis is most grave, 
for death may ensue in any attack and an attack may come on at any time. On 
the other hand, patients sometimes go long periods without a fatal attack, partic- 
ularly if the mode of life can be quiet and the pulse tension can be reduced by the 
iodides and nitroglycerin. Much depends in prognosis upon the degree of vascular 
and myocardial change which can be found. In many of these cases the feeble first 
sound shows how weak and dilated the ventricles have become. 

Treatment. — The treatment of angina pectoris may be divided into that which is 
devoted to the improvement of the circulatory condition with the object of pre- 
venting paroxysms of the disease, and to that which is devoted to the relief of the 
patient during the paroxysm. As the treatment of a paroxysm requires very active 
procedures, it will be considered first. If seen as a paroxysm is commencing, the 
patient should inhale from 3 to 5 minims of nitrite of amyl, or if this drug is not at 
hand a few whiffs of chloroform should be used. Nitroglycerin should also be 
given hypodermically in the dose of T ^ or even ^ of a grain. If the patient has 
become accustomed to this remedy, larger doses are indicated. Sometimes it is 
advantageous to give simultaneously with the nitroglycerin \ of a grain of morphine; 
but in those cases in which the paroxysm is not of long duration, the attack com- 
monly passes away before the morphine has an opportunity to exercise its pain- 



ANGINA PECTORIS 493 

relieving influences. If the patient can swallow, a very useful remedy is 1 or 2 
drachms of Hoffmann's anodyne given in a little cracked ice and water; or, if 
this is not at hand, J to 1 drachm of spirit of chloroform may be given in a similar 
manner. The employment of nitrite of amyl, nitroglycerin, and chloroform is 
useful in direct proportion to the degree of arterial spasm which is present. In 
that somewhat unusual class of cases in which attacks of angina occur with a state 
of low arterial tension, these drugs, manifestly, cannot be of the same value as in 
those patients in which the systemic arteries are tightly contracted. Should the 
patient be seen in a paroxysm and the physician possesses none of the remedies 
just named for his relief, a drink of hot water, containing some capsicum, or some 
brandy, may be given, since this not infrequently causes the belching up of a 
considerable quantity of gas followed by some degree of relief to the patient. 

The treatment between the paroxysms is dietetic, hygienic, and medicinal. 

The patient must take a sufficient quantity of food for the purpose of maintaining 
his nutrition, and must be forbidden to eat anything more than is absolutely neces- 
sary for this purpose. Sweet and fatty articles of diet should be entirely avoided, 
as should be champagne and all sweet wines. If any alcoholic stimulant is required, 
Scotch or rye whiskey, or a dry gin with lime-juice and sparkling water should be 
ordered. There is no objection to the diet being largely one of meat, if the kidneys 
are in a fairly healthy state; the more so, as starchy foods are prone to cause the 
formation of gas in the stomach and bowels, which may reflexly upset the cardiac 
balance and precipitate an attack. 

As distention in the stomach sometimes causes an attack, it is often necessary 
to feed the patient with small quantities of food four or five times a day rather 
than to permit him to eat two or three hearty meals. 

The hygienic treatment consists in having the patient take as much sunshine 
and fresh air as possible; in forbidding him to expose himself to blustering winds, 
and to warn him that if his peripheral circulation is chilled the consequent contrac- 
tion of his capillaries may result in an attack of heart pang. Flannel should be 
worn next the skin both winter and summer. Sudden effort, as going up stairs 
rapidly or running for a car, or entering into any heated debate, either in court or 
in a business argument, should be avoided. 

Care must be taken that the bowels do not become overloaded with feces, and 
that they be moved every day by some vegetable laxative or one of the mild saline 
waters. 

The medicinal treatment consists in the administration of iodides in as large 
doses as the patient can readily bear without danger of disordering his digestion. 
If there is a history of syphilis in the case, larger doses are needed than if the history 
is not specific. The patient should take at least 60 grains a day of the iodide of 
sodium or iodide of strontium if possible, divided into four doses, which should be 
taken one hour after food. In some cases syrup of hydriodic acid, in the dose of 
2 to 4 drachms three or four times a day, may be given with advantage, well diluted 
with water. The iodides under these circumstances lower arterial tension and do 
whatever can be done toward arresting the process of fibroid overgrowth in the 
bloodvessels. The patient will also be much benefited if he receives nitrite of 
sodium in the dose of 1 grain four or five times through the twenty-four hours, the 
dose being controlled, not by the number of doses administered, but by the effects 
which it produces upon arterial tension. In some instances it is wise to alternate 
the nitrite and iodide. If the heart muscle is very feeble, full doses of mix vomica, 
10 or 20 drops of the tincture, or moderate doses of digitalis — say, 5 minims of the 
tincture— may be given three times a day. The patient should be instructed to 
carry glass pearls of nitrate of amyl in his pocket and to crush one and inhale its 
contents if at any time he feels threatened by an attack. 

Symptoms of gastro-intestinal dyspepsia are to be relieved not only by regulating 



494 DISEASES OF THE HEART 

the diet in the way indicated, but by the use of pancreatin and taka-diastase to 
aid digestion. A very useful capsule under these circumstances is one which con- 
tains 2 grains of taka-diastase, 2 grains of pancreatin, 1 grain of capsicum, and J 
grain of extract of mix vomica. This should be taken thrice daily. Donovan's 
solution is often useful. 

CONGENITAL CARDIAC DEFECTS. 

Two abnormal conditions may arise in the heart of the foetus and persist after 
birth, namely, defects of development and defects produced by an attack of endo- 
carditis. In some instances the endocarditis is responsible for the defect in develop- 
ment. The most common of these defects is the persistence of the foramen ovale, 
which permits the blood to make a short circuit through the interauricular septum 
instead of passing into the right ventricle and thence through the lungs. Some- 
times this opening is partly guarded by a membrane, but in other cases no such 
membrane is present. If the opening is large and entirely unguarded by a mem- 
brane the patient is apt to present intense cyanosis, particularly if any effort is 
made; but in some cases the defect does not produce this symptom and the patient 
lives to adult years, no one suspecting the presence of such a defect, the existence 
of which is revealed only at autopsy. Thus, my colleague, Coplin, made an autopsy 
upon a woman, dead of croupous pneumonia. During her life and in her filial 
illness there were no signs of cardiac disease, but at the autopsy a twenty-five-cent 
piece could be dropped flatwise through the foramen ovale. More or less oblique 
communications between right and left auricles are present in about 2 to 5 per 
cent, of adult hearts. 

A very rare congenital defect is a patent ductus arteriosis which produces no 
definite symptoms, save that it is sometimes associated with stunted development, 
but definite physical signs, namely a distinct thrill and pulsation in the second 
left interspace close to the sternum with a loud, rasping, prolonged, humming-top 
murmur extending all over the precordium, to the vessels of the neck, to the scapula, 
and along the vertebral column. The second pulmonic sound is also accentuated. 

A much more rare condition is that in which there is an absence of the septum 
between the right and left sides of the heart, and as a result "bilocular heart" is 
present. In others again the absence of an interventricular septum produces a 
"trilocular heart." At times a condition is met with in which a perforation exists 
in the upper part of the ventricular septum, in the so-called "undefended space." 
A perforated interventricular septum is characterized by a systolic murmur and 
an absence of marked cyanosis. 

Stenosis of the right conus arteriosus, of the pulmonary artery, and of the pul- 
monary orifice are often associated, and form a large proportion of the congenital 
lesions seen at autopsy in persons who have suffered from these defects, but lived 
for years. It is a noteworthy fact that these lesions are not rarely complicated 
by a patulous interventricular septum, an open foramen ovale, and an open ductus 
arteriosus. Considerable hypertrophy of the right ventricle is naturally found in 
these cases if life is prolonged. Congenital pulmonary stenosis when severe enough 
to produce marked circulatory disorder in early infancy is characterized by cyanosis 
and enlargement of the area of cardiac dullness and often a well-marked thrill on 
palpation. 

Valvular anomalies also occur. The three aortic semilunar valves may be 
replaced by two leaflets. This state while not at all incompatible with life is, 
nevertheless, prone to become grave, in that the semilunar valves usually become 
thickened and distorted. The pulmonary valves are much more rarely abnormal, 
and the valves protecting the auriculo ventricular orifices on both sides of the heart 
are even more rarely anomalous from defective development. These valves may, 



AORTITIS 495 

however, be the subject of endocardial disease prior to birth, and the result is, 
in one sense, not very different from that met with in the heart of the ordinary 
individual who suffers from rheumatic endocarditis; for we find the auriculo ventricu- 
lar valves thickened and the chorda? tendinese broadened and shortened so that they 
interfere with the free action of the valves. That form of acute or chronic endo- 
carditis which results in the production of granular or warty nodules on the valves 
is rarely encountered in fetal endocarditis. 

The orifice of the pulmonary artery is very commonly found to be in a state 
of stenosis, as a result of gluing together of the valves and contraction of the ring 
around the orifice itself. The agglutination of the segments may be so perfectly 
accomplished as to leave a smooth, funnel-like opening, or the valves may be rough- 
ened by vegetations. Patients with this defect may live for years, but it is a 
curious fact that they are very prone to die of pulmonary tuberculosis. 

Narrowing of the aortic orifice is a rare congenital defect. Malposition or trans- 
position of the heart is sometimes seen. Transposition is always associated with 
transposition of the other viscera. 

Occasionally ectopia cordis, a state in which the heart is not protected by the 
chest- wall, is met with. The heart has also been found in the abdominal cavity. 
Peacock reported one such case in a man of forty-seven years, and Rezek one in a 
man of thirty-two years. It is important to bear in mind that congenital cardiac 
defects are often multiple. 



DISEASES OF THE ARTERIES. 

The tubes carrying blood are subject to many alterations, some of which depend 
upon changes in the perivascular tissues, including with these peri-arterial inflam- 
mations, infection, trauma, etc. The most important group of vascular changes, 
however, result from alterations in stress and tension under which the circulation 
is maintained, and, to a greater degree, are the results of the irritant action of 
poisons circulating in the blood. The intravascular irritants may be bacterial 
or of bacterial origin (toxins), unusual quantities of normal salts, or the presence 
of abnormal compounds that irritate the endothelium. 

With the acute and subacute inflammations involving the intima (endarteritis), 
and the relation of this change to later alterations in the vessels, we are at present, 
through the studies of Thayer and others, becoming more familiar. The clinical 
importance, however, of these alterations is not as yet fully appreciated. Hyaline 
and fatty degenerative changes occur in the intima and subintimal tissues in a 
number of pathological processes. The deposit of pigment in the vessel walls, 
infiltration by lime salts (calcification), and amyloid disease are rarely, if ever, 
primary in the vessels, but depend upon a number of primary conditions, and there- 
fore are rarely, if ever, recognized independently of the conditions by which they 
are caused. Infections acting within the vessels give rise to proliferative or necrotic 
changes in the endothelium with the formation of thrombi (thrombo-arteritis and 
thrombophlebitis), which, by mechanical interference of the circulation, influence 
the nutrition of the organs, or, by causing embolism and distribution of infectious 
material through the system at large, constitute the basis of septicemia and pyemia 
as already considered. 

AORTITIS. 

Closely allied in its symptomatology and pathology with angina pectoris and 
arteriosclerosis is aortitis, a condition usually due to an old syphilitic infection or 



496 DISEASES' OF THE ARTERIES 

to gout. It is characterized by the morbid changes described under Arteriosclerosis 
and by the presence of more or less constant distress or gnawing pain under the 
upper sternum. There are often acute exacerbations of this pain particularly at 
night, and on exertion and this pain may extend down one or both arms. 

The treatment consists in rest and, when there is a specific history, in the use of 
salvarsan and mercury, particularly the latter, associated with, or followed by, 
iodide of potassium in large doses. If the general arterial system is degenerated 
the use of salvarsan must be cautious or avoided. 

ARTERIOSCLEROSIS. 

Definition. — Arteriosclerosis, as we understand it today, evidently comprises 
a number of pathological processes, the exact relation of which, one to the other, 
is still somewhat uncertain. Two important processes, often, if not constantly, 
associated, are, first, an affection involving particularly the smaller arteries (arteri- 
oles), and commonly termed arteriocapillary fibrosis; and, second, a type of arterial 
change involving particularly the larger vessels and called atheroma, or, on account 
of the changes in the conformation of the affected vessels, arteritis deformans. 
Writers are not agreed that these two processes are independent, for they are 
very constantly associated, and the clinical picture embraced under the term 
arteriosclerosis includes them both. 

Etiology. — Certain individuals, and often whole families, seem peculiarly liable 
to arteriosclerosis. The change is often a manifestation of age, and the trite 
but true saying " that a man is as old as his vessels" indicates the belief in premature 
aging of those in whom arterial change occurs in early life. Alcohol, and intem- 
perance in work and eating, and overexertion, mental or physical, are also causes. 
The auto-intoxications, lead poisoning, syphilis, and gout are important factors 
in the production of arterial disease. The demonstration of the Treponema pallidum 
in aortic lesions has substantiated some of the earlier claims as to the frequency 
of syphilitic aortitis. There is not unanimity of opinion, however, that syphilitic 
aortitis is always to be differentiated anatomically from the ordinary atheroma 
or that the former, as some assert, is the cause of the great majority of aneurysms 
of the aorta. Certain forms of chronic interstitial nephritis may precede, accom- 
pany, or follow arterial change. (See Etiology of Chronic Interstitial Nephritis.) 

Some studies, experimental and pathological, seem to indicate that possibly 
arteriosclerosis may bear some definite relation to morbid processes affecting the 
adrenals. Josue, Ziegler, Erb, Pearce, and others have produced atheroma, or a 
closely allied lesion, by the intravenous injection of adrenalin. Vaquez reported 
an instance of adenoma of the adrenal associated with heightened arterial tension, 
and Josue and Bernard, and, my colleague, Coplin, have shown that in patients 
having arteriosclerosis the adrenal is rarely, if ever, a normal organ. The observa- 
tions are not, however, as yet conclusive, since similar lesions have been produced 
in animals by the use of agents other than adrenalin, agents moreover that do not 
cause increased blood pressure. Steinbiss has recently secured lesions he describes 
as identical with the adrenalin cases by feeding animals on liver albumin, on which 
they will live for about three months. 

The relation of heightened stress to arteriosclerosis is one of the problems upon 
which authorities are not agreed. Allbutt recognizes a mechanical arteriosclerosis 
depending upon prolonged high tension of whatsoever origin. There can be no 
doubt that in some cases prolonged stress is an important etiological factor, as is 
shown by the fact that typical arteriosclerosis is rare in the pulmonary artery 
and its branches, except when mitral disease or pulmonary lesions increase the 
tension in this vessel, under which circumstance sclerotic changes are not of infre- 
quent occurrence. Heightened stress in the veins also tends toward the develop- 



ARTERIOSCLEROSIS 



497 



merit of phlebosclerosis, as is shown by the occurrence of this lesion in the veins 
of the lower extremity, when for any reason the tension in these tubes is heightened, 
and also by the development of similar changes in the portal area in cirrhosis of the 
liver with venous obstruction. 

Pathology and Morbid Anatomy. — Lesions in the Terminal or Small .Arteries. — 
The change in the arterioles is characterized by proliferation of the endothelium 
and subendothelial tissues, fragmentation of the elastica, and alterations in the 
media. There has been much dispute as to the primary alteration in the muscle 
layer, some holding that there is evidence of a distinct hypertrophy, which others 

Fig. 92 




Left coronary artery. Advanced arteriosclerosis, from a case of fatal angina pectoris. Magnified 30 
diameters. But little of the adventitia is shown. The media is thinned and at points encroached upon, 
but the most conspicuous change is in the intima, beneath the endothelial layer of which there has 
been extensive proliferation and leukocytic accumulation, most marked in the upper segment, greatly 
altering the lumen of the vessel, lessening its carrying capacity, and rendering it practically inelastic. 
There was a marked fibroid myocarditis in the area supplied by the vessel. 



fail to recognize. Whether or not there be an initial increase in the muscle layer 
of the arteriole, there is, sooner or later, if the condition persists, a degenerative 
change, hyaline in tendency, with loss of elasticity, thickening of the intimal and 
subintimal tissues, and narrowing of the lumen, and hence increased peripheral 
resistance. 

Lesions in the Larger Arterial Trunks. — In the second conspicuous alteration 

of arteriosclerosis there develops in the larger arteries a succession of changes 

greatly influencing the elasticity of these structures. Councilman recognizes 

at least three divisions of this type of arterial change. In the nodular form a 

32 



498 



DISEASES OF THE ARTERIES 



cellular infiltration occurs around the vasovasorum, as originally pointed out 
by Martin, extending into the media and subintimal layers. Fragmentation of 
the elastica with efforts at production of new elastic tissue occurs. Later necrotic 
and degenerative changes weaken the wall and, as pointed out by Thoma, endothe- 
lial proliferation tends to restore the smooth lumen. The cells forming the node 
undergo hyaline and fatty degeneration, giving rise to a mass of cellular detritus 
constituting the so-called atheromatous abscess. Should the overlying endothelium 
give way an atheromatous ulcer is formed; these areas are particularly prone to 
develop around smaller branches given off by relatively large trunks, and lessen 
the blood-carrying capacity of the affected branches. 

Fig. 93 




Atheromatous plaques on the lining of the aorta. (Graupner and Zimmermann.) 



The nodules, seen on the vascular surface of the larger arteries, are elevated, 
yellowish, and often soft from degenerative changes, and, later, are infiltrated 
by calcareous material, becoming rigid so that they break when bent. Often 
associated with this nodular form is a diffuse arteriosclerosis, which may also occur 
independently. The affected vessels are dilated, thin-walled, with irregular 
elevations at points, taking on more or less fully the character of the nodules 
already described. Sometimes the intima is almost unchanged. 

The senile arteriosclerosis, so classified by Councilman, would appear to represent 
that late stage of the nodular type in which so-called atheromatous ulcers and 
abscesses form with calcareous scales, giving rise to rigid "pipe-stem" or "slate- 
pencil" vessels that can be rolled under the fingers as tortuous, inelastic, rigid 
tubes. The blood-carrying capacity of such vessels is materially diminished, and 
the resistance offered to the circulation proportionately increased. 

These briefly described alterations in the arteries may be associated with similar, 
though usually much less marked, changes in the veins (phlebosclerosis), the 
combined arterial and venous lesions constituting what Thoma has called angio- 
sclerosis. 

The thoracic aorta is the one large vessel which usually presents the greatest 
atheromatous change. Its entire inner surface may be so roughened that it no 



ARTERIOSCLEROSIS 499 

longer presents any of the appearances seen in health. In other cases, in 
which the process has not gone so far, we find patches, or plaques, of atheromatous 
change all over its lining. These patches may cover areas of softening or areas 
of calcification, and on them thrombi may form. They are particularly prone to 
appear about the origin of branch vessels, and this is the reason that fatal disease 
of the coronary arteries so often occurs as part of the aortic changes. 

In vessels of the intermediate class and in the aorta these changes may so weaken 
the resistance of the vessel wall that it yields to pressure and an aneurysm develops. 

When changes occur in the small vessels their intima becomes thickened by an 
outgrowth of the endothelial cells, and the connective-tissue cells in the media 
also proliferate, so that the vessel becomes fibroid, the elastic coat being rendered 
rigid and the calibre of the vessel diminished. If this process proceeds far it 
causes an obi iterative endarteritis. 

The secondary effects of these vascular changes have already been largely con- 
sidered when discussing the causes of cardiac hypertrophy and myocardial degenera- 
tion. The heart, if its own tissues are not invaded, undergoes hypertrophy to 
enable it to pump blood through rigid, unyielding vessels, and finally, when the 
pressure becomes too high, develops a leak at the mitral valve to relieve pressure, 
or breaks down and fails, suddenly or gradually, under the strain thrown upon it. 
The hypertrophy chiefly affects the left ventricle, because it is upon this part 
that the strain falls. 

Symptoms. — If the heart is examined the apex may be found displaced a little 
downward and to the left, and palpation will show that the impulse against the 
chest wall is forcible if hypertrophy is present. 

A symptom of greater importance is the accentuation of the aortic second 
sound at the second right costal cartilage, and, indeed, wherever it is heard else- 
where in the chest. If the radial or temporal arteries are palpated they may be found 
thickened and corded, often elongated and tortuous and so rigid it is difficult to 
extinguish the pulse by pressure. This high arterial tension is one of the most 
important clinical conditions that can be estimated by the physician. While 
it is true that the degenerative process is practically universal nevertheless in some 
cases the palpable vessels may seem so soft that far-advanced sclerosis of important 
deep vessels is not suspected. 

A patient presenting these signs and symptoms may continue in apparently 
excellent health for several years, but as life progresses the cardiovascular changes 
also progress, and cardiac failure, attacks of angina pectoris, or renal disease ensue. 
Much depends in these cases upon how widespread the lesions are and where they 
are most developed. If the coronary arteries are the parts chiefly affected, anginoid 
attacks soon come on. If the cerebral arteries are calcareous apoplexy ends 
existence, or, if the stroke be mild, it were better for the patient if death ensued. 
Not rarely attacks of vertigo, of fleeting monoplegia or hemiplegia, and aphasia 
may take place as the result of the arteriocapillary fibrosis, without being due 
necessarily to rupture of a cerebral vessel. If, again, the renal vessels are involved, 
then the general manifestations of chronic contracted kidney are produced. 

Among the complications may be named cerebral and pulmonary embolus, and 
gangrene of the extremities from the same cause. 

Treatment. — The treatment consists in the use of the iodides, whether there 
be a history of syphilis or not, in the administration of nitrites to lower that part 
of the arterial tension due to spasm and so relieve the heart of labor, and in the 
use of gentle exercise and electric cabinet baths in moderation to flush the capillaries 
with blood. After the circulation begins to fail in the advanced stages of the 
disease strychnine and digitalis may be urgently required. Highly seasoned dishes 
are also to be avoided. If the heart is tired, atrophanthus is to be given to sup- 
port this organ. High altitudes are dangerous for such patients. Great muscular 



500 DISEASES OF THE ARTERIES 

and mental strain are dangerous because the increased arterial pressure may rupture 
a vessel or weary the heart. 

As chronic interstitial nephritis is nearly always present the treatment for that 
state should be instituted if any sign of renal disease can be discovered. (See 
Chronic Interstitial Nephritis.) 

ANEURYSM. 

Definition. — -An aneurysm is a localized dilatation of an artery and depends 
upon a weakening of its wall so that it is unable to withstand the pressure of the 
blood. This dilatation may involve the entire circumference of the vessel, forming 
a cylindrical or fusiform aneurysm, or it may chiefly affect only a part of the cir- 
cumference, forming a sacculated aneurysm. The walls of the aneurysm are 
composed of the thinned coats of the vessel, but as the sac develops some of these 
may in part disappear. 

The term "dissecting aneurysm" is applied to that form in which the blood 
escapes through the intima and forces a passage for itself into the middle area 
of the vessel wall, between the media and the adventitia. By "false aneurysm" 
is meant a state in which all the coats of the vessel give way so that the blood 
escapes into the surrounding tissues, where a pulsating sac usually forms, owing 
to the development of fibrous tissue around it. An "aneurysmal varix" or "vari- 
cose aneurysm," is one in which the artery communicates with a vein through an 
abnormal opening, so that the vein and its neighboring veins are distended with 
pulsating blood. An " embolic aneurysm" is one in which a vessel is plugged by an 
embolus and then undergoes dilatation in its proximal part. "Mycotic aneurysm" 
is often multiple and occurs as a result of the infection of the vessel by micro- 
organisms, as in ulcerative endocarditis. 

Etiology. — Aneurysm is due to arterial degenerative changes whereby the normal 
elasticity of the vessel is impaired and its lining membrane injured. (See Arterio- 
sclerosis.) The primary causes of aneurysm are, therefore, identical with those of 
ordinary arterial disease, and consist in syphilis, alcoholism, and excessive toil 
or sudden strain. Thus syphilis, for example, weakens the vessel and a strain 
causes it to give way. There are also cases, not so commonly met with, in which 
congenital defects seem to exist in the vessel walls. Thus, I saw a few years ago 
a young man of about twenty-eight years, who developed a popliteal aneurysm 
and then a thoracic aneurysm and finally died of cerebral aneurysm, but who at 
no time suffered from syphilis or from strain. It may also arise from injury, as 
when a vessel is damaged by a stab wound or by a bullet, and these injuries may 
result in the development of the aneurysm many years after, and only when the 
arterial changes of advancing age still further weaken the area which was damaged. 
In other cases the acute infectious diseases, without causing general or widespread 
arterial change, may produce localized vascular inflammation and necrosis. 

Pathology and Morbid Anatomy. — In fusiform aneurysm the wall of the vessel 
dilates in its full circumference, but certain spots give way more rapidly than others, 
so that the surface of the dilated vessel is slightly nodular or uneven. As it increases 
in size its walls become thinner, but if an inflammatory process is set up in the 
surrounding tissues the actual thickness of the wall may be increased, and finally 
a marked deposit of lime salts may take place. 

In sacculated aneurysm the dilatation may originate in at least two ways. In 
one, the entire vessel having become weakened, dilates, and the middle coat atro- 
phies. This process of atrophy becomes further advanced in one area than in 
another, and here bulging rapidly progresses. In other cases the low-grade inflam- 
matory process results in degeneration of the tissues lying under the intima, thereby 
greatly weakening the sustaining lamina, which eventually yields, so that the 



ANEURYSM 



501 



fibrous sheath of the vessel may be all that is left of the arterial wall. In either 
case, however, a process of compensation or repair may develop and the sac 
become filled with a clot, which is usually laminated and remarkably tough. Such 
aneurysmal sacs often grow to an enormous size, becoming as large as a child's 
head. 

Frequency. — The relative frequency of aneurysm as compared to other diseases 
is not of much interest, and there are no very large statistics which deal with this 
point. There is, however, interesting information at hand in regard to the relative 

Fig. 94 




Zcnx. 



Double sacculated aneurysm of the thoracic aorta, the upper sac rupturing into the pleura. On the 
right is the aorta, in which can be seen the two oval openings communicating with the aneurysmal sacs. 
The inferior margin of the lower sac has been pushed upward, showing the erosion of the body of the 
vertebra, which, above the point shown, has exposed the spinal canal, but had not, in this case, com- 
pressed the cord. 



frequency of the most frequent and important forms of aneurysm. Thus, at St. 
Bartholomew's Hospital, Browne found that in thirty years there were 468 cases 
of aortic aneurysm, 80 of popliteal aneurysm, 21 of femoral aneurysm, 14 of sub- 
clavian aneurysm, 8 of carotid aneurysm, and 6 of external iliac aneurysm. 

Aneurysm of the Thoracic Aorta. — Not only is aortic aneurysm the most com- 
mon lesion, but it is, by reason of the importance of this vessel and of the tissues 
about it, capable of causing very characteristic and also very obscure symptoms, 
both by disturbing the circulation and by pressure on neighboring organs. 



502 DISEASES OF THE ARTERIES 

For convenience of study the aorta is usually divided into three parts: the 
ascending, the transverse, and the descending. Each of these may be the seat of 
an aneurysm, but the ascending portion is most frequently affected. Some years 
ago one of my assistants, Holder, and myself studied the statistics derived from 
953 cases of aortic aneurysm, and obtained the following results. No less than 
570 of these were cases of aneurysm of the ascending portion of the arch. Of these, 
544 were sacculated and 466 occurred in males and 78 in females. The remaining 
26 cases were fusiform, and all of these 26 cases occurred in males. These statistics 
emphasize very forcibly the far greater frequency of sacculated aneurysm than 
the fusiform variety. When we consider that of nearly 1000 cases analyzed, 
aneurysm of the ascending aorta occurred no less than 570 times, while aneurysm 
of the transverse portion occurred only 104 times, and of the descending portion 
110 times, the great difference in the relative frequency of the lesion in different 
parts of the aorta is also marked. 

Of the 466 cases of sacculated aneurysm occurring in males, it is interesting 
to note that the great majority of them occurred in persons between thirty-five 
and forty-five years of age, that the next greatest frequency was in persons between 
twenty-five and thirty-five, then between forty-five and fifty-five. 

When we come to the consideration of aneurysms involving the second or trans- 
verse portion of the aorta we find, once again, that the most common age for the 
development of this lesion is between thirty-five and forty-five; for out of 88 males 
suffering from this lesion 37 were between these ages, 21 between forty-five and 
fifty-five, 14 between twenty-five and thirty-five, 10 between fifty-five and seventy, 
and 2 between fifteen and twenty-five. The same facts as to age also hold true 
for aneurysm of the descending arch. It is evident, therefore, that aneurysm is 
not a disease of old age, but of the middle period of life. As Coats has well expressed 
it, " aneurysm occurs when the period of greatest bodily vigor overlaps the period 
of occurrence of atheroma." 

Symptoms. — Aneurysm of the aortic arch not infrequently lasts for some time 
before producing any symptoms, and is then spoken of as a "latent aneurysm." 
In other instances it causes symptoms almost as soon as it develops, and the differ- 
ence in the promptness with which the signs appear depends largely upon the site 
of the growth and the parts pressed upon. 

When the convex surface of the ascending arch is involved we find the patient 
presenting engorgement of the wins of the head, neck, and arm on the right side, 
and the voice is often altered or lost from the pressure upon the recurrent laryngeal 
nerve of the right side. The pupil of the right eye may be dilated, due to irritation 
of the sympathetic; or it may be contracted because the ciliospinal nerves are para- 
lyzed by pressure. There is often severe pain due to pressure, and attacks of 
anginoid pain may be present. 

The physical signs are dulness on percussion over the second right interspace, 
a bruit, or roaring sound, produced by the passage of blood through the sac, and 
perhaps bulging of the first, second, or third interspace on the right side. If the 
hand is placed over the area of bulging, a distinct, expansile, heaving movement 
is felt. Some displacement and hypertrophy of the heart is often present, and, 
if the sac is a large one, the apex beat of the heart may be far below and outside 
the normal spot near the nipple. If the sac develops on the concave part of the 
arch, then the downward displacement of the heart is still greater, for obvious 
reasons. 

Hypertrophy of the heart is by no means a constant sequel of aneurysm. 
Not rarely the heart is not increased in size at all, but its apex may be displaced 
and the impulse transmitted to the chest wall more markedly than normal because 
of the pressure produced by the aneurysmal sac. 

When we come to the consideration of the direction in which sacculated aneurysms 



ANEURYSM 



503 



of the ascending arch most commonly rupture, or, in other words, when we study 
the neighboring tissues into which the blood forces its way when the wall of the 
aneurysm bursts, we find that the vast majority rupture into the pericardium. 
Thus, out of 289 cases in which death was stated to have been due to rupture in 
males, 75 ruptured into the pericardium and 58 into the pulmonary artery; 23 
ruptured into the right auricle, 3 of these taking place some time before death; 
23 ruptured externally; 14 ruptured into the superior vena cava; 11 into the esopha- 
gus; 9 into the left auricle; 8 into the right ventricle; 8 into the trachea; 6 into the 
left ventricle; 6 into the left pleura, and 5 into the right lung; 3 burst in the posterior 
mediastinum and 1 burst simultaneously into the trachea and esophagus; in 20 
others no statement was made as to the direction of the rupture. It is, moreover, 
a fact that death is much more commonly due to pressure symptoms than to 
rupture. 

Fig. 95 




Aneurysm of the ascending and transverse part of the aortic arch, with erosion of the chest wall. 



Aneurysm of the transverse portion of the arch usually causes a ringing, brassy 
cough, dysphagia, expansile pulsation in the suprasternal notch, and dulness on per- 
cussion on the first and second left intercostal spaces. Its pressure on the innomi- 
nate vein may cause congestion of the left side of the face and neck. Dyspnea 
from tracheal pressure may be present, and there may be aphonia from paralysis 
of the left vocal cord, arising from pressure on the left recurrent laryngeal 
nerve. If the growth is so situated that it presses upon the left bronchus it 
may cause bronchiectasis and even bronchial suppuration by preventing drainage. 
Again, if the sac be a large one, it may involve the innominate artery, the left 



504 DISEASES OF THE ARTERIES 

carotid, and even the subclavian, and in this manner the radial pulse may be absent 
on one side. Even the pulse in the arteries of the trunk and lower extremities may 
be greatly lessened in vigor. The bruit may be loud and angry, but if the laminated 
clot be large it is often absent. The aortic second sound is usually accentuated or 
ringing in character unless aortic regurgitation is present. 

When the descending arch is affected it often occurs that the aneurysm extends 
posteriorly, and the bruit and pulsation are found in the back, between the scapula 
and the spinal column on the left side. In these cases severe pain due to pressure 
on the intercostal nerves is often present, and the pressure on the vertebrse may 
cause erosion and even paraplegia by destroying the spinal cord. 

Aneurysms of the ascending and transverse portions of the aorta often produce 
an extraordinary degree of erosion, and so pass through the wall of the chest by 
causing the absorption of the bony tissues, and by pushing the fragments of the 
ribs to one side. This is well shown in the accompanying cut. The surface of 
this tumor is often shining from distention of the skin, it is discolored by blood, 
and the surface may weep bloody serum for days as the end approaches. 

Under the name tracheal tugging a symptom of aortic aneurysm, which consists 
in the transmission of a tugging sensation to the trachea, has been described by 
Oliver and studied by MacDonnell. To make this test, the patient stands erect 
with his head slightly tipped backward, so as to stretch the tissues of the front of 
the neck. The cricoid cartilage is now grasped by the thumb and finger and 
drawn toward the chin, when if aneurysm is present a tugging sensation will some- 
times be felt with each beat of the heart. I have seen many cases and have met 
this sign. Sewall has shown that this sign is present in cases which have adhesions 
in the left pleura, and in some healthy persons when they take a deep inspiration. 
•Occasionally in aortic aneurysm incurvation of the finger-nails and clubbing 
of the finger-tips on one side may be present. 

Blood-spitting is due to the formation of an erosion of the mucosa at the spot 
in the bronchial tube where the tumor causes pressure. Such a cause produces 
only a slight blood stain of the sputum. When the blood passes by a process of 
leakage through the wall of the sac and escapes into a bronchus it may be in con- 
siderable amount, and death may be due to a free hemorrhage of this sort. 

Very rarely there develops in the chest, as the result of aortic aneurysm, an 
adhesion between the sac and the superior vena cava, so that on the development 
of ulceration a communication between the two vessels is established, forming on 
a large scale an arteriovenous aneurysm. The most exhaustive study of this 
state has been made by Pepper and Griffith, and was reported to the Association 
of American Physicians in 1890. They could find only 28 cases in literature in 
addition to the one they observed. Less commonly the aneurysm communicates 
with the pulmonary artery. 

Diagnosis. — The symptoms of aneurysm, on which the diagnosis must be chiefly 
based; have already been mentioned. They may be briefly named as follows: 
The presence of bruit, expansile pulsation, pressure symptoms, dulness on percussion 
over the second and third interspace anteriorly on either side, unilateral sweating, 
and mydriasis or myosis, and thoracic pain. Swellings due to aneurysm nearly 
always are expansile, but care must be taken that swellings which pulsate by 
reason of transmitted impulse are not mistaken for a true dilated vessel. 

Nothing is more difficult to diagnosticate correctly than the early manifestations 
of aortic aneurysm. Scarcely a physician of experience can look back and not 
recall cases in which its early signs completely misled him. The inconstant pain 
in the chest is often thought to be rheumatic or neuralgic. In other instances 
dyspneic seizures are thought to be asthmatic, or attacks of severe cardiac pain 
are considered to be due to true angina pectoris. The persistence of symptoms 
like these, despite treatment, the age of the patient, the degenerated state of the 



ANEURYSM 505 

palpable arteries, the sounds of the heart, and the history of syphilis, of alcoholism, 
and of strain or blow or wounds, are all at least capable of arousing suspicion of 
the real condition. The pain of aneurysm is often dull, gnawing, and constant, 
but in some cases pain may be absent. Occasionally an unsuspected aneurysm 
may cause an attack of stridor or paroxysmal dyspnea, resembling somewhat a 
laryngeal crisis in locomotor ataxia. This should excite suspicion of aneurysm 
causing pressure on the recurrent laryngeal nerves. A hemorrhage from the 
lungs in the absence of tuberculosis should also be regarded as significant. This 
hemoptysis may be frothy and mucoid, or rusty, like that of pneumonia, or prune- 
juice in hue. 

A very valuable aid in the diagnosis of thoracic aneurysm is the use of the x-rays, 
either the fluoroscope being used or x-ray pictures being taken. The chest should 
be x-rayed not only anteroposteriorly but laterally to discover the direction in 
which sacculation is occurring. The advantage of the fluoroscope is the fact that 
the physician can see the expansile movement of the mass. 

Prognosis. — The prognosis of aortic aneurysm is, in the vast majority of cases, 
inevitably fatal, but in some cases life is preserved for many years if nature succeeds, 
by the deposition of laminated clot, in walling off the sac. An old scrub-woman 
presented herself to my clinic during thirteen years, each season, with a massive 
aneurysm of the aorta which had eroded the sternum years before, and which had 
not grown since to any extent. She worked hard for her living and had little dis- 
comfort. Her case is the exception that proves the rule, however. If the growth 
is of any size, life rarely lasts more than a few months. Even when it is small 
a rupture may occur. As already stated, death from aortic aneurysm is usually 
due to pressure on adjacent parts, and not most commonly to rupture, as is 
generally thought. 

Treatment. — Aneurysm of the peripheral arteries is best treated by compression 
and ligation, and the methods to be employed will be found discussed in works 
devoted to surgery. 

In aortic aneurysm there are two plans of treatment which may be insti- 
tuted, namely, medicinal and dietetic, on the one hand, and operative on the 
other. 

The medicinal treatment depends to some extent upon the underlying cause of 
the aneurysm. If it be due to syphilis, in the sense that this disease is chiefly 
responsible for the vascular degeneration, it is hardly necessary to state that the 
iodides in full doses are advisable, not that they can cure the aneurysm in the sense 
of regenerating an old vessel, but that they may, by their specific influence, arrest 
the degenerative influence in the vessel wall, and so delay the progress of the malady. 
Even if there is no history of syphilis in the case, the iodides are often of value in 
that they seem to arrest in some unknown manner degenerative changes in the 
vessels. They should be given in sufficiently large dose to produce some evidence 
of iodism, but not in sufficient dose to seriously disorder digestion. 

The second point in the treatment of the case is the institution of the greatest 
degree of rest which is compatible with comfortable existence. The patient should 
be placed in bed and required to use a bedpan in order that he may not disturb 
his circulatory equilibrium by getting up. He should also be given small doses 
of the bromides, if necessary, to overcome nervous irritation and restlessness, 
and if the action of his heart is exceedingly tumultuous and fails to become more 
quiet, by rest in bed, I have known small doses of aconite, such as 10 minims of 
the tincture, three or four times a day, to be advantageous. In other cases tincture 
of veratrum viride is useful. Such a plan of rest treatment is useless unless it 
is carried out for weeks, and sufficient time must be allowed for a laminated clot 
to form in the aneurysm and reinforce its walls. 

The so-called Tufnell treatment of aneurysm consists in a more rigorous method 



506 DISEASES OF THE ARTERIES 

than that just described. The patient is not only put at absolute rest, but he 
is also given considerable quantities of iodide of potassium and as low a diet as is 
compatible with existence. Indeed, the treatment may be called the starvation 
plan of treatment, for it is the deliberate purpose, when this plan is instituted, 
to lower the activity of the circulation by the depression which is associated with 
semistarvation. I have seen this plan instituted in only a few cases, and I have 
never seen good results from it. Surely, no advantage can accrue except by 
diminishing the activity of the circulation, and this can be obtained by the use 
of aconite or veratrum viride. 

The use of digitalis in these cases is not advisable because, while the drug steadies 
the heart, it increases arterial tension and so tends to increase the pressure upon 
the aneurysmal sac. 

The operative treatment of thoracic aneurysm is only possible when the tumor 
is of the sacculated type. The fusiform type of aneurysm contra-indicates its 
employment. A large number of operative procedures have been suggested, 
but there is only one which has at the present time received general recognition 
by the profession, namely, the so-called Corradi method, in which there is intro- 
duced into the aneurysmal sac several feet of fine platinum-gold wire which has 
been previously wound about a glass spool, both the spool and the wire being 
carefully sterilized by boiling before they are used. After the skin over the sac 
has been carefully sterilized, the greatest gentleness being used lest it be damaged, 
a hollow needle, which is insulated by being coated with porcelain, is pushed into 
the sac, and then through it is passed from ten to thirty feet of wire, according to 
the size of the growth. A larger number of feet have been used, but ten or fifteen 
feet will be sufficient in the vast majority of cases. As soon as all the wire, save 
about six inches has passed into the sac, the external end of the wire is made fast 
to an electrode which is attached to the positive pole of a galvanic battery. A 
large, wet, clay electrode attached to the negative pole is placed under the back 
to complete the circuit and by means of a "current controller" the electricity 
is gently turned on. At first about 5 milliamperes are used; at the end of five 
minutes the current is raised to 10 milliamperes, and after this the current is in- 
creased every iive minutes by 5 milliamperes until about 50 milliamperes are 
employed. A higher number of milliamperes have been used, but with increasing 
experience I am confident that they are unnecessary and perhaps harmful. As 
the result of this method of procedure it not infrequently happens that by the end 
of the first twenty minutes or half-hour the sac is found to be somewhat more firm 
than before, and that pulsation in it has diminished owing to the fact that the 
acid reaction produced by electrolysis about the gold wire has resulted in the for- 
mation of a clot, which, as time goes by, becomes more and more firm and solid. 
At the end of from thirty minutes to an hour the wire is disconnected from the 
battery, its external end is pushed underneath the skin, and the external wound 
is closed by collodion. Absolute quiet must be maintained for ten days or two 
weeks after the operation, in order that the clot may become thoroughly con- 
solidated. 

I have now performed this operation twenty-nine times, and my experience 
has been that in no instance did the patient suffer much pain. Indeed the relief 
of pain is one of the chief advantages of the procedure. In several instances 
the patient has stated during the operation that he had less pain, and in every 
instance he has voluntarily expressed his pleasure at the subsequent improvement. 
Unfortunately, the condition of the aorta is often such that when we close one bulging 
spot in this way, it is not long before another area gives way under pressure, and 
so another aneurysm is formed. In most of my cases this accident has ultimately 
occurred. One patient operated on the first time five years ago and a second time 
three years ago is alive and at work as I write. One case a year after operation 



ANEURYSM 507 

lost his life not by the disease but because he was struck by a freight car as 
he was walking along the track in very excellent health. In one case operated 
on by Stewart some years ago the patient lived in comparative health for a period 
of three years, and then died from pneumonia following an alcoholic debauch, 
although at the time of operation the aneurysm could be seen as large as a fist 
outside the chest wall. Considering the slight pain of the operation, it is indicated 
in many cases, if only for the relief which it gives. 

Aneurysm of the Abdominal Aorta. — Aneurysm of the abdominal aorta usually 
occurs near the diaphragm, and it is far more rare than aneurysm of the thoracic 
aorta. Out of 325 cases of aortic aneurysm collected at Guy's Hospital in forty- 
six years, 54 involved the abdominal aorta. Of these 63 per cent, occurred between 
the ages of twenty-one and forty years and 77 per cent, between twenty-one and 
fifty years ; over 90 per cent, occurred in men. The growth usually arises from the 
neighborhood of the celiac axis. Like that in the thorax, its sacculated form is 
more common than its fusiform type. It usually projects forward, but it may 
extend backward and cause erosion of the vertebrae, followed by pressure on the 
spinal cord. Pain is usually a constant symptom, which is often referred to the 
region of the heart or to the back. On inspecting the abdomen distinct pulsation 
may be seen at once, but care must be taken that the transmitted pulsation of 
the aorta in a state of health is not mistaken for true expansion. These two states 
can be separated by careful palpation. In some instances the aorta can be clearly 
felt through the belly wall; in other cases a morbid growth in the stomach or in 
the omentum can be felt, but although it pulsates it is not expansile. If the patient 
is placed in the knee-elbow position so that the growth falls away from the aorta, 
the diagnosis may be readily made. Auscultation may reveal a bruit if aneurysm 
is present, but if a stethoscope is used it is easy by pressure on the aorta to narrow 
its lumen and cause a bumming sound, which is not a sign of aneurysm. Again, 
in hysterical persons a very marked pulsation of the aorta may be complained of 
by the patient and felt by the physician. I have seen an hysterical male who had 
rhythmical contraction of his abdominal rectus muscles synchronous with his 
pulse. It was only possible to diagnose his case by giving him ether to the point of 
relaxation. 

A larger proportion of these cases end by rupture than is the case in aneurysm 
of the thoracic aorta. Thus, out of these 54 cases no less than 43 died from rupture. 

Aneurysm of the abdominal aorta may rupture into the retroperitoneal tissues, 
through the diaphragm into the pleural spaces, or into the general peritoneal 
cavity, or more rarely into an intraperitoneal viscus, as, for example, the stomach. 
Rarely death ensues from the vessel becoming closed by a thrombus. 

Abdominal sacculated aneurysms may be treated by wiring and electricity. 
(See Aortic Aneurysm.) 

Even more rare than aneurysm of the abdominal aorta is aneurysm of its branches. 
Cases have been reported in which a blow upon the belly has caused aneurysm 
of the hepatic artery, and in a case seen by the writer it followed ulceration produced 
by a malignant growth of the gallbladder. That this condition is very rare is 
shown by the fact that up to 1898 only 26 cases had been recorded. The symptoms 
are usually mistaken for hepatic colic, and this error is all the more easy because 
jaundice from pressure is often present. In most of the recorded cases the ante- 
mortem diagnosis has been "gallstones" or "duodenal ulcer." 

Aneurysm of the splenic artery is rarer than aneurysm of the hepatic artery, 
and causes symptoms like those of gastric ulcer. 

Aneurysm of the superior mesenteric artery is also rare. Rolleston has collected 
20 cases. Embolism is the usual cause, and injury may be responsible for it. 
This growth may cause jaundice by pressure on the gall-duct, as in a case reported 
by J. A. Wilson; or it may press on the renal arteries and cause uremia, as in a case 



508 DISEASES OF THE ARTERIES 

recorded by Burney Yeo. Aneurysm of the inferior mesenteric artery is practically 
unknown. 

Aneurysm of the renal artery is also rare, although small multiple sacs are some- 
times seen. If the sac be very large hematuria may occur, or wasting of the kidney 
may ensue. Sometimes by the sudden rupture of an aneurysm of this vessel the 
retroperitoneal space has been filled with blood. In the surgical clinic of the 
Jefferson College Hospital, my colleague, Dr. W. W. Keen, cut down on a kidney 
because of severe renal symptoms, and found a large aneurysm of the artery. 
He was forced to remove the aneurysm and the kidney. 



DISEASES OF THE DIGESTIVE TRACT. 



DISEASES OF THE MOUTH. 



STOMATITIS. 



Definition. — As its name implies, stomatitis is an inflammation of the mouth. 
Of the many forms that have been described three are important: catarrhal stoma- 
titis, aphthous stomatitis, and ulcerative stomatitis. All these forms of stomatitis 
usually occur in childhood. The catarrhal and aphthous forms are more common 
in early infancy, but the ulcerative type is practically never met with in children 
who have not as yet gotten teeth, and is more common in those past puberty than 
are the other forms. 

Catarrhal Stomatitis. — In catarrhal stomatitis there is hyperemia of the mucous 
membrane of the tongue and cheeks, with an increase in secretion on the part of 
the mucous and salivary glands. It arises from injury, as by some foreign body 
being taken into the mouth which acts as a mechanical irritant, or by hot or irrita- 
ting liquids. These are, however, only predisposing causes. Difficult dentition, 
or the use of a rubber nursing nipple which is dirty, are more common factors. 
It also occurs as one of the manifestations of the acute eruptive diseases, as in 
scarlet fever and measles, and it may be a symptom of some metallic poisoning, as 
mercury, lead, or arsenic. 

Symptoms. — The symptoms of catarrhal stomatitis are intense hyperemia of the 
mucous membrane of the mouth with some swelling which is particularly visible 
on the gums. If the finger be placed in the mouth a sense of increased heat is felt. 
The child evidently suffers a good deal of pain. When given the breast or bottle 
it eagerly seizes it because of hunger and thirst, and then, as the nipple touches 
the tender mucous membrane, gives a cry of pain and disappointment. Cool 
water is usually taken with avidity if given from a cup or spoon. The flow of saliva 
is so free that constant dribbling on the chin is present or the excess is swallowed 
and disturbs digestion. If the mouth be carefully examined it may be that tiny 
blisters at the opening of the mucous glands will be seen and the papillae of the tongue 
will be found enlarged, swollen, and unduly red in hue. Some digestive disturbance 
and diarrhea are nearly always present. Whether these symptoms are the result 
of the condition of the mouth, or whether the state of the mouth is secondary to 
disturbed digestion, is often difficult to determine. 

Prognosis. — Recovery from catarrhal stomatitis is usually rapid, the condition 
rarely lasting for more than a few days after the disordered digestion is corrected 
and proper cleanliness of the mouth is obtained. 

Aphthous Stomatitis.— The aphthous form of stomatitis, sometimes called fol- 
licular or vesicular stomatitis or canker, may be considered as a still further develop- 
ment of the catarrhal form. In this condition we not only have a diffuse hyperemia 
of the mucous membrane of the mouth, but in addition small spots appear which 
look as if the superficial epithelium had been snipped off with curved scissors. 
These spots are, of course, exquisitely sensitive. All the symptoms of the catarrhal 
form are much exaggerated, and in addition to more marked digestive disturbance 

(509) 



510 DISEASES OF THE MOUTH 

the patient often has systemic disturbance, as is shown by some fever and general 
wretchedness. Nutrition is interfered with materially only by the inability to 
take food. 

Ulcerative Stomatitis. — The ulcerative form of stomatitis, sometimes called 
fetid stomatitis, or putrid sore mouth, is a much more serious type, but it is often 
so mild that the dividing line between it and the aphthous form is not readily 
made. When well developed, the mucous membrane is seen to be studded by 
small ulcers which may coalesce, forming rather large areas of superficial necrosis. 
If the child is badly nourished, or suffering from some malady which impairs its 
general nutrition, ulcerative stomatitis may become a very serious affection, causing 
great suffering, interfering seriously with proper feeding and rapidly undermining 
the strength of the patient. The ulcers are situated chiefly along the edges of the 
gums which recede from the teeth, or on the margins of the tongue, on the buccal 
membrane, and even on the lips. The breath is often very foul and the corners of 
the mouth become excoriated from the salivary flow. When the patient is a 
sufferer from scurvy, it may be an important factor in preventing recovery. In 
adults it is usually due to mercurialism. 

In many cases the condition arises from carious teeth and occasionally the 
disease occurs epidemically. On the other hand, I have repeatedly seen mild 
ulcerative stomatitis occur in otherwise healthy young girls past puberty, in whom 
none of these causes was apparent. 

In severe cases the ulceration may be very deep and may even cause loosening 
of the teeth or superficial necrosis of the lower jaw. 

Treatment. — The treatment of all these forms of stomatitis may be considered 
simultaneously. All of them are to be treated by careful attention to cleanliness 
of the mouth itself and of all objects entering the mouth, by careful regulation of 
the bowels and the food, and by a mouth- wash of chlorate of potash and myrrh in 
the following formula: 

1$ — Potassii chlorat. ' . . gr. xxx. 

Tinct. myrrhae . . ■ . . TTL x. 

Elix. calisayse f 5 iij . — M 

Sig. — Dilute one tablespoonful with two of water, and use as a mouth-wash. 

When very young children are treated this solution may be applied to the mucous 
membrane by means of a swab tied to a small stick or pencil. These measures are 
usually efficient in the catarrhal and aphthous type. 

In the ulcerative form it may be necessary in addition to touch each ulcer with 
a solid stick of nitrate of silver or with a solution of this drug of the strength of 60 
grains to the ounce. This is painful, but efficacious. Only a few spots should be 
touched at each sitting. When the teeth are not carious peroxide of hydrogen 
may be used locally. The system should be well supported by nutritious foods 
such as cold consomme or cold chicken-jelly, by ordinary foods if they can be taken 
into the mouth, and, if anemia is present, by the use of iron and quinine in moderate 
doses. 

When for any reason chlorate of potash cannot be applied locally the physician 
may give the drug internally in the dose of 2 grains every three hours, since, as it 
is eliminated by the salivary glands, the saliva bathes the diseased mucous mem- 
brane with the drug. This plan of treatment is contra-indicated if any renal 
irritation or marked gastric disturbance is present. 

In scorbutic cases fresh vegetables, fruit, and beef -juice are absolutely needful 
in the treatment of the patient. 

There still remain to be discussed in this connection two forms of sore mouth 
which do not, strictly speaking, fall under any of the headings just given, since 
in each of them definite specific causes have been isolated, namely, so-called thrush 
or parasitic stomatitis and gangrenous stomatitis. 



STOMATITIS 511 

Thrush. — Thrush, or parasitic stomatitis (Soor or Muguet), is due to the pres- 
ence in the mouth of a parasite variously named Saccharomyces albicans, or Oidium 
albicans or Endomyces albicans. This parasite has been classed with yeasts, and 
grows with branching filaments at the ends of which egg-shaped, torula cells are 
produced. Thrush is distinctly associated with impaired health of the mucous 
membrane, and in children, in whom it is most commonly met with, it is due, as a 
rule, to the use of dirty nursing nipples or nursing bottles, or to general impairment 
of health. When the latter cause is present, thrush may appear in the mouth of 
adults, and for this reason it sometimes aids in increasing the miseries of those 
whose vitality is impaired by tuberculosis, diabetes, and by prolonged exhausting 
fevers. It is also seen in children suffering from marasmus. The parasite can be 
readily conveyed from one person to another by utensils. 

Symptoms. — The subjective symptoms of thrush consist in the same discomfort 
in the mouth which is met with in aphthous stomatitis. The objective symptoms 
are, however, to be carefully separated from that state. Instead of denudation 
or depression of the surface of the mucous membrane there is seen on the tongue 
small particles or specks in the form of tiny pearly white spots, which are raised 
and may gradually coalesce and seem to form a membrane that is usually easily 
removed, although its removal may leave a bleeding surface. From the tongue 
the growth may extend to the entire mucous membrane of the mouth and the soft 
and hard palate. Very rarely it even spreads to the pharynx and esophagus, and 
even into the stomach and small intestine. Holt states that the fungus has been 
found in the lungs of babies suffering from bronchopneumonia. Thrush is separated 
from aphthous stomatitis by the fact that the profuse salivation of the latter is 
replaced by great dryness of the mouth, and by the aid of a microscopic examination 
of the growth. 

Prognosis. — The prognosis depends upon the health of the patient. In the 
robust the condition may last but a few days, but in the feeble and impoverished 
it may persist for weeks. It does not materially influence the general health 
except by interfering with the taking of nourishment. 

Treatment. — The treatment consists in cleanliness, good feeding, the use of a 
mouth-wash of borax in the strength of 10 grains to the ounce, or of a mouth-wash 
of permanganate of potash, 1 grain in 8 ounces of water, or by diluting peroxide 
of hydrogen, 1 part in 5 of water. Any underlying disorder of nutrition should 
be carefully removed if it be possible. All sweets and syrups should be carefully 
avoided. 

Gangrenous Stomatitis, Cancrum Oris, or Noma. — Noma is a term applied to 
all forms of severe ulceration of a localized character attacking mucous membranes, 
but the state may be present without the mucous membrane being broken, the 
tissues of the cheek being chiefly affected. The condition occurs so rarely in those 
who are past puberty that it may be said to be a disease of early childhood. It 
affects the buccal mucous membrane and cheek so constantly that the word "noma" 
has come to mean a malignant and sometimes a perforating gangrenous process 
involving the cheek, although, strictly speaking, noma may affect the ear, the 
vagina, the buttock, the nose, or the external genitalia. 

In the vast majority of cases noma results in the death of the patient, not so 
much because it is in itself a fatal disease as that it is a terminal infection; that is, 
one which develops only in a child or adult whose vital resistance is so lowered by 
disease or poor nutrition that the pathological process known as noma is possible. 

The disease is rarely seen in private practice, but has its greatest frequency 
in institutions for poor children, where because of mismanagement, or of the 
wretched state of the child on admission, it readily falls a victim to infections of 
all kinds. 

Noma more commonly follows measles than any of the other eruptive diseases, 



512 DISEASES OF THE MOUTH 

but it also sometimes complicates or follows scarlet fever, typhoid fever, whooping- 
cough. It is practically never a primary lesion at the point of development, but 
begins in a solution of continuity such as an ulcer due to a carious tooth or as a 
sequence of ulcerative stomatitis. In all probability it is not due to an infection 
by any single micro-organism, but to several organisms which may be associated. 
Cases have been recorded in which the ulceration seemed to be due to the bacillus 
of diphtheria, but mixed infection is the rule. An attempt to establish specificity 
for any single organism has been futile. 

Not only has the ulcerative process a tendency to rapidly become deep and so 
to perforate the cheek, but it lacks the sharp line of demarcation marking the wall 
often built by nature to prevent the spread of gangrene. That is to say, the ulcer 
is bounded by an extending area of necrosis, often branching and discolored, which 
spreads from day to day, with no apparent effort on the part of the system to 
limit its progress. The soft parts melt into the fetid ulcer, and cartilage and bone 
undergo necrosis. When recovery does occur, which is exceedingly rare, a line 
of demarcation forms, and the extension of the disease is arrested in this way; the 
ulcer clears up and repair slowly takes place. 

Symptoms. — The local symptoms of noma are a foul breath, a state of localized 
ulceration with deep induration of the tissues near by, and the speedy development 
in the centre of the ulcer, of a dirty-looking slough of necrotic tissue. The side 
of the face is usually much swollen and distorted, and when felt by the fingers the 
tissues feel brawny and hard. If the ulceration extends to the gums, the teeth 
become loosened. So great may be the destructive process that the teeth and 
alveoli may be seen through the perforated cheek. 

The systemic symptoms are not characteristic of any specific state, but are those 
of profound systemic poisoning, depression, and exhaustion. The pulse is rapid 
and feeble, the appearance of the patient markedly septic and cachectic, and the 
temperature mildly febrile. The height of the temperature depends, however, to a 
considerable degree, upon the vitality of the patient. When the sufferer is pro- 
foundly exhausted and the vital state is very low marked febrile movement does 
not occur. 

Treatment. — From the description just given it is evident that the treatment 
of noma, to be successful, must depend upon its early institution and thorough 
character. It must also consist in the use of such nutritious food and such medicines 
as will serve to support the strength of the patient. The local treatment consists 
in the early and complete cauterization of the part affected by the electrocautery 
or its excision by the knife, so that the necrotic mass is at once destroyed and 
removed. The physician must not limit the operation to the dead tissues, but 
extend the excision to the living tissues as well in order that none of the infected 
tissue may remain. The local process may be temporarily treated by swabbing 
the part with peroxide of hydrogen or by using permanganate of potash. In 
cases in which the streptococcus or the bacillus of diphtheria are present, the serum 
therapy needed for these specific infections should be used. 

ECZEMA OF THE TONGUE. 

Under this distinctly erroneous term is described a condition in which there 
is a superficial overgrowth and desquamation of the epithelium covering the tongue. 
As a rule, the centre of each spot of desquamation begins to heal while the periphery 
is still spreading, so that the appearance of the inflammatory zone is distinctly 
circinate. Its irregular outline has given it the name of "geographical tongue." 
In other instances the appearance of the tongue is that of a worm-eaten leaf. In 
some patients it produces no discomfort whatever. In others the patient may 
have some itching and tingling, and on examining the tongue is surprised to find 






FUNCTIONAL DISORDERS OF THE SALIVARY GLANDS 513 

the curious outlines which have been described. Not infrequently nervous patients 
are wont to consider that it is an evidence of syphilis, or perhaps of a malignant 
growth. A modified form of this condition is very frequently seen in children as a 
result of catarrhal condition of the stomach and bowels. 

Treatment. — In adults it is best treated by the local application of nitrate of 
silver, 20 grains to the ounce. In children the correction of the gastro-intestinal 
disorder usually results in a normal growth of epithelium, so that the condition 
is relieved. As a rule, such children require some simple bitter such as tincture 
of gentian with 5 or 10 grains of bicarbonate of soda. 

LEUKOPLAKIA BUCCALIS. 

Leukoplakia buccalis is sometimes called smoker's tongue, ichthyosis lingualis, 
and buccal psoriasis. It is characterized by the development of white spots of 
considerable size on the mucous membrane of the mouth and tongue, which are 
due to cellular infiltration of the subepithelial connective tissue and a thickening 
of the epithelium. When the spots occur on the edge of the tongue and are indented 
by the teeth they sometimes look like the scars or puckerings which are seen on 
the edges of the tongue in cases of advanced syphilis. Occasionally these areas 
may be slightly ulcerated, and in some cases are thought to be the seat of epithelio- 
matous degeneration. In the majority of instances, however, they are benign, 
and after removal of the eause require no treatment unless the surface is ulcerated, 
in which case they may be touched with nitrate of silver and the patient directed 
to avoid taking hot, irritating substances into the mouth, and particularly to 
avoid smoking or chewing. Leukoplakia is sometimes looked upon as a precancer- 
ous condition, and this is probably true in the sense that the state if permitted to 
continue it may lead to cancer. 

MUCOUS PATCHES. 

Mucous patches are opaque, white, flattened swellings on the mucous membrane 
of the mouth and lips, and are characteristic of secondary syphilis. (See Syphilis.) 
From them the Treponema pallidum is readily communicated. Not infrequently 
their surface is somewhat ulcerated. 

Treatment. — The treatment, of course, consists in the active employment of 
salvarsan and the use of nitrate of silver locally. 



DISEASES OF THE SALIVARY GLANDS. 

FUNCTIONAL DISORDERS OF THE SALIVARY GLANDS. 

Ptyalism. — Ptyalism, or salivation, occurs as the result of poisoning by mer- 
cury or the iodides. It is also produced by such drugs as jaborandi, and occasionally 
occurs because of irritation of the mucous membrane of the mouth by the develop- 
ment of stomatitis in one of its severe forms. Rarely a form of idiopathic ptyalism 
is met with in young children. Under these conditions the salivation is probably 
the result of a neurosis. 

When due to the influence of a drug, the condition is to be arrested by stopping 

the use of that substance and aiding in its elimination by the employment of sodium 

bicarbonate if the iodides have been taken, and mild saline purgatives if mercury 

has been used. A mouth-wash containing 10 grains of chlorate of potassium and 

33 



514 DISEASES OF THE SALIVARY GLANDS 

2 drachms of fluidextract of rhus glabra in an ounce of water will be useful to 
improve the condition of the mucous membrane and arrest the flow of saliva. 
Sometimes moderate doses of atropine are useful. In other cases, 10 to 15 grain 
doses of camphoric acid given thrice a day may be used. 

DRY MOUTH. 

Dry mouth, or xerostomia, is frequently met with in all fevers, but sometimes 
occurs as an independent condition. Under these circumstances the tongue is 
seen to be red and dry, with lessened superficial epithelium, so that it is smooth 
and shiny. It is said to be most frequent in women after great nervous excitement 
or in those suffering from hysteria. 

Treatment. — Temporary relief from dryness of the mouth may be produced 
by washing it with a mixture of 1 part of glycerin to 2 of water, to which has been 
added a little lemon-juice. 

INFLAMMATION OF THE SALIVARY GLANDS. 

The most important and most common inflammation of the salivary glands is 
the swelling of the parotid gland in mumps, which has already been considered. 
The next most frequent cause of inflammation of the salivary glands is a septic 
condition of the mouth in the course of one of the prolonged adynamic fevers, such 
as typhoid fever, and in persons who are suffering from cerebral softening. In 
these cases it would seem that infection may pass through the salivary duct, and 
so cause inflammation of the gland itself. Occasionally a similar accident occurs 
in pyemia, pneumonia, syphilis, and scarlet fever. In some of these diseases 
the infection undoubtedly enters the glands by way of the bloodvessels and lym- 
phatics. Pyogenic infection of the parotid, whether hemal, lymphatic, or by a 
duct, produces a suppurative interstitial parotitis, or parotid abscess, also called 
" parotid bubo." A curious form of inflammation of the parotid gland with stenosis 
of Steno's duct is sometimes seen in cases of sulphuric-acid poisoning. While it is 
possible for the sublingual and submaxillary glands to be involved, the parotid 
is the gland which nearly always suffers. 

The inflammation may be treated in its early stages by cold compresses, by the 
application of leeches, and by the administration of circulatory sedatives like 
aconite, provided the patient is not already depressed by disease. So far as possible 
the treatment should also be addressed to the relief of the underlying cause of the 
condition. If the gland is suffering from a subacute inflammation, mercurial 
ointment, iodine ointment, or ichthyol ointment may be thoroughly rubbed into 
the skin over it, unless perchance the gland is swollen as the result of mercurial 
or iodide influence. When an abscess forms it must not be forgotten that it should 
be opened promptly, but with great care. Not infrequently a parotid abscess is 
so closely associated with an important bloodvessel, or indeed with the external 
carotid artery, that a careless incision may produce disaster. Such an abscess 
should always be opened by careful dissection. 

Chronic indurative or sclerosing parotitis is a well-known pathological condition, 
the clinical features of which are still obscure. It has been observed in diabetes 
with and without pancreatic disease, but the exact relationship, if any, is not 
known. 

Mikulicz's Disease. — Bilateral Salivary Swelling. — This is a condition character- 
ized by bilateral swelling of the salivary glands, often associated with an involve- 
ment of the lachrymal glands and sometimes accompanied by a considerable degree 
of anemia. In some instances the blood changes are closely allied to or identical 
with leukemia and in still others there may be swelling of the spleen and lymph 



ACUTE PHARYNGITIS 515 

nodes with the picture of lymphatic pseudoleukemia. According to Thursfield 
there are at least eight groups of these cases. In one group it appears in a con- 
genital or hereditary family affection; in another group it occurs in a single in- 
dividual; in still a third there is involvement of the lymphatic apparatus; in the 
fourth there is leukemia; in the fifth it is associated with tuberculosis; in the sixth 
with syphilis; in a seventh with gout; while the eighth form manifests an inter- 
mittent or periodic salivary swelling, the so-called sialodochitis fibrinosa. The 
prognosis in the simple form without involvement of the lymph nodes is good as 
to life, although some years may elapse before a cure develops. In the leukemic 
cases the prognosis is evil for obvious reasons. In the tuberculous and syphilitic 
the prognosis depends upon the treatment usually carried out for these maladies. 



DISEASES OF THE PHAEYNX. 

ACUTE PHARYNGITIS. 

Definition. — Acute pharyngitis is an acute catarrhal inflammation of the mucous 
membrane lining the pharynx in which there is hyperemia and congestion, with 
some infiltration of the submucous tissues, and, later, an increased secretion of 
mucus. 

Etiology. — Acute pharyngitis is caused, as a rule, by simultaneous exposure to 
cold and infectious dust. Cold and damp air first impair the vital resistance of 
the pharyngeal mucous membrane, and then dust, laden with micro-organisms, 
falling upon it speedily produces infection. There can be no doubt that systemic 
conditions also favor the development of this state. 

Aside from the fact that lowered vitality always permits infection to take place 
readily, there can be no doubt that the excessive use of alcohol, tobacco, or rich 
foods, or the presence of a torpid liver, or a catarrh of the nose, mouth, or stomach 
aid materially in permitting the condition to arise. Pharyngitis also arises as a 
result of lithemic states. Sometimes infection seems to come from a chronic 
tonsillitis or is an extension from the nares. The condition is particularly prone 
to arise in those who work for a number of hours a day in imperfectly ventilated 
rooms. 

Pathology. — After a preliminary dry stage the engorgement of the bloodvessels 
of the mucous membrane and the inflammation of the mucous glands results in 
the pouring out of considerable quantities of mucus, marked epithelial desquama- 
tion, and in severe cases some fibrin. If pyogenic organisms are present the secre- 
tion may be distinctly mucopurulent. In some instances the swelling of the 
submucous tissues is very marked. In others, although severe, it may be superficial 
In very rare cases the exudate may be so fibrinous as to form a false membrane 
which is not always due to the presence of the bacillus of diphtheria. Not rarely 
in such cases the uvula and the tonsils are also involved. 

Symptoms. — Acute pharyngitis usually comes on suddenly, with the symptoms 
of what is popularly called "sore throat," so that the patient feels that the mucous 
membrane is swollen and sore, and there is some pain on swallowing. On inspection 
it will be found that the posterior wall of the pharynx and neighboring parts are 
dry and red, with the capillaries injected. After secretion is established the parts 
are thoroughly moistened by serum and mucus. In some instances, if the infiltra- 
tion of the submucous tissues is marked, the patient may complain of a sense of 
constriction in the throat, and at times a good deal of pain may extend along the 
Eustachian tube into the ear. If the pain is not too great, the patient may con- 



516 DISEASES OF THE PHARYNX 

tinually clear his throat in an effort to . relieve the irritation. Constitutional 
symptoms are usually mild, but the tongue is coated and the patient may be some- 
what depressed. 

Prognosis. — Recovery always ensues unless some unforeseen complication arises. 

Treatment. — The treatment consists, if the patient is seen in the early stages, 
in the application of a cold compress to the neck below the angle of the jaw. This 
compress is made by dipping cloths in ice-water, wringing them out, and then 
binding them against the part. They should not be allowed to become warm 
and so produce the relaxing effects of a poultice. Internally, if the patient is an 
adult, he may be given from 10 to 15 drops of the tincture of aconite with a drachm 
of sweet spirit of nitre in a glassful of hot lemonade. Before taking this he should 
be put to bed in order that when perspiration develops he will not be chilled. 
Small pieces of ice may be held in the mouth, but, as a rule, better results will be 
obtained if the patient gargles with as hot water as he can bear. This water may 
be fortified by adding to it an equal quantity of the distilled extract of witch-hazel. 
If the bowels are at all constipated, saline purgatives, such as citrate of magnesia, 
should be used to unload them. If there is any rheumatic or gouty tendency, the 
patient will do best if, in addition to the purgatives, he is given 20 grains of bicar- 
bonate of potash in large draughts of water every four or five hours; or, instead, 
10 grains of aspirin may be given every three hours until 40 grains have been used. 

Local treatment aside from the use of the gargle is usually unnecessary. /If the 
condition is due to a gouty tendency, the use of any one of the oily substances 
commonly employed in atomizers produces increased discomfort, in the writer's 
experience. If it is not due to this cause, some relief may be obtained by spraying 
the parts with 3 drops each of oil of sandal-wood and oil of sassafras in an ounce 
of liquid albolene. In other cases, when the oils cause discomfort, my colleague, 
Dr. Kyle, strongly recommends applying hydrochloric acid, in the proportion of 
5 to 10 drops of the dilute acid in an ounce of water, for the purpose of contracting 
the dilated bloodvessels. 

When the second stage is reached 5 to 10 grains of chloride of ammonium may 
be given in equal parts of fluidextract of licorice and water four or five times a day. 
Or, instead, 10 grains of benzoate of ammonium may be given in capsule four 
times a day. 

ULCERATIVE OR PHLEGMONOUS PHARYNGITIS. 

Etiology. — This condition, sometimes called ulcerated sore throat, or phlegmonous 
pharyngitis, is due to an infection of the mucous membrane of the throat by micro- 
organisms. It is not uncommonly seen in physicians and nurses who are attending 
children suffering from scarlet fever and diphtheria. Many years ago it was 
frequently met with in medical students who were dissecting cadavers which had 
been imperfectly preserved. This form of pharyngitis is exceedingly painful 
in its early stages, and is characterized by changes much like those just described 
in acute catarrhal pharyngitis, except that a superficial necrosis of the mucous 
membrane rapidly occurs, so that in a few hours small, irregular ulcers may be 
seen upon the soft palate, the half-arches, and the pharyngeal wall. If the infection 
is severe, so that the submucous tissues are involved, it becomes a phlegmonous 
pharyngitis. 

Symptoms. — A patient with infectious pharyngitis usually complains of much 
pain in the throat and in the muscles of the neck. This is greatly increased when 
he attempts to swallow. There may be slight febrile movement and depression. 

Treatment. — The treatment consists in spraying the inflamed mucous membrane 
with a normal salt solution, and following this by a gargle or spray of 1 per cent, 
solution of carbolic acid and water or albolene. This in turn is followed by a 



FOLLICULAR PHARYNGITIS 517 

spray of menthol, 4 grains to the ounce. Cold compresses applied under the jaw 
are advantageous. If one or two ulcers are particularly active, they may be touched 
with nitrate of silver. Usually it is advisable to give the patient a moderate 
purgative dose of calomel and to follow it by a saline purge, such as a Seidlitz 
powder. 

CROUPOUS PHARYNGITIS. 

Etiology. — Croupous pharyngitis occurs in two forms; as diphtheria, which has 
already been described, and as a simple membranous pharyngitis, which commonly 
is due to infection by the Pneumococcus or Streptococcus pyogenes. The chief 
difference between this form of pharyngitis and diphtheria is that the mucous 
membrane is not deeply involved, that true ulceration never occurs, and the Klebs- 
Loeffler bacillus is absent. The inflammation is, however, of such a character 
that a false membrane develops with desquamation of the epithelium. If the 
membrane is removed, the tissues beneath may bleed, very much as they do in 
diphtheria. Although there is usually a slight chill and some fever, the degree of 
systemic disturbance is by no means as marked as in the well-developed case of 
true diphtheria. 

Treatment. — The treatment consists in washing the infected parts thoroughly 
by a spray of normal salt solution, and following this by a solution of hydrogen 
peroxide and water half and half, and this in turn by gargling and spraying with 
distilled extract of witch-hazel. Usually this treatment is sufficient. If the 
condition persists Loeffler's solution may be applied locally. Antitoxin is to be 
used if diphtheria is present. (See Diphtheria.) 

CHRONIC PHARYNGITIS. 

Etiology. — A condition of chronic inflammation of the pharyngeal mucous mem- 
brane is frequently met with in certain climates, particularly that of the Atlantic 
seaboard. It is also found in persons who continually use the voice, and so it 
has obtained the name of "auctioneer's" or "clergymen's" sore throat. It is 
also met with in persons who use tobacco to excess, and sometimes in those who 
take too much alcohol. Obstructions in the nasal passages seem distinctly to 
predispose to this state. 

Pathology. — The pathological condition consists in a thickening of the mucous 
membrane of the pharynx and an increase in the connective tissues of the mucous 
membrane itself, and of the submucous tissues. This may result in a secondary 
atrophy of the glands in the mucous membrane. 

Symptoms. — The symptoms consist in a thickening of the pharyngeal secretions 
and irritation of the mucous membrane, so that the patient is continually attempting 
to clear the throat, which often feels dry and harsh. The cough is spasmodic, 
unproductive in its result, and is made much worse by exposure to cold and dust. 

Treatment. — The treatment consists in a regulation of the digestive system, 
in giving tone to the circulation if it is feeble, in rest for the nervous system if the 
patient is overworked, and in the internal administration of benzoate of ammonium 
in 10 grain doses several times a day. Before going to bed at night the patient 
should gargle his throat with hot water or with hot salt solution, and if the blood- 
vessels are much dilated a spray of dilute hydrochloric acid, 10 drops to the ounce 
of water, should be used. 

FOLLICULAR PHARYNGITIS. 

Etiology. — Under the name of follicular pharyngitis a closely related condition 
to that just described exists, in which an annoying cough is persistent, and in 



518 DISEASES OF THE TONSILS 

which a considerable number of enlarged follicles, surrounded by an injected 
mucous membrane, can be seen on the posterior wall of the pharynx. 

Treatment. — The treatment is of the same character as that just described for 
chronic pharyngitis. Occasionally it is necessary to cauterize the follicles. An 
excellent application is tincture of iodine 1 part in 2 parts of glycerin. 

EPIDEMIC SORE THROAT. 

Definition. — This very general term is applied to a form of more or less severe 
pharyngitis and tonsillitis occurring in epidemic form, sometimes causing death. 
The earliest reports deal with an epidemic in England in 1875. Very noteworthy 
outbreaks have occurred in Boston in 1910 and 1911, in Chicago and Baltimore in 
1911 and 1912, and in Jacksonville, Illinois, in 1913. In Chicago no less than 10,000 
persons suffered from it. 

Etiology. — The cause exists in infected milk derived from cows suffering from 
an acute inflammation of the udder due to a streptococcus, which organism is 
found to be identical in the milk and in the throat of the patient. The micro- 
organism is easily destroyed in sour milk, but may be found in ice-cream after 
three weeks. 

Symptoms. — These consist in more or less severe inflammation of the pharynx 
and tonsils with swelling of the cervical lymph nodes, fever as high as 105° F., and 
great prostration. When death has ensued it has been due to erysipelas, septic 
pneumonia, peritonitis, appendicitis, or general septicemia. 

Treatment. — This consists in preventing further infection by excluding the milk 
previously used and using only pasteurized or boiled milk and in the general plan 
of treatment carried out in combating any one of the conditions named. 



DISEASES OF THE TONSILS. 



ACUTE TONSILLITIS. 



Definition. — As its name implies, this disease consists in an acute inflammation 
of the tonsils, accompanied by great swelling of their tissues, and an associated 
pharyngitis. It occurs in two forms, the follicular and diffuse. The follicular 
form is distinctly infectious. 

Etiology. — Acute tonsillitis is the result of an infection by pathogenic micro- 
organisms, which are practically always present in the crypts of the tonsils, but 
do not penetrate the mucous membrane until its permeability is increased by con- 
gestion, or by general causes affecting perhaps the vital resistance of the entire 
body. In many instances the suppurating form arises because the organisms 
attempt to enter the general system by way of the tonsils, and the suppurative 
process is the result of an effort to prevent such an entrance. The streptococcus 
is a cause in some cases. In other cases the organism which Poynton and Payne 
think is the cause of acute articular rheumatism is responsible, and the bacillus 
of diphtheria is also a common factor. 

Follicular tonsillitis is more common in the period of life from five to twenty 
years than at any other time, and is rare in infancy. Some individuals suffer 
from frequent attacks until they reach forty or fifty years of age. After this time 
of life it is very rare. 

Although follicular tonsillitis is rare in adults, the suppurating form is frequently 
met with in this class of patients. Persons who have a lymphatic temperament 



ACUTE TONSILLITIS 519 

are far more susceptible than persons of the wiry type, and it is particularly prone 
to occur in those who, because of obstruction of the nasal passages, are "mouth 
breathers," or who suffer from subacute or chronic hypertrophic catarrh of the 
nasopharynx. One attack distinctly predisposes to another. My experience 
leads me to believe that it is distinctly infectious, for I have repeatedly seen healthy 
persons develop the malady after being exposed to the breath of those who were 
ill with it. Another predisposing cause is the breathing of vitiated air, and air 
that is contaminated by sewer gas or smoke. How much these influences act 
directly as sources of infection and how much as agents which, by diminishing 
vital resistance, make infection possible, is difficult to determine. 

Pathology and Morbid Anatomy. — In acute follicular tonsillitis there is an inflam- 
matory swelling of the parenchyma of the gland. The mucous membrane covering 
the gland is intensely hyperemic and may even show vesicles on its surface. Each 
follicle exudes a cheesy-looking mass, and these masses dot the surface of the tonsil 
or coalesce and produce a tonsillar coating, which at first glance closely resembles 
the false membrane of diphtheria. If some of this material is examined micro- 
scopically it is found to consist of dead epithelial cells, micro-organisms, and pus 
cells. In addition to these superficial changes there is hyperemia of the tonsillar 
capillaries, and proliferation of the lymphoid cells in the deeper tissues of the glands. 
In the more deeply situated and intense inflammations of the gland, sometimes 
called quinsy, there is a necrosis of the tissues, suppuration takes place, and the 
pus escapes from the tonsillar abscess, either by the aid of the surgeon's knife or 
by rupture of the abscess wall. In any of these conditions the passage of bacteria 
or their toxins into the lymphatics may produce glandular enlargement in the neck. 

As general systemic infection often enters the body by way of the tonsils it is 
wise to be on the watch for signs of endocarditis. Doubtless the association of 
rheumatism with tonsillitis by many practitioners is due more to the development 
of septic arthritis from the entrance of pathogenic germs by these pathways than 
to any real relationship between acute rheumatism and tonsillitis. I have seen 
many cases of severe endocarditis and acute arthritis follow an acute tonsillitis. 

Symptoms. — A patient suffering from the earliest stages of acute tonsillitis may 
first feel soreness of the throat, with a sense of local swelling or constriction, or the 
systemic signs of the infection may first be manifested. Creeping, chilly sensations, 
or even a true rigor, may develop, and there is very frequently an amount of aching 
and pain in the limbs which is extraordinarily severe, so that the patient complains 
most bitterly, not only of this symptom, but of the degree of illness, so that he 
fears a serious malady. Violent headache is often a prominent symptom, and the 
temperature soon becomes very high, mounting to 103° or 104° or even 105° in a few 
hours. Rarely nausea and vomiting may occur. An examination of the throat 
will show the presence of distinct swelling of the tonsils, which not rarely extend 
as far across the fauces as the uvula, and even press against one another. These 
swellings are intensely congested and frequently covered with exudate, and are 
often very foul in appearance. The breath of the patient is often exceedingly foul, and 
unless ventilation is very good the odor may fill the room. Owing to the swelling 
of the tonsils and adjacent glands and stiffness of the muscles of the sides of the 
neck, an examination of the patient's throat may be very painful. It is a note- 
worthy fact that acute follicular tonsillitis is practically always bilateral, while the 
deeper form, sometimes called quinsy, is often unilateral. 

In the suppurating form of the disease the systemic manifestations are often 
less severe than in the follicular types just described, but the local pain is often 
very severe, and opening the mouth may be very painful. The tonsil is often 
enormously enlarged, but is rarely dotted with follicular spots. Instead it may 
be smooth and shining in appearance. The inflammation often extends to the 
uvula, which may be so swollen and elongated as to cause great distress. 



520 DISEASES OF THE TONSILS 

Treatment. — The treatment of both forms of tonsillitis is largely identical. To 
the surface of the tonsil, in the first twenty-four hours of the inflammation, there 
is nothing better to arrest the process and relieve pain than pure guaiacol applied 
by a cotton applicator. This often causes great pain for the moment; but it is 
remarkably efficacious. Externally, over the gland, a small ice-bag is a valuable 
application. It should be kept constantly applied for several days. Internally 
in the very early stages the use of biniodide of mercury is very useful in the dose 
of 5-jyo" of a grain every half-hour till 5V grain has been taken. 

After the stage of onset is past the best internal treatment is 10 to 20 minims 
of tincture of iron chloride well diluted with water every three or four hours and 
potassium bicarbonate, or citrate, in copious draughts of water to flush the kidneys 
and diminish the backache. 

Many practitioners rely largely on aspirin or salicin at this time, giving them in 
full doses. They are efficacious, but they increase headache, disorder the diges- 
tion, and may irritate the kidneys, which are prone to irritation in this disease. 

Some cases get relief from gargling with very hot water or by holding ice in the 
mouth. 

When the tonsils are chronically enlarged and repeated attacks of tonsillitis 
occur they should be removed between attacks. The application of caustics like 
nitrate of silver often makes them larger than before. 

In the suppurating form the pus should be evacuated as soon as it is formed, 
the tonsils being punctured by a bistoury or a tenotome, the tip of which is exposed 
after being run through a small cork so as to guard it and prevent any movement 
of the patient from causing the physician to injure an important bloodvessel. 

In all cases of follicular tonsillitis cultures of the secretions from the throat 
should be examined for the Klebs-Loeffier bacillus, for in all cases before making 
a diagnosis of follicular tonsillitis the physician should carefully exclude diphtheria. 
(See Diphtheria.) When children are in the household the patient should be 
carefully isolated. 

LUDWIG'S ANGINA. 

In 1836 Ludwig described a condition in which, in association with an acute 
inflammation of the mucous membrane of the mouth, cheek or tonsillar region there 
developed a phlegmonous cellulitis resembling that produced in other portions of 
the body by virulent infections. This cellulitis is particularly prone to involve 
the tissues under the tongue. It may spread with great rapidity and rapidly reach 
a fatal termination in ten days. The sub-maxillary area is intensely swollen, the 
lower jaw almost immovable. The extension of the swelling posteriorly may 
produce suffocation. Whether Ludwig's angina is a specific infection is not as 
yet determined, but almost every bacteriological investigator has found one or 
more common pathogenic germs present. Some have isolated the streptococcus, 
others the bacillus of malignant edema, and sometimes the streptococcus and 
staphylococcus have both been present. The pneumococcus has also been 
found in the pus. Even when fluctuation cannot be found if pressure symp- 
toms exist free drainage should be obtained. Ludwig considered the following 
symptoms as characteristic of the disease : More or less inflammation of the throat 
which often disappears early. A board-like hardness of the sub-maxillary swelling; 
a condition also characteristic of the sub-lingual swelling so that the same sensation 
is given to the finger both inside and outside the lower jaw. There is a sharp 
line of demarcation between the indurated tissues and the surrounding healthy 
ones, and this is true even when the loose connective tissue is involved. There 
is an irregular septic fever, profuse sweats, delirium and a rapidly developing 
typhoid state if free drainage is not given early. The swelling may rupture in 
the floor of the mouth discharging a thin grayish or reddish-brown offensive fluid, 



CHRONIC HYPERTROPHIC TONSILLITIS 521 

more like a putrefactive process than ordinary suppuration. Aside from free drain- 
age the patient should be supported by good food, administered through a tube, by 
stimulants and if possible by the use of autogenous vaccine. If the chief swelling 
is sublingual the incision may be made between the tongue and the teeth, or a 
median incision may be carried through the mylohyoid muscle under the jaw. 

VINCENT'S ANGINA. 

Vincent's angina is an acute inflammatory diphtheroid inflammation of one or 
both tonsils, which condition in severe cases extends to peritonsillar tissues and is 
often accompanied by marked swelling of the cervical lymph nodes. Two asso- 
ciated microorganisms are present, a spirillum and a fusiform bacillus readily 
differentiated by Gram's method of staining. These organisms do not grow on 
ordinary culture media and can only be found by using a smear. It is probably 
far more common than supposed, being diagnosed as acute tonsillitis. The false 
membrane when removed leaves a bleeding surface. The blood shows a marked 
lymphocytosis. There is little fever but considerable prostration. If the peri- 
tonsillar tissues are involved and the patient is already feeble death may occur. 
The treatment consists in the local use of tincture of iodine, hydrogen peroxide or 
nitrate of silver, and good food with iron and arsenic. Rolleston and others 
advise dipping a cotton applicator in glycerin which is in turn dipped in salvarsan 
and applied to the lesion. The results are remarkably good. 

CHRONIC HYPERTROPHIC TONSILLITIS. 

Definition. — Chronic hypertrophic tonsillitis is a condition of overgrowth, or 
hyperplasia of the tonsils, which affects all parts of both tonsils and usually involves 
the so-called pharyngeal tonsil. In some instances the lymphoid tissue of the 
glands is chiefly affected, while in others it is the connective tissue. In the one 
instance the enlarged tonsils present themselves as projecting masses, soft in tex- 
ture. In the other they are remarkably hard and cut with a resistance almost 
cartilaginous in character. In some instances there is overgrowth of the tonsils 
without the adenoid of the pharynx being involved. Nearly always patients 
with this affection suffer from associated nasal catarrh, often from secondary 
middle-ear disease, and they present a peculiar expression of stupidity or lack 
of intelligence. 

Symptoms. — Aside from organic disease of the great viscera there is no chronic 
malady which produces such extraordinary changes in the physical appearance, 
growth, and mental development as does this one. The obstruction to free nasal 
breathing results in mouth breathing, and this in turn causes the child to hold the 
mouth open in a silly manner, which detracts from its facial appearance. So, 
too, the lack of free respiration results in a failure of physical development, so 
that the chest is often poorly developed, and even the entire body is dwarfed. Finally, 
this same cause produces restless nights and so causes loss of physical rest, which 
may be emphasized by attacks of spasmodic croup or night screaming. Constant 
cough at night on lying down is also often a troublesome symptom and is due to 
undue dryness of the nasopharynx or to thickening of the uvula by the edges of 
of the projecting tonsils. 

After the disease has lasted for years the child is often stupid, morose, and 
apathetic to a degree, and the open mouth, stunted nose, and heavy eyes make a 
diagnosis of the tonsillar state easy. When the child is stripped the chest is often 
found to be barrel-shaped or the patient is pigeon-breasted, or it presents the 
Trichterbrust of the Germans, or the so-called funnel chest of English writers, in 
which there is a deep depression of the lower part of the breast-bone. These 



522 DISEASES OF THE ESOPHAGUS 

thoracic changes are due to two chief causes: first, the general impairment of 
nutrition produces malnutrition of the thoracic walls as in rickets, and, second, in 
the effort at sufficient respiration the chest walls undergo faulty development. 
The breath is often quite fetid, due to retained secretions and particles of food in 
the crypts of the tonsils, and if the tonsils be pressed upon a surprisingly large 
amount of material can be expelled from their cavities. 

The nasopharyngeal spaces of such children are first-rate culture fields for the 
growth of bacteria of all sorts and for acute infections, such as diphtheria and 
scarlet fever. 

Treatment. — When the tonsils are ragged and chronically enlarged this does 
not in itself indicate operative interference. There can be no doubt, as J. 
Noland Mackenzie points out, that there has been a massacre of the tonsil in the 
last decade. If the enlargement obstructs breathing, causes night cough, or results 
in frequent attacks of acute tonsillitis the tonsils should be removed, particularly 
if they induce peritonsillar abscess. Mere enlargement of the tonsils does not 
necessarily predispose the child to the severe complication of the acute infectious 
diseases, such as diphtheria and scarlet fever. If, however, the tonsils are so 
large as to obstruct breathing, and particularly if the postnasal adenoids are greatly 
enlarged, making the child a mouth-breather, then operative interference is essential. 
If we except the effects produced by the use of thyroid gland in cretinism it is not 
possible to find any state in which the physician can cause such a complete meta- 
morphosis in his patient as to health of mind and body as in this type of case. 
The removal of the enlarged tonsils by tonsillotomy and the scraping away or 
curetting of the pharyngeal adenoid results in free and easy breathing and in an 
extraordinary change in growth and spirits. Children who have been stunted in 
mind and body for years gain, it may be, thirty pounds in a few months, become 
rosy and bright-looking, and are able for the first time to keep up with their fellows 
in school and in sport. 

The use of cod-liver oil and syrup of the iodide of iron after the operation is a 
great aid to speedy recovery. 



DISEASES OF THE ESOPHAGUS. 

ESOPHAGITIS. 

An acute inflammation of the esophagus often ensues after the ingestion of 
irritant poisons, such as concentrated lye, ammonia-water, carbolic acid, and 
similar substances. Under these conditions it is but a part of the general inflamma- 
tion of the gastrointestinal tract which all irritant poisons induce, and has little 
interest except from a toxicological standpoint and the strictures that commonly 
follow. When esophagitis is due to disease it may arise from an extension of a 
diphtheria from the pharynx or from an extension of the inflammation in the 
pharynx in cases of scarlet fever. So, too, in certain cases of typhoid fever the 
esophagus may undergo inflammatory changes, and these may progress to such 
an extent that ulceration ensues. (See Typhoid Fever.) Sometimes, too, the 
esophagus is involved in cases of aphthous stomatitis and in thrush. 

A membranous esophagitis occurs, but it is rare. It may follow the swallowing 
of escharotics and is occasionally seen after prolonged alcoholic excess. A cast 
of the entire esophagus may be expelled. 

The mucous membrane in ordinary inflammations of the esophagus is reddened 
and hyperemic. There may be some pain beneath the breastbone, which is in- 



DILATATION OF THE ESOPHAGUS 523 

creased by the swallowing of food or drink, but in the milder types no symptoms 
are present, and unless ulceration is followed by cicatrization, neither the physician 
nor the patient may be aware of the fact that the esophagus has suffered from an 
inflammatory process. 

Should symptoms of pain and discomfort exist, they may be relieved by the 
use of demulcent drinks, of which perhaps the best is emulsion of sweet almonds, 
or milk with arrowroot. Sometimes swallowing small pieces of ice gives relief. 

In cases of heart disease and cirrhosis of the liver a form of chronic esophagitis 
sometimes develops, in which the mucous membrane suffers from a chronic catarrh 
and the smaller bloodvessels become varicose and rupture, causing the vomiting 
of blood. 

ORGANIC STRICTURE OF THE ESOPHAGUS. 

As has already been intimated, stricture of the esophagus usually follows the 
healing of an ulcer which is produced by the ingestion of some corrosive substance, 
or by ulceration developing in the course of typhoid fever or syphilis. Stricture 
may be cylindrical or annular, symmetrical or asymmetrical, single or multiple. 
The usual sites are behind the cricoid cartilage, opposite the bifurcation of the 
trachea, and at the hiatus esophagei. Occasionally inflammation of a lymphatic 
gland, the pressure of a tumor in the mediastinum, or of an aneurysm, causes a 
narrowing of the gullet, and, more rarely still, a polypoid tumor may grow from 
the mucous membrane. Malignant stricture will be discussed later. 

Symptoms. — The symptoms consist in difficulty in swallowing food, the patient 
stating that it lodges part way down to the stomach, and that if any considerable 
quantities are taken regurgitation takes place, the regurgitated materials containing 
no trace of gastric juice or the products of digestion. If an esophageal bougie 
is passed it is found to be arrested at the level of the stricture, and it may be im- 
possible to push it past this point. 

Treatment. — The treatment consists in the use of a small bougie to dilate the 
stricture, followed by the employment of larger, graduated bougies. If the stricture 
is so tight that food cannot pass and the life of the patient is endangered by inani- 
tion, and if the use of a bougie fails to overcome the obstruction, surgical interference 
will be necessary. 

Sometimes stricture of the esophagus is a congenital condition, in which case the 
child rarely lives, and little can be done for its relief. 

DILATATION OF THE ESOPHAGUS. 

Etiology. — Dilatation of the esophagus occurs in two forms, namely, the diffuse 
and the localized. In the diffuse form the entire tube is dilated, and there may 
be some overgrowth of the muscular fibres, which has occurred in an endeavor 
on the part of the esophagus to force food past an obstruction which exists near 
the cardiac orifice of the stomach. 

When a localized dilatation occurs it takes the form of a diverticulum, which 
may be divided into two types, namely, "pressure diverticula" and "traction 
diverticula." The pressure diverticula are very rare and are found usually at 
the junction of the pharynx and the esophagus, where the muscular fibres are 
weakest. Their origin is supposed to depend upon pressure upon this point of 
the gullet in deglutition, and they are thought to develop in those who are in the 
habit- of bolting their food. The diverticulum arising from this cause is lined 
with mucous membrane, its submucous tissues are thickened, and the muscular 
coat is atrophied so that the mucous coat bulges through it as a hernia-like pro- 
jection. The lesion always occurs in the posterior or posterolateral wall of the 
esophagus. 



524 DISEASES OF THE ESOPHAGUS 

Traction diverticula occur more frequently than the type just mentioned, but 
are very seldom recognized during life. They are thought to be due to contraction 
of tissues which have become attached to the esophagus by inflammatory adhesions, 
as in cases in which inflammation of the bronchial lymph glands has taken place. 
This lesion is usually found in the anterior wall of the gullet, and a number of 
diverticula may be present in a single case. 

Atonic dilatation of the esophagus is occasionally observed; the dilated tube 
may be fusiform or flask-shaped, the part of the organ corresponding to the neck 
of the flask being upward. Such dilatation occurs independently of organic disease 
below, and has been attributed to spasm of the cardia. The dilated esophagus 
may be extremely capacious, holding a pint or more of fluid. 

Symptoms. — The symptoms of diffuse dilatation of the esophagus due to stenosis 
are those produced by stricture of the gullet, and consist chiefly in difficulty in 
swallowing. It is a condition rarely recognized during life. The small diverticula 
due to traction by adhesions are also rarely recognized, unless one of them becomes 
so large that it forms a pocket in which food accumulates, until by reason of its 
decomposition or fermentation it produces so much irritation and inflammation 
that the stomach, esophagus, and all the muscles of the chest and abdomen endeavor 
to expel it by a process akin to that of vomiting. Sometimes a diverticulum of 
this character is capable of holding a very considerable quantity of fluid. 

Diagnosis. — The diagnosis of a diverticulum is reached by the use of a stomach 
tube, which is passed as far as it will go and then used as it would be in lavage, or as 
a stomach pump would be employed. Under these circumstances liquids which 
have been swallowed are brought up when the tube has not been passed far enough 
to make it possible that the liquids are obtained from the stomach. Such large 
diverticula are usually of the traction type. A diverticulum may be discovered by 
filling the cavity with bismuth and syrup of acacia and using the x-rays. 

Treatment. — The treatment consists in the use of a stomach tube for the purpose 
of feeding the patient, provided the physician or the patient is successful in passing 
the tube past the diverticulum. In those cases in which the diverticulum is so 
large that it prevents the ingestion of food, by pressure on the esophagus, and so 
interferes with the patient's nutrition, the only resort is a surgical operation and 
rectal alimentation. 

SPASM OF THE ESOPHAGUS. 

This affection, sometimes called " esoyhaqismus" is rarely met with except in 
persons suffering from hysteria or insanity. It is sometimes seen in hydrophobia, 
and it is this difficulty in swallowing water, rather than an actual dread of water, 
which has given that disease its name; for with the thought of swallowing, at the 
sight of water, the spasm develops. The difficulty in swallowing usually points 
to the presence of spasm or stricture, and if there is no history of the ingestion of 
an irritant some time before, or other causes which would be likely to produce 
ulceration and stricture, the strong possibility of spasm is to be considered. Usually 
in spasm it is much easier to pass an esophageal bougie than it is in cases of stricture. 
But occasionally the spasm is sufficiently tight to oppose the passage of the bougie, 
and to give to the hand guiding the bougie the sensation which is produced by the 
end of the instrument coming in contact with a true organic obstruction. 

Treatment. — The treatment consists in the passage of a bougie once or twice a 
day; in the administration of nervous sedatives if the patient is in a condition of 
nervous excitation; of stimulants, if she is in a condition of profound depression, 
and of measures devoted to the improvement of the general health, both mental 
and physical, if it is impaired. As the spasm may be due to a fissure, ulcer, or 
other tender spot the food should not be bulky, but preferably liquid and never 
taken in large amounts. 



ACUTE GASTRIC CATARRH 525 

CANCER OF THE ESOPHAGUS. 

Cancer of the esophagus usually occurs in the form of squamous epithelioma, 
and affects men more frequently than women. Occasionally a medullary cancer 
is found in this region. The growth soon undergoes ulceration, and not infrequently 
the entire circumference of the tube may be involved, and in this manner a stenosis 
may be developed with dilatation of the esophagus above the point of growth. 
The disease is quite rare, for of 7290 cases of cancer collected by Williams but 6 
per cent, were primary in the esophagus. Tanchon in 9118 cases of cancer found 
only 13 in the esophagus. Cases have been recorded as early in life as nineteen 
years, but most patients are past forty. The disease is about equally divided as 
to its occurrence in different levels of the tube. Thus, if the statistics of Kraus, 
von Hacker, and Newmann are added together, making 1477 cases, we find 
that 582 were near the cardia, 453 near the middle third, and 440 at the upper 
third. 

Symptoms. — The symptoms, as in cases of ordinary stenosis due to stricture, 
consist in difficult deglutition and not infrequently considerable pain, both at the 
time of swallowing and when the esophagus is at rest. The food is often regurgitated 
almost as soon as it leaves the pharynx, and sometimes the effort at regurgitation 
is followed by the appearance of some blood and mucus. Blood and mucus also 
very frequently appear if a bougie is used to pass the stricture. The age of the 
patient, the absence of a history of the ingestion of a corrosive poison, the emaciation 
and weakness, and the presence of primary or secondary growths elsewhere render 
the diagnosis possible. Sometimes an aneurysm of the thoracic aorta by pressing 
on the esophagus may produce somewhat similar symptoms, but under these 
circumstances the physical signs of aneurysm may be found. 

Prognosis. — The prognosis in esophageal cancer is, of course, exceedingly bad. 
Death comes from exhaustion and starvation, from pneumonia due to the inhala- 
tion of septic materials, or to ulceration of a large bloodvessel. Sometimes the 
lymphatic glands of the neck are secondarily involved. Occasionally the physician 
is chagrined at the autopsy to find that an unsuspected esophageal cancer has 
been present for weeks without presenting symptoms, and without his having 
recognized its existence. 

Treatment. — Medicinal measures are of course fruitless except for the relief of 
pain. Surgical measures are of little value, since the patient is usually so exhausted 
by the time that the diagnosis is confirmed and he is willing to resort to an operation, 
that life is prolonged but little by the operative interference. Exner has recently 
reported a case in which improvement followed the use of radium in a tube attached 
to a bougie. 



DISEASES OF THE STOMACH. 

ACUTE GASTRIC CATARRH. 

Definition. — Acute gastric catarrh, or acute catarrhal gastritis, as its name indi- 
cates, is a state in which the mucous membrane of the stomach becomes hyperemic 
and then swollen, with lessened secretion, followed by excessive production of 
mucus and reduction in the quantity of digestive ferments. The term acute 
gastritis is sometimes employed to describe this state. This is unfortunate because 
a true inflammation of all the coats of the stomach is not present except when 
irritating foods have been taken in excess, or when some irritant poison has been 
swallowed. 



526 DISEASES OF THE STOMACH 

Etiology. — The causes of acute gastric catarrh are very various. In children 
it is often a sequel to taking cold, with some resulting interference with the activity 
of the liver. It also follows the excessive use of sweets in this class of patients. 
In older persons it is nearly always due to the taking of an excessive amount of 
indigestible food or overloading the viscus with ordinary foodstuffs, particularly 
if alcoholic drinks and highly seasoned articles have been swallowed. 

Symptoms. — The symptoms of acute gastric catarrh in children are quite different 
from those met with in adults in most instances. The child has nausea and vomiting, 
and some epigastric discomfort. Fever, varying from 100° to 102°, often develops 
and persists for several days. The bowels may be constipated or several loose move- 
ments may occur daily. The appearance of the tongue in this class of cases is very 
characteristic. It is evenly coated by a thin white fur which is dotted by many 
tiny red spots where the enlarged papillae exist. The tongue is also somewhat 
drier than normal and the breath slightly foul and hot. The urine is usually decreased 
in amount and high colored. 

In adults acute gastric catarrh presents somewhat different symptoms. There 
is often some pain or tenderness on pressure in the epigastrium and a loss of appetite 
amounting to disgust for food. Nausea may be quite persistent and vomiting 
may occur. 

In both children and adults the attacks may last for from one to four days. 

Diagnosis. — When the physician is called to see a child who is suffering from 
moderate fever, a somewhat coated tongue and epigastric distress, he must not 
be hasty in stating that the case is one of acute gastric catarrh, because many of 
the acute infectious diseases begin by moderate gastric disorder and a coating of 
the tongue. Whenever the gastric symptoms persist for more than four or five 
days, enteric fever should be suspected as being the cause of the illness, but care 
must be taken that the common error of calling mild typhoid fever "gastric fever" 
is not made. Uncomplicated acute gastric catarrh is so rare in adults, who have 
not abused alcohol, that great care should be taken before the physician is satisfied 
with this diagnosis. 

Treatment. — The treatment consists in unloading the portal and hepatic circula- 
tion, which is nearly always disordered, by the use of small doses of calomel, giving 
| of a grain every half-hour for eight doses, and following this in five hours by a 
Seidlitz powder or some other mild and cooling saline purge. If the stomach is 
very irritable the Seidlitz powders should be divided into fourths and taken at 
fifteen-minute intervals. After this treatment has acted the patient should receive 
small doses of bismuth subnitrate and oxalate of cerium. For a child 2 grains of 
the former and 1 of the latter may be given every hour for five or six doses. Adults 
may take 5 grains of the bismuth at a dose. 

The rest of the treatment consists in the use of small quantities of liquid food, 
such as whey or barley-water, or scalded toast. Small quantities of milk and 
lime-water may be used. In some instances total abstinence from food for twelve 
or twenty-four hours gives the best results. Rest in bed is also very advantageous 
for both children and adults. 

PHLEGMONOUS GASTRITIS. 

Definition. — The term "phlegmonous gastritis" is applied to a condition in 
which the inflammation is of such a character that it proceeds to suppuration, the 
chief part of the suppurative process developing in the submucous tissues, and 
sometimes extending to the muscular coat of the stomach and even to the peri- 
toneum. 

Etiology. — The disease is exceedingly rare, and has appeared with about equal 
frequency at all ages from ten to eighty years. In some instances it is primary, 



DIPHTHERITIC GASTRITIS 527 

the seat of the infection beginning in an ulcer or growth, or more rarely from some 
direct traumatism. The secondary cases are those in which the process develops 
during the course of one of the acute infections, such as typhoid fever, puerperal 
fever, pyemia, and variola. Fifty cases have been gathered by Jacoby and 85 
by Leith, but these figures of course include many of the same instances of the 
disease. Phlegmonous gastritis is of two kinds: a diffuse form with a rapid course, 
profound systemic disturbances, and speedy death, and a circumscribed form in 
which the symptoms are much less severe; the patient living, it may be, for weeks, 
but usually dying as the result of the disease. 

The pyloric portion of the stomach is chiefly affected. Its walls are greatly 
thickened, and the submucous tissues are riddled with pus, having undergone 
almost complete necrosis. Not infrequently many perforations of the mucous 
membrane occur, so that the internal surface of the stomach has a sieve-like 
appearance. 

Several cases of suppurative gastritis have been reported in the United States, 
and they are remarkable enough to demand notice. In Kinnicutt's case the disease 
followed an alcoholic debauch. In Hemmeter's case the patient had vomited 
blood, was treated for gastric ulcer, and did not die until two months after the 
onset of severe symptoms. The infection had here occurred through a healed 
ulcer. In Smith's case violent epigastric pain with collapse and death in two and 
a half days took place, the entire submucosa being infiltrated with pus. In Loomis' 
case abdominal pain, bilious vomiting, and a feeble pulse with delirium preceded 
death, which occurred at the end of four days. In Hun's case the gastric walls 
were fully one-half inch in thickness and the tissues between the peritoneum and 
the mucous membrane were purulent. 

In the circumscribed form of phlegmonous gastritis the abscess may be single, 
or multiple abscesses may be present. 

Symptoms. — The symptoms in the diffuse form consist in the sudden development 
of violent epigastric pain, followed by faintness and collapse, with incessant vomiting. 
After the vomiting has continued for some time, the vomited matter may be stained 
with bile. 

When the disease is secondary to malignant growth, it is stated that vomiting 
does not often develop. Notwithstanding the severity of the process, pus is 
never found in the vomit in the acute cases. The temperature varies from 103° 
to 105°. The pulse is rapid and feeble, and becomes more and more so until death 
occurs in collapse, preceded by a stage of apathy. 

Diagnosis. — There is practically no array of diagnostic symptoms in cases of 
this disease save the onset of violent epigastric pain. 

The pus may escape into the peritoneal cavity, the patient dying with symptoms 
of perforation and collapse. The most extraordinary case of this character so 
far recorded is the one reported by Callow, in which the patient vomited a pint 
of pus, pus appeared in the stools, and there were seven pints of it in the peritoneal 
cavity. All this pus was traced to a large abscess cavity in the wall of the stomach 
which had, however, not been accompanied by pain during its formation. 

Treatment. — When it is possible to make a diagnosis prompt operative interference 
is strongly indicated. So far, this has not been attempted early enough in any case 
to give satisfactory results. The parts should be drained and a gastroenterostomy 
performed. (For an excellent paper on this subject see Moynihan in the Medical 
Chronicle for November, 1903.) 

DIPHTHERITIC GASTRITIS. 

Inflammation of the stomach with the formation of a false membrane due to 
the Klebs-Loeffler bacillus is very rarely encountered. It nearly always follows 



528 DISEASES OF THE STOMACH 

diphtheria in the upper air-passages. Still more rarely in cases of septicemia, 
scarlet fever, and smallpox a false membrane may develop in the stomach. The 
condition is of interest solely from a pathological stand-point. * 

MYCOTIC GASTRITIS. 

Inflammation of the stomach due to the growth of specific micro-organisms 
upon its mucous membrane is very rare. The thrush fungus, Oidium albicans, 
has been found in certain cases. Anthrax of the stomach has also followed anthrax 
of the mouth. The yeast fungus is not infrequently present, but rarely produces 
severe inflammation of the stomach. Cases which are in the nature of medical 
curiosities have been reported in which acute inflammation of the stomach was 
due to the action of maggots deposited about the mouth by the common fly, or 
swallowed with various articles of food. In all such instances the functions of the 
stomach have been profoundly depressed, as otherwise the ability of this organ to 
destroy invading micro-organisms and parasites prevents it from becoming infected. 

CHRONIC GASTRITIS. 

Definition.— By chronic gastritis is meant a state in which the gastric mucous 
membrane suffers from prolonged and persistent inflammation of a low grade, 
or repeated acute or subacute attacks, which result in more or less well-marked 
pathological changes. The term "chronic gastric catarrh" is often used as a 
synonym to describe this condition. 

Etiology. — The causes of chronic gastritis are very numerous. In the majority 
of cases they consist in the frequent entrance into the stomach of irritating foods 
or drinks, as in alcoholics, or in persons given to the excessive use of highly seasoned 
foods. In these cases a very large part of the disorder in the gastric mucosa is 
also dependent upon the engorged portal circulation and the hepatic torpor which 
such dietary indiscretions induce. Cardiac diseases which lead to hepatic conges- 
tion very frequently induce gastric catarrh. Alcohol, bad food, or badly chewed 
food, hepatic cirrhosis, and congestion of the liver are, therefore, the chief causes 
of this condition. 

Pathology and Morbid Anatomy. — The changes in the stomach in chronic gastritis 
may be divided into two classes: In the first there is a proliferation of the con- 
nective-tissue cells and formation of new tissue, which, like similar forms of over- 
growth elsewhere, results in atrophy or degenerative changes in the gastric glands. 
In other words, the lesions are not limited to the superficial portion of the mucous 
membrane, but extend well down into the deeper layers. As the contraction of 
the overgrown connective tissue proceeds, it may cause the projection on the 
surface of the inner wall of the stomach of wart-like masses, so that broad, raised 
patches of mucous membrane are discernible, or even polypoid formations 
appear (gastritis polyposa). The entire gastric mucosa may be contracted or 
plicated. 

In other cases the lesions appear to be more of a degenerative type; the sclerosis 
or fibrosis is inconspicuous, and the epithelial or granular atrophy is most marked. 
In other cases cystic alteration, with little fibrous hyperplasia, may be the dominant 
alteration. In the pyloric end of the stomach the contraction which follows the 
overgrowth of connective tissue may produce stenosis, a condition which is empha- 
sized in some cases by the inflammatory process extending to the muscular layer 
of the stomach, by which means still greater thickening takes place. The closure 
of the pyloric orifice is, therefore, due to a true hyperplasia. The cause of the 
nipple-like projections found in the gastric mucous membrane in some of these 
cases is unknown. It may be due to the constricting influence of connective tissue 



CHRONIC GASTRITIS 529 

formed between the tubules, or it may arise from overgrowth of the submucous 
coat of the stomach. 

The second type of chronic gastritis is that characterized, not by overgrowth 
of connective tissue, as has just been described, but by wasting or atrophy of the 
glands. In some cases, however, there is at first some hyperplasia of connective 
tissue, and this is followed by atrophic changes. The mucous membrane becomes 
thin and smooth and is often pigmented, while the epithelial cells lining the gastric 
tubules suffer from atrophic, fatty or necrotic changes. The deeper tissues in 
some cases escape, but in others they also undergo wasting, so that even the sub- 
mucous coat and the muscular coat atrophy. To this condition has been given 
the unfortunate, but etymologically correct, name of phthisis ventriculi. In such 
a case it is quite possible for gastric dilatation to develop. 

Atrophic gastritis is much more rare than the hyperplastic type, and is often, 
if not always, associated with another grave condition, pernicious anemia. Finally, 
in very rare instances, cases of atrophic gastritis may develop into ulceration of the 
gastric mucosa, the ulcers being small, round or irregular in shape, and rarely 
penetrating very deeply (erosive gastritis) . They are found chiefly near the pylorus 
and may bleed very freely. 

Symptoms. — The symptoms of chronic gastritis consist in loss of appetite, impair- 
ment of the sense of taste, and nausea, which is particularly prone to be present 
in the morning and may often amount to actual vomiting — the "morning vomiting 
of the drunkard." The vomited matters are but partly digested and are often 
mixed with much mucus. Most cases frequently belch up gas, and with it a mouth- 
ful of acid fluid may be brought up which scalds the pharynx. Hydrochloric acid 
may be lacking in the gastric contents, but in its place an excess of butyric and 
acetic acids is often present, particularly if the stomach is feeble and is unable 
to expel its contents into the bowel with sufficient promptness. Lactic acid is 
also present in some cases. It is the presence of these acids that causes heartburn, 
or pyrosis. In some cases, however, an excess, or at least a normal amount, of 
hydrochloric acid is secreted. 

The tongue is moderately coated, the bowels are prone to constipation, and the 
general nutrition is slightly impaired, partly because of poor digestion, but chiefly 
because of the fact that the patient has cut off from his diet list one article after 
another, with the thought that it "disagrees" with him. There is not, however, 
an impairment of nutrition sufficient to cause great loss of weight in many cases, 
because the digestive function of the duodenum is not always impaired. If the 
liver is diseased, a very considerable loss of weight is usually present. Digestion 
is, of course, as is clear from a consideration of the state of the gastric mucous 
membrane, greatly delayed and very imperfect, and as a result the patient becomes 
inert, low-spirited, and vitally depressed, so that he presents the clinical picture 
of what is commonly called by the laity "a confirmed dyspeptic." 

If the cause of the gastric disorder is alcoholic cirrhosis of the liver, the symptoms 
of cirrhosis are associated with those of gastric catarrh. 

A constant, unproductive cough is often present without any lesions being 
found in the lungs. 

When the atrophic form of chronic gastritis is present, a very profound degree 
of anemia is often developed, as already stated. 

Diagnosis. — The separation of chronic gastritis from gastric cancer is by no 
means easy in many instances, for in many cases of cancer gastritis is also present. 
The presence of a mass, of considerable pain, of coffee-ground vomit, and an absence 
of HC1 in the gastric fluids would point to the diagnosis of cancer; but as pain is 
not always present in cancer, as ulcers of the stomach may be present in chronic 
catarrh, giving rise to bloody vomit, and as HO is often diminished or absent in 
this state, these signs are not entirely reliable. Lactic acid is not commonly present 
34 



530 DISEASES OF THE STOMACH 

in large amount in chronic gastritis, but it is usually present in excess in cancer. 
Since we have had adequate information about cholecystitis, duodenal ulcer, and 
appendicitis the diagnosis of chronic gastric catarrh is less frequently made. 

Prognosis. — The prognosis in a case of chronic gastritis must be given guardedly, 
for while one patient may speedily recover under proper treatment, other patients 
remain ill for long periods, even with the most skilful treatment. Much depends, 
too, upon the course of the disease and upon the general health of the patient. 
While, on the one hand, the malady does not cause death, on the other, complete 
recovery may seem impossible. 

Treatment. — Theoretically, chronic gastritis may be prevented by avoiding the 
use of irritating and indigestible foods and alcoholic drinks, but, practically, patients 
are not seen until after the condition has been developed by the various causes 
which have been enumerated. After the condition has developed the treatment 
must be devoted to the removal of the habits which act as causes, to the relief of 
the conditions which exist in other portions of the body, and to the cure of the 
symptoms already present in the stomach. In cases in which errors in diet exist 
these must be rectified, and if alcohol is used it must be stopped. If an examination 
of the heart shows that it is feeble, and that the gastric condition is due to an 
impaired circulation, rest and the use of moderate doses of digitalis must be resorted 
to, but it must not be forgotten that digitalis in full doses is capable of causing 
gastric distress. Usually it is necessary, in order to get the best results, to admin- 
ister, every few days, small doses of blue mass, which not only unloads the liver, 
but seems to increase the efficiency of the digitalis. 

The local treatment of the stomach consists in the employment of lavage, by 
means of which the excessive quantities of mucus and undigested food are removed. 
Emetics should not be employed, as they are too violent and apt to increase the 
inflammatory process. Not infrequently the mucus which is secreted is so thick 
and tenacious that there is some difficulty in removing it from the stomach. Under 
these circumstances, various medicinal substances may be added to the water 
which is employed for the lavage. A salt solution may be used, composed of J 
ounce of sodium chloride and 1 ounce of sodium bicarbonate, placed in a quart 
of warm water. After the stomach has been thoroughly cleansed, it may be washed 
a second time with boric acid, 1:100; salicylic acid, 1:1000; chloroform-water, 
1:200; hydrochloric acid, 1:200. When chloroform-water is used, great care 
should be taken that the chloroform is thoroughly mixed with water and that the 
mixture is then allowed to stand for a sufficient time to permit of the separation 
of any excess of chloroform. 

Lavage should be carried out, as a rule, not oftener than twice in twenty-four 
hours; in many cases once every alternate day is often enough. The best time 
to perform lavage is usually in the evening at about 9 o'clock, so that the stomach 
may have complete rest for the next ten hours. In those cases, however, in which 
the taking of food in the morning produces great distress, it is often advantageous 
to use lavage on first arising, in order that mucus may be removed. 

In regard to drugs, it may be said that the one which has the greatest reputation 
is the nitrate of silver given in pills containing J grain, or in solution in the dose of 
from J to 1 grain to 2 drachms of one of the aromatic waters, as cinnamon-water or 
peppermint-water. Another drug which has a high reputation is the subnitrate 
of bismuth, which -should be given in large doses, about 1 drachm twice or thrice 
a day. Both of these forms of treatment possess the disadvantage that they are 
constipating, and therefore the patient usually has to take a small dose of one of 
the mild laxative saline waters on first arising in the morning. 

For the relief of loss of appetite and for absence of hydrochloric acid, the various 
simple bitters, such as cinchona, quassia, and cardamom, may be given. Of the 
compound tincture of cardamom, 1 or 2 drachms may be given once or twice a 



GASTRIC DILATATION ■ 531 

day with meals. If, in addition, it is believed that the stomach lacks motive 
power, strychnine may also be used, and the fluidextract of condurango may be 
given in the dose of a drachm three times a day. If digestion is delayed because 
of a lack of hydrochloric acid, 15 drops of this dilute acid may be given with each 
meal, combined with a good essence of pepsin. The administration of nitrate of 
silver one hour before meals usually diminishes pyrosis, or heartburn, but, if it 
does not, magnesium carbonate or bicarbonate of sodium may be used for this 
purpose. These alkalies frequently diminish pain by decreasing acidity. 

The diet should consist of easily digested foods, and it is to be remembered that 
small meals given five of six times a day are better than large meals given three 
times a day. Chicken, beef, and mutton broths, free from fat and fortified by the 
addition of barley or rice, are exceedingly useful. If solids are taken, the patient 
must be instructed to chew both the meats and starches thoroughly. Often it is 
advisable to have the meat made tender by pounding it, or by cooking it in such 
a way that its fibres are readily dissolved by the gastric juice. 

The digestion of starches, like baked potatoes, toasted bread, zweiback, and 
pulled bread, should be aided by the use of taka-diastase or pancreatin. Often a 
konseal containing both of these digestive ferments will be advantageous in its effect. 

Milk may be given to those with whom it agrees. In some instances, when it 
cannot be taken pure, it can be digested readily if diluted with some sparkling 
water, particularly Vichy-water. In other instances the addition of a small quantity 
of salt aids in its digestion, and in still others lime-water may be given with it. 

The question as to the use of the light wines by a patient suffering from chronic 
gastritis is debatable. If any fermentation is present, they must not be used. 
If patients are accustomed to drinking wine with each meal, it may be advisable 
to permit small quantities, particularly with luncheon and dinner. Champagnes 
are usually distinctly harmful. 

GASTRIC DILATATION. 

Definition. — By dilatation of the stomach is meant a condition in which this 
viscus loses its propulsive power to a greater or less degree and also undergoes a 
certain amount of dilatation, so that its capacity is increased. It is sometimes 
called "gastric ectasy," or "gastrectasis." 

Etiology. — While it is true that dilatation is the state which impresses itself 
most forcibly upon the clinician when a patient is examined who is suffering from 
this malady, it is also a fact that the dilatation is always the result of some primary 
difficulty in expelling the contents of the stomach into the duodenum. In some 
instances this is due to stenosis of the pylorus produced by a thickening, as in 
chronic gastric catarrh; in others it may be due to what is called hypertrophic 
stenosis of the pylorus, and in still others the obstruction may be offered by a 
tumor at this point or by a cicatrix or other form of stricture. Rarely the pylorus 
becomes so glued to nearby tissues that it is held abnormally high, and is so fixed 
that it is almost impossible for the stomach to force its contents past the orifice. 

A second cause of difficulty in emptying the stomach exists in a weakness, con- 
genital or acquired, which so impairs the motor power of the viscus that it is too 
feeble to empty itself. Neither obstruction nor inherent weakness of the muscle 
fibres in the gastric wall are necessarily associated with dilatation, but it can be 
readily understood that these causes may so result. It is conceivable that in the 
obstructive cases the stomach may undergo some hypertrophy, and this takes 
place in a considerable number of cases as a primary result of the obstruction. 
The constant endeavor of the stomach to empty itself, however, ultimately causes 
fibroid changes in the muscle fibres from fatigue, and this condition is emphasized 
by impaired nutrition of the stomach, and perhaps by impaired nerve supply as 



532 DISEASES OF THE STOMACH 

well. Finally, it is undoubtedly true that, in some persons at least, the repeated 
distention of the stomach by large amounts of food and drink may cause permanent 
dilatation, particularly if these materials be of such a character that they produce 
chronic gastritis, and so impair the tone of the gastric walls. Workmen in breweries 
who partake of large amounts of beer, and diabetics who eat and drink to excess 
because of their disease, often suffer from gastrectasis. 

Dilatation of the stomach is usually a disease of middle age or of adult life, 
but cases are not uncommon in children. The youngest case I ever saw was in a 
child of eighteen months. The dilatation due to obstruction is the type in which 
the greatest enlargement of the stomach develops. 

Pathology and Morbid Anatomy. — The size of the stomach may be greatly in- 
creased, so that the average capacity of a quart (1000 c.c.) increased to even four 
quarts. Under these circumstances, the lower border of the stomach extends far 
below the normal level. Its walls are decreased in thickness, there is atrophy of 
the lining mucous membrane, and the muscular fibres are even more wasted, so 
that many of them disappear and are replaced by connective tissue. When primary 
atrophy of the muscularis has been present, it not rarely happens that an excess 
of muscle fibres are found in the pyloric region, although advanced secondary 
wasting has occurred elsewhere. In some cases of dilatation the gastric walls 
do not become thin, but may appear thicker than normal, because of an overgrowth 
of connective tissue which supplants the muscular layer of the organ. 

Gastric dilatation does not always result in an equally well-developed increase 
in size. In some instances the cardiac orifice and the pylorus are near one another, 
so that the great curvature hangs like a plumber's trap; in other cases cicatrices 
distort it and even cause an hour-glass form, with a dilatation on either side. 

Symptoms. — The symptoms of gastric dilatation are usually considered by the 
patient to be those of "chronic dyspepsia." There is usually loss of appetite, a 
sense of gastric discomfort and weight, or a feeling of dragging down in the abdomen 
and a good deal of belching of gas, which is often accompanied by some particles 
of food mixed with fluid. The sense of distention and distress gradually increases 
until it is almost insupportable, and then the viscus finding the burden too great, 
unloads itself by an attack of vomiting, in which the patient is surprised to find 
articles of food ingested, perhaps, several days before. Both the physician and the 
patient are, not rarely, amazed at the quantity expelled, for the volume shows that 
it represents the ingested fluids and solids of several days. Such an attack of 
vomiting, in which the quantity expelled is far in excess of the amount recently 
swallowed, is a very important diagnostic point. These attacks of vomiting usually 
occur at night. When the dilatation is severe, so that the stomach cannot com- 
pletely empty itself, the relief given by vomiting is only partial, and perhaps no 
relief follows. 

The bowels are constipated, and the stools when passed are scanty, because so 
much of the food ingested is not passed on into the duodenum. The urine is also 
scanty. Not rarely it is decreased to one-third the normal quantity. 

Many of the symptoms are due to stasis of the food in the stomach, fermentation, 
and the absorption of toxic materials from bacterial growth. 

In cases in which bile appears in the urine, the cause of the dilatation probably 
does not depend upon gastric dilatation alone, but upon some obstruction in the 
duodenum, which dams back the food in the pyloric orifice and so forces the stomach 
to undergo distention. 

The physical signs of gastric dilatation are as follows: On inspection in some of 
these cases, it may be possible to outline the stomach if it is distended with food 
and gas. This determination of its area and limitation is, however, much better 
accomplished by percussion after the stomach has been emptied by the use of the 
stomach-tube and then has been distended by gas. This distention may be pro- 



GASTRIC DILATATION 533 

duced either by giving the halves of a Seidlitz powder separately (or by the use 
of 30 grains of tartaric acid in a half-glass of water and 2 drachms of sodium 
bicarbonate in another half -glass of water), or by introducing a stomach- tube, 
attaching a Davidson syringe to it and then pumping air into the stomach until 
it is distended. This latter plan is probably the safer of the two if ulcer is supposed 
to be present, but if the patient is not accustomed to the use of the tube its presence 
causes so much retching and gastric unrest that it is usually impossible to make a 
satisfactory examination of the true area of gastric tympany. 

The tympanitic note produced by the percussion of a stomach so distended 
very clearly outlines it in many cases. If there is doubt as to the presence of 
gas in the colon, which may cause tympany, the large intestine should be filled 
with fluid, by the injection of a large clyster, when the areas of gastric tympany 
and intestinal flatness on percussion can be readily defined. In other cases the 
stomach may be filled with fluid, and, if need be, the bowel filled with air to develop 
the same outlines. 

It has been held by some clinicians that the use of carbonic acid for the purpose 
of dilating the stomach for diagnostic purposes is dangerous, but when we consider 
the hundreds of instances in which it has been used in every part of the world 
without evil effect, we must conclude that it rarely does harm. Behrend has 
reported 3 cases, however, in which death followed its use, the patient in one instance 
suffering from a profuse hemorrhage, another patient bringing up froth and blood, 
and the third, who did not die for five days, suffering from great distress and 
prostration. Wharton and Musser have reported a perforation of the stomach 
after drinking a glass of carbonated water. All of these cases were complicated 
by gastric ulcer. 

Auscultation of the epigastrium may reveal splashing, or succussion, in many 
cases of gastric dilatation, but this sign should never be regarded of very great 
import, for not rarely the same sound is produced by fluid in the bowel. 

Another means of diagnosis is the use of the a>rays after the patient has received 
a large dose of bismuth subnitrate (J to 1 ounce). By this means the area of the 
stomach can be determined. 

The use of drugs, which are dissolved only in the intestine, to test the motor 
power of the stomach is of some diagnostic value. Salol, for example, is given 
in the dose of 15 or 20 grains, and the urine tested after five hours for salicyluric 
acid by means of the perchloride of iron test, which consists in adding tincture 
of iron chloride to the urine, when, if this acid is present, a purple color is obtained. 
When dilatation is present there may be no response for twenty-four hours. 

Finally, as a means of determining that the digestive power of the stomach is 
greatly impaired, a test meal should be used after the stomach has been cleaned 
by lavage. If dilatation is present, the digestive process will always be very slow 
and imperfect. 

Cases of gastric dilatation sometimes develop a state called gastric tetany, in 
which tetanic spasms develop in the extremities. This is preceded by a sensation 
of formication, or numbness, associated with drowsiness. It has ensued, as a rule, 
upon the employment of lavage. Following the sensory symptoms the patient 
is seized with violent vomiting, and after or during this attack of emesis the muscles 
of the thumb and fingers contract, so that the thumb is drawn into the palm of 
the hand and the fingers are flexed. The wrist is also strongly flexed, but it may be 
extended. The forearm is flexed on the arm, and the biceps is hard and tense. 
These positions may not be maintained, but be changed into extension. Both 
sides are involved, but one side usually suffers more than the other. When the 
legs are affected the toes are flexed and the knees bent. The facial muscles may 
be in spasm and the patient may have explosive speech, as if in a shouting delirium. 
If the affected arm be pressed upon over the course of its vessels or nerves, the 



534 DISEASES OF THE STOMACH 

attacks may be reproduced (Trousseau's sign); if the point of exit of the facial 
nerve be tapped, facial spasm develops (Chvostek's sign) ; if electricity is used it is 
found that the muscles are excessively irritable (Erb's sign). The cramp-like 
contractions are painful. In severe cases death may occur from exhaustion. Out 
of 101 cases reported by European clinicians, no less than 75 died. 

Although the employment of the stomach-tube has induced attacks of gastric 
tetany in some cases, attacks not due to this cause are to be prevented by frequent 
and thorough lavage, and are to be combated, when present, by nerve sedatives 
such as morphine or hyoscine hypodermically. Their occurrence in a mild form 
urges upon the physician the need of operation for the gastric state. 

Gastric tetany occurs in cases of dilatation more frequently than in cases of ulcer. 

Diagnosis. — As a rule, the diagnosis of gastric dilatation, in its well-developed 
stage, is not difficult. Care must always be exercised, however, that dilatation 
and gastroptosis are not confused, for in both affections the lower border of the 
stomach may be found far below the normal level, particularly if it is distended 
with liquid or gas. The use of any of the methods of percussion and palpation, 
or the other means of diagnosis just described, will speedily separate the one state 
from the other, and the relatively limited capacity of the stomach in ptosis and 
its large capacity in dilatation will be another factor in deciding upon the real 
state which is present. 

Treatment. — The treatment of gastric dilatation is not promising unless the 
patient is seen and his condition recognized in the early stages of the disease. At 
this time, and later on as well, his diet should be most carefully regulated. He 
should be instructed to avoid all fatty articles of food which may give rise to lactic 
and butyric acid fermentation, and should also avoid the use of sweet materials, 
which may also undergo fermentative changes. The food which he takes should 
be thoroughly masticated and insalivated, it being remembered that the saliva 
is an important digestive juice, and that much may be done in aiding the digestion 
by thoroughly moistening the food with this secretion. The patient must also 
be warned not to eat a large amount of food at any one time, but rather to subsist 
on four or five small meals a day. He should also be instructed not to take large 
quantities of liquids with his meals. 

As to the articles of diet, he may have beef, mutton, chicken, or other simple 
varieties of meats, broiled or roasted, but not fried. Potatoes should only be taken 
when baked, and then in moderation. Zweiback, or soda biscuits which have 
been once more cooked by pouring scalding water over them, may be taken in 
moderation. The digestion of the starches should always be aided by the simul- 
taneous ingestion of a konseal containing 2 grains of taka-diastase and 2 grains of 
pancreatin. If the diet is largely a meat diet, digestion should be aided by the 
use of hydrochloric acid and pepsin, 5 to 20 drops of the dilute acid and 2 teaspoon- 
fuls of a good essence of pepsin being used. Often it is wise to add to this mixture 20 
drops of the tincture of nux vomica, or -£% of a grain of strychnine, for its effect as a 
bitter tonic and for the purpose of improving, if possible, the activity of the stomach. 

In no case should the patient be allowed to accumulate fluid and food in the 
stomach for more than twenty-four hours. In other words, we should not wait 
until nature relieves the stomach by an attack of vomiting. 

As in chronic gastric catarrh, lavage should be performed once in every twenty- 
four hours, preferably at night before going to bed. In all cases it should be 
remembered that the stomach is loaded with fermenting matter and is therefore 
incapable of dealing with new food, which if taken simply adds to the decomposing 
mass already present. 

In many of these cases it is advisable, after emptying the stomach of its contents, 
to wash it out with one of the solutions named in the article on the Treatment of 
Chronic Gastric Catarrh. 



GASTRIC DILATATION 535 

Emptying the stomach by means of the stomach-tube and forbidding the use 
of excessive quantities of food are not only advantageous in that they permit 
digestion, poor as it may be, to proceed, but also do good in that they prevent the 
stomach from being overloaded and distended, and so further dilated, by its con- 
tents. It seems hardly necessary to add that beer, sweet wines, and champagnes 
should be absolutely forbidden for such patients. 

Some physicians of experience resort to the use of faradic electricity in these 
cases, introducing a stomach-tube containing the positive electrode and applying 
the negative electrode to some point on the surface of the body. 

In cases in which the dilatation is so severe and the symptoms so distressing 
that none of the measures so far suggested give adequate relief, the question of 
operative interference must be considered. Under these circumstances, the 
question as to the cause of the dilatation becomes an important factor. If it is 
dependent upon pyloric stenosis, a gastroenterostomy or pylorectomy is indicated. 
But if, .on the other hand, it does not depend upon this cause, but upon inherent 
atony and failure of the gastric walls, pylorectomy is, of course, of little value, 
and a gastro-enterostomy is indicated. Before proceeding to operation, however, 
it must be remembered that there is some difference between an operative recovery 
and benefit to the patient. Not infrequently in these cases the patient survives 
the operation and makes a surgical recovery, but abdominal discomfort persists, 
either because of the presence of adhesions, irritation of nerve fibres, or other 
causes which it is difficult to determine, and which may be dependent upon the 
altered course of food from the stomach to the bowel. 

Acute Gastrectasis. — Under the names acute gastric dilatation, gastro-intestinal 
paralysis, atonic gastrectasis, toxic gastrectasis, and paralytic dilatation of the 
stomach, there occurs an acute, often rapidly fatal, dilatation of the stomach 
alone or of the stomach and intestines. 

Etiology. — Some cases are apparently causeless, and even at autopsy no cause 
may be demonstrable. Others occur in the course of acute infectious processes, 
some of which are systemic, such as scarlet fever and typhoid fever; in others the 
lesion is some distance from the affected viscus, as in pneumonia and meningitis, 
while still others depend for their development upon infectious processes in the 
neighborhood of the stomach or intestine, conspicuous among which may be men- 
tioned peritonitis. The condition occasionally follows surgical anesthesia, and 
it has been suggested that swallowing of mucus saturated with the anesthetic may 
be the cause in some cases. It has been attributed to acute pyloric obstruction, 
as by foreign bodies or spasm, but that this is not always the cause is shown by 
the reported instances in which dilatation extended through the pylorus and first 
and second parts of the duodenum or even into the ileum. It has been thought 
to depend upon obstruction of the duodenum by the superior mesenteric vessels. 
It sometimes follows operation involving the peritoneum, and may commence after 
labor. Reynier strongly urges the influence of the nervous system in the production 
of acute gastro-intestinal paralysis. 

Morbid Anatomy. — At autopsy the stomach is large, thin, and flaccid; it may 
extend almost to the pubes. It contains gas and fluid; the latter may be thick 
and viscid, but it is usually thin, watery, greenish or occasionally brownish in 
color, and frequently contains flocculi. The gastric mucosa may weep blood and 
the vessels be widely distended. 

Symptoms. — These usually come on rapidly. In operative cases they may be 
delayed twenty-four to forty-eight hours. There is marked abdominal distention 
amounting to actual ballooning', the dilated organ occupies the middle and upper 
left areas of the abdomen, and may be outlined through the abdominal wall. Peri- 
staltic waves are rarely recognizable. Vomiting is nearly always present. In 
the few reported cases in which vomiting has been absent, it has been suggested 



536 DISEASES OF THE STOMACH 

that the associated relaxation in the abdominal wall has rendered emesis impossible. 
The vomited fluid is thin, watery, greenish or brownish. Profound depression 
or symptoms bordering on collapse quickly appear. The pulse is small, rapid, 
and weak; the respirations shallow and frequent; the temperature, in the absence 
of complications, is usually low and may be subnormal. Thirst is intense, and, 
on account of suppressed absorption and prompt vomiting, is unrelieved by drinks. 
The urine is scanty or even suppressed. 

Diagnosis. — The acuteness of the symptoms and rapidly progressing collapse 
differentiate the condition from chronic dilatation. The vomiting is more incessant 
and the pain less than in volvulus of the stomach, which in some respects it closely 
resembles. The gastrorrhea that accompanies it and the character of the vomit 
is unlike acute indigestion, and, ordinarily there is no expulsion of fragments of 
the mucosa as in true toxic gastritis. The relaxed abdominal wall is quite unlike 
the rigid wall of peritonitis. 

Prognosis. — The mortality is high; in Herff's series of 34 cases, 29 died. In 
the so-called reflex group — those unassociated with any intra-abdominal lesion — 
prompt treatment promises some relief. 

Treatment.- — Its prevention after operation may be accomplished by lavage 
immediately at the end of anesthesia, and if vomiting appear and persist, lavage 
should be repeated. As it is probable that the condition is of toxic origin, free 
lavage should repeatedly be practised, and the stomach kept empty by the frequent 
use of the stomach-tube. Water and food had best be given by enema. Strychnine 
and pituitrin have been used. As early as possible saline purgatives should be 
administered in small, but often repeated, doses. As relapses are possible as late 
as the third day, feeding, and even the administration of fluids, must be begun most 
cautiously in cases fortunate enough to survive. 

GASTRIC ULCER. 

Definition. — Ulcer of the stomach, often called peptic ulcer, or ulcus ventriculi, 
is due to necrosis of a part of the mucous membrane of this organ, so that an exposure 
of the submucous tissue is present. 

Etiology. — Almost ever since the processes of gastric digestion have been known, 
animated discussions have arisen as to why the stomach is not digested by its 
own juices and a large number of explanations have been offered, many of which 
have been anything but satisfactory. At present the conditions which result 
in gastric ulcer are known to be closely connected with the inability of the gastric 
mucosa to resist the action of the gastric juice. If, by any cause, the vital resistance 
of the mucous membrane is impaired, at the point of greatest impairment an ulcer 
may be developed. In very rare instances an injury to the surface of the abdomen 
may extend, or be transmitted, deeply enough to cause a lesion in the gastric wall; 
but it is more common for injuries to occur by internal agents, as by the use of 
certain articles of food which may interfere with the circulation in the wall of the 
stomach, as, for example, boiled tea, taken very hot, which contains an excess 
of tannic acid. So, too, an embolus or thrombus in a branch of a gastric artery 
may deprive an area of its blood supply, and subsequent digestion remove the dead 
tissue and so form an ulcer. Another predisposing cause of ulcer is the secretion 
of superacid juice or of an excess of ordinary juice, and finally, in some cases, a 
local necrosis of the tissues is produced by the entrance of infecting micro-organisms, 
which, however, cannot enter the mucosa if normal vital resistance is maintained. 

Frequency. — The frequency of gastric ulcer in some parts of the world is far 
greater than in others. Even between England and the United States the difference 
is extraordinary. Out of 59,762 medical cases in the London hospitals, there were 
1649 cases of gastric ulcer; while out of 75,612 medical cases in hospitals in different 



GASTRIC ULCER 537 

cities in the United States, there were only 446 cases. According to these figures 
the morbidity of gastric ulcer is more than four times as great in England as it 
is in the United States. Since these figures were compiled Howard has confirmed 
them by others. 

In regard to the relationship of age and ulcer statistics vary slightly, but those 
of Welch are still to be considered the most competent. He found that the largest 
number of cases of ulcer occurred between twenty and thirty years of age, and Lebert 
also found that seven-tenths of 252 cases were between twenty and forty years 
of age. A case of ulcer in an infant only thirty hours old had, however, been 
recorded by Goodhart. Cutler, in an exhaustive search in literature, found only 
24 cases under ten years of age with autopsy and 2 without autopsy, and has 
added 3 more which occurred in the Massachusetts General Hospital; 29 in all. 

Women suffer from ulcer far more frequently than men. This is shown by all 
statistics and is illustrated by the following figures: Of 1548 cases of gastric ulcer 
collected from the official reports of hospitals in the United States and England, 
1273 occurred in women and 275 in men. Of 1699 cases examined postmortem 
and studied by Welch, 1020 were in women and 679 in men. Cantlie states that 
out of 20,586 cases in Montreal there were 85 cases of gastric ulcer, and of these 
82 were women. The average age was twenty-seven and a half years. W. J. 
Mayo thinks that the percentage in the two sexes is nearly equal. This may 
be so in the severe cases but it is untrue of the average case. 

Other etiological factors of interest are occupation and associated disease. Thus, 
seamstresses and servant girls are singularly prone to ulcer, as are also tailors 
and shoemakers. Such persons are usually chlorotic or anemic. So, too, ulcer 
is sometimes a complication of tuberculosis, and it may be in itself tuberculous. 

Moynihan believes that in the majority of cases gastric ulcer is not primarily 
or chiefly a lesion in the stomach, but is the outcome of a chronic infection, as a 
rule in some abdominal organ. This view he supports by the fact that in cases 
of chronic gastric and duodenal ulcer there is frequently found a focus of infection 
in the abdomen, most commonly in the appendix. 

Gastric ulcer may be divided into four classes : In the first the lesion is very mild, 
the mucous membrane being eroded in such a manner that its superficial epithelium 
is destroyed. All authors do not agree, however, that these erosions are a form 
of peptic ulcer. The second type is characterized by an ulcerative process which 
penetrates more deeply, so that the submucous tissues are affected. The third 
invades the submucous, muscular, and even the peritoneal coat, and may cause 
perforation. The fourth type is that in which as a result of cicatrization and con- 
traction scars and deformities develop, which produce serious consequences. 

Pathology and Morbid Anatomy. — Gastric ulcer is usually single, but cases are 
not very rare in which the ulcers are numerous. When acute it forms rapidly 
and presents a peculiar punched-out appearance. In the usual chronic form the 
edges are more shelving, indurated, and not so sharply defined. The size of the 
ulcer varies from a small spot scarcely larger than a pinhead to an enormous excava- 
tion covering nearly two-thirds of the gastric surface. These large ulcers are, 
however, very rarely met with. • 

The depth to which the ulcerative process extends is also variable. The mucous 
membrane nearly always suffers most, but the tissues beneath it are affected as 
well, and the destructive process may, as just stated, extend as far as the peritoneal 
coat. Undermined ulcers are extremely rare. Around the edge of the ulcer there 
is usually marked hyperemia, and the surrounding tissues, especially in chronic 
ulcers, are often infiltrated by formative cells or by the development of connective 
tissue. Usually the rest of the stomach exhibits more or less marked chronic 
gastritis. 

Ulcer of the stomach is usually found on the posterior wall of the viscus near the 



538 DISEASES OF THE STOMACH 

pylorus and on the lesser curvature (75 per cent.), probably because this is the part 
of the stomach which carries out the grinding process and urges the food into the 
duodenum, and therefore is exposed to injury and abrasion. Armstrong has 
however, analyzed 440 cases of gastric ulcer and found the anterior wall affected in 
125 cases, the posterior wall in only 32. 

If the healing process is not rapid enough to arrest the ulcerative process, the 
wall of the stomach may be perforated and so produce severe abdominal symptoms. 
More commonly, however, as the inflammatory process approaches the surface 
of the stomach it causes this viscus to become glued to a neighboring organ, and 
so it happens that the floor of the ulcer may be formed by an adjacent viscus. 
In this way neighboring organs may be involved in the inflammatory and septic 
process, and not rarely subphrenic abscess is due to this cause. Sometimes a per- 
foration takes place into the colon or duodenum, and cases have been recorded 
in which the pericardium and pleura have been involved in this manner. The 
liver is also sometimes infected. Fenwick, in an analysis of 127 cases, found the 
stomach adherent to the pancreas in 49, to the liver in 33, and to the liver and 
pancreas in 10. 

Fig. 96 




Diagram showing the situation of ulcers of the stomach on the lesser curvature and near 

the pylorus. (Modified from English.) 

Ulcers on the anterior surface of the stomach are less common, but more prone 
to perforation into the peritoneum than those situated posteriorly. It is held 
that the anterior wall is more movable than the posterior, and hence time for 
adhesion to opposed tissue is less. 

In many cases, a tendency to healing asserts itself and gradually, the exposed 
tissues are healed by the formation of a cicatrix which may cause considerable 
puckering as it develops. 

If the ulcer has been near the pylorus this may cause pyloric stenosis, or if it 
be near the middle of the stomach and the ulcer has been extensive an hour-glass 
contraction may result. (See Hour-glass Stomach.) 

Symptoms. — Ulcer of the stomach, at least in its milder forms, may exist for 
years without its presence being suspected, the patient suffering from a train of 
moderate gastric symptoms, generally described as dyspeptic. In most cases, 
however, it makes its presence known by symptoms which sooner or later send 
the patient to her physician for relief. The symptoms now complained of are 
discomfort and pain, with a constant gnawing between meals when the stomach 
is empty. Not infrequently this gastric distress is relieved by taking some food, 
and then increases as an excess of gastric juice is poured out to digest the food. 
The pain, when characteristic, is peculiar in its distribution, for it radiates from 
the epigastrium back to the shoulder-blade, or to a spot between the shoulder-blade 



GASTRIC ULCER 539 

and the spine. Head has also shown that in gastric ulcer there is an area of cuta- 
neous hyperesthesia in a small triangular spot in the left epigastrium. This is 
demonstrable by a light touch, and not on deep palpation. At times the pain 
is exceedingly severe, and it may require active medication because of its intensity. 
Oftentimes the patient attempts to find relief by lying on the stomach or placing 
a pillow against it, but as a rule the epigastrium is so tender that any pressure 
on the part of the physician makes the patient wince. Careful palpation may, 
however, reveal an area of thickening or induration, if the ulcer is a chronic one. 
Associated with these symptoms there is often vomiting of very acid fluid, and an 
examination of the gastric contents will show an excess of hydrochloric acid both 
as to percentage and actual quantity. Constipation is usually marked. 

It is important to remember that ulcer of the stomach does not by any means 
always cause the same train of symptoms. Attention has already been called 
to the fact that the symptoms may be latent. In other cases there may develop, 
with great suddenness, a profuse hematemesis or symptoms of collapse from perfora- 
tion, and one of these accidents may be the first symptom of any importance. In 
other instances there is a general failure of health, marked emaciation, and a develop- 
ment of profound anemia. In still others violent neuralgic pains (gastralgia) are 
the chief manifestations. In some instances the disease lasts but a few weeks; in 
others it is prolonged for years. 

The symptoms so far described are chiefly those of acute or subacute ulcer. 
Chronic ulcer, on the other hand, may produce none of these symptoms when the 
patient presents herself for treatment. Beyond a history of gastric distress, which 
may have existed for many years, there may be no pain on pressure and no soreness, 
in the sense of tenderness. Indeed, the symptoms may be those of gastric dilata- 
tion, or of pyloric stenosis. The patient is emaciated by reason of voluntary 
starvation, to decrease discomfort, and by the loss of food by vomiting. So, too, 
a cicatrix near the middle of the stomach may produce an hour-glass stomach. 
This may become evident on distending the stomach with gas or fluid, but it is 
to be recalled that there is danger that rupture may ensue from this practice. 
(See Pyloric Stenosis and Dilatation of the Stomach.) 

In no other disease, save pernicious anemia, is there such a notable diminution 
of red blood cells as takes place in many cases of chronic gastric ulcer. This is 
due to the more or less constant loss of blood which escapes by the bowel, the loss 
of which is usually not recognized. When hemorrhage does not occur great anemia 
is rare, although the patient may appear pallid. 

When hemorrhage from the stomach takes place the blood may be vomited or be 
passed by the bowel. The hemorrhage may follow many weeks of suffering or it 
may be the first sign that the gastric mucous membrane is diseased. The quantity 
of blood lost may be very small or so large as to almost exsanguinate the patient, 
the variation depending upon the size of the bloodvessel which is eroded. If a 
large vessel is perforated by a small ulcer it is not difficult to understand why it is 
that hemorrhage may be the first symptom. In other words, the hemorrhage 
may be the first symptom of ulcer. On the other hand, not infrequently gastric 
hemorrhage, particularly if it be from a chronic ulcer, may be so scanty as never 
to cause bloody vomiting, the small amount of blood escaping with the food into 
the bowel. Moynihan believes that all ulcers bleed at some time in their existence. 
(See Diagnosis.) 

In studying the question of perforation of gastric ulcer it is well to recall that 
this accident may or may not be preceded by symptoms which will serve as a 
warning to the physician if not to the patient. There is, in some cases, a pro- 
gressive increase in discomfort and pain, a greater degree of tenderness or pain 
over the epigastrium, and more frequent vomiting. When such signs are present 
the patient must be placed at absolute rest, and if the symptoms do not speedily 



540 DISEASES OF THE STOMACH 

become modified operation must be considered. On the other hand, the literature 
on this subject contains cases in which the history of gastric disorder was entirely 
absent, and the patient was suddenly seized by symptoms of perforation. 

When perforation does develop, it is usually in the anterior gastric wall, and 
from what has been said of the various ways in which perforation of the stomach 
occurs, it must be evident that the symptoms may vary over a wide range of 
severity. When no inflammatory adhesions have been formed and the gastric 
contents escape suddenly into the general peritoneal cavity, the onset is, of course, 
startling in its acuteness and the pain is exceedingly severe, but the locality of the 
pain is frequently far removed from the area of the accident. Vomiting and collapse 
may soon develop, and general peritonitis begins if operative relief is not promptly 
given. 

If the perforation is more gradual the symptoms are less violent and the opening 
may at first be so small that only a little of the gastric contents escapes into the 
peritoneal cavity. In those cases in which adhesions have formed before perfora- 
tion takes place subphrenic abscess may result. In such instances the perforation 
is usually on the posterior wall of the stomach. . 

Sometimes perforation of the stomach may take place without the sharp and 
decisive symptoms just described. 

While the pulse usually is rapid it may not be materially increased in rate. 

Again, it is important to remember that after perforation of the stomach there 
may be a "period of repose," or "fallacious calm," during which time the patient 
feels less pain and distress, and the pulse approximates its normal speed. 

At one time, it will be recalled, a decrease in the area of liver dulness was sup- 
posed to be indicative of gastric or intestinal perforation, but we now know that 
the absence of this sign does not negative perforation. Thus, Pearson found a 
decrease in the area of liver dulness in 33 per cent, of 140 cases of gastric ulcer at 
some period during their stay in the hospital, yet perforation took place in none 
of them. 

Diagnosis. — Gastric ulcer in some instances is so manifestly present that there is 
little difficulty in determining the cause of the illness. In other cases a correct 
diagnosis is almost impossible; it is more a supposition than a diagnosis. 

The irritation produced by gallstones may produce symptoms resembling gastric 
ulcer, but in these cases the history of gallstone colic may be given and the taking 
of food has no immediate influence upon the pain. Then, too, the pain in the 
back due to ulcer is to the left of the middle line near the twelfth dorsal vertebra 
whereas that due to gallstone is on the right of the median line and a little lower 
down. So, too, palpation of the neighborhood of the gallbladder may reveal an 
enlargement of this viscus, and jaundice points to cholelithiasis rather than to 
ulcer. (See Cholelithiasis). 

Cases of chronic ulcer of the stomach with much cicatricial tissue around the 
ulcer, or at the seat of an ulcer which has healed, may present symptoms almost 
identical with those of gastric cancer. Pain and obstruction to the passage of 
food through the pylorus, gastric dilatation due to this latter cause, and emaciation 
from all these causes may combine to present a clinical picture of gastric cancer, 
particularly if the physician finds, on palpation, that he can feel a mass or masses 
in the gastric wall. The comparative youth of the patient in cases of ulcer, the 
absence of cachexia even if anemia is marked, and a remembrance that ulcer of the 
stomach is more common in the female sex helps to make the diagnosis possible. 
Again, in ulcer the gastric contents show an excess of hydrochloric acid after a 
test meal, whereas in cancer this acid is usually absent or less than normal. (For 
the tests of the stomach contents see article on Gastric Cancer.) 

There can be no doubt that the use of the axrays affords a valuable means of 
investigating these cases, particularly when a bismuth meal is given and the fhioro- 



GASTRIC ULCER 541 

scope is used. Sometimes the ulcer causes spasmodic hour-glass contractions which 
if shown in an x-ray photograph may give rise to the belief that this deformity is 
permanent. The contraction chiefly affects the greater curvature but it is impor- 
tant to exclude neuroses, tabes, renal colic and even hepatic cirrhosis since spas- 
modic hour-glass stomach has been met with in such patients. Again, the retention 
of the bismuth in the stomach for more than six hours is significant, but not diag- 
nostic of ulcer, the retention being due to pyloric spasm or cicatricial tissue. Some- 
times the bismuth adheres to the ulcer and gives a shadow. When an ulcer is 
old enough to have induced scar formation there is often delayed emptying, a 
shadow at the cicatrix, sometimes reversed gastric waves of marked intensity or 
the stomach may be fixed by an adhesion. 

Care must be taken that the pain of appendicitis, gallstone colic, renal colic, and 
intense menstrual colic is not taken for that due to perforation. Moynihan speaks 
of 3 cases operated upon for gastric perforation in which menstruation was the cause 
of the pain. Severe pain in the stomach due to locomotor ataxia (gastric crises) 
can usually be excluded by the presence of Argyll-Robertson pupils, absence of 
knee-jerks, and swaying when the patient stands with the eyes shut. Epigastric 
and umbilical hernia must be excluded. Aortic aneurysm may mislead as may 
also lead colic. 

Finally it must be recalled that duodenal ulcer may cause symptoms so closely 
resembling gastric ulcer that a differentiation may be impossible. If blood is 
passed in the stools in considerable quantity without hematemesis the lesion is 
probably duodenal. (See Duodenal Ulcer.) 

The demonstration of minute quantities of blood in the feces is of great value 
in the diagnosis of both gastric and duodenal ulcer, but does not separate them. 
It has been proven experimentally that the ingestion of so small a quantity as 
3 c.c. of blood gives a positive reaction for blood in the feces, and this fact shows 
that even minute hemorrhages may give rise to similar positive reactions. Hemor- 
rhage in ulcer is often absent and when it occurs is apt to be inconstant. In cancer, 
if ulceration is present, it is constant. 

Before performing the test for blood all other sources of hemorrhage, such as the 
swallowing of blood from wounds in the mouth or from lesions in the respiratory 
tract must be guarded against, and the absence of hematuria, and in women 
metrorrhagia and menstrual blood, must also be assured. No red meat, fish, or 
sausages are allowed for two days before the test is made. 

Boas prefers the aloin test as recently recommended by Klunge and Schaer to 
the older guaiacum test. It is performed as follows: 5 to 10 grams of feces, which, 
if hard, are to be softened by the addition of a small quantity of water, are mixed 
with 20 c.c. of ether, 3 to 5 c.c. of glacial acetic acid, and the mixture is well shaken 
in a reagent glass. Then more ether is added, and also 20 or 30 drops of an old 
oil of turpentine. If to this mixture there now be added 10 or 15 drops of a solution 
made by dissolving in 3 to 5 c.c. of 70 per cent, alcohol as much aloin as can be 
taken up on the tip of a small spatula, a light red color is soon produced if blood 
is present. This light red gradually assumes a cherry-red hue if the mixture is 
allowed to stand. If no blood is present the mixture remains of a yellow color 
for from one to two hours, when it changes to rose-red. 

The possibility of parenchymatous gastric hemorrhage, and of hemorrhage 
from varicose or atheromatous bloodvessels in the esophagus or stomach, must of 
course be taken into consideration before a diagnosis in doubtful cases is reached. 

Prognosis. — The prognosis of cases of gastric ulcer must, of course, vary greatly 
with the severity of the lesion, and the time during which it has lasted. In those 
cases in which superficial erosions are present, the patient probably recovers in 
the great majority of instances. When actual ulceration is present, the proposition 
is, of course, a different one. The most divergent views exist as to the prognosis. 



542 DISEASES OF THE STOMACH 

Whatever may be the percentage as to recovery, it cannot be doubted that in 
many instances it is once an ulcer always an ulcer, in the sense that relapses take 
place soon after the ulcer seems well. In a collection of 500 cases at the London 
Hospital, made by Bulstrade, 211 had had ulcer before, 18 per cent, died, and 42 
per cent, were not cured on discharge. The surgeon who sees an old ulcer which has 
produced such severe symptoms that the patient is forced to submit to the knife, 
readily comes to believe that recovery never occurs except by operation and even 
goes so far as to state that the ulcers that have been cured by the medical man 
were only supposititious. That complete recovery of a well-developed ulcer takes 
place is still a subject for debate; probably it does not. Often after a period of 
good health a relapse occurs or worse still an old quiescent ulcer undergoes malignant 
change. The surgeon says "operate to avoid these evils;" the physician says 
"sometimes the patient dies of the operation." The direct mortality from ulcer 
in hospital practice is about 12 per cent.; in private practice about 3 per cent. 
The question is one of a comfortable life rather than one of life or death. (See 
Treatment.) 

Ulcers near the pylorus heal more slowly than those which occur elsewhere. 

The mortality in cases which suffer from hemorrhage is not high. The direct 
mortality from this cause is only 2.1 per cent., according to Russell. So far as 
recovery from the ulcer is concerned, when it is severe enough to cause hemorrhage 
the outlook is not good — 44.7 per cent, continued in ill health and 42.6 per cent, 
recovered (Russell). 

Treatment. — The treatment of gastric ulcer may be medical or surgical depending 
on the lesion and the character of the symptoms. The percentage of "cures" 
under medical treatment naturally varies greatly with the class of patients, in what 
the patient and physician considers as a "cure," and in the time which elapses 
before a case is recorded as "cured." Leube, in Germany, reports 90 per cent, 
of cases as clinically cured within a few weeks. These statistics are of little value 
because the longer such cases are followed the greater is the number that relapse. 
Greenough and Joslin some years ago found 82 per cent, "cured" but only 40 per 
cent, remained so, and Joslin has just published results in another series which 
are practically identical. Statistics collected by others give similar results. Lock- 
wood in cases followed for three years found 50 per cent, cured. On the other hand, 
surgical treatment gives by no means perfect results. Deaver after operations 
found that 42 per cent, still had symptoms and 14 per cent, died from some 
surgical complication. In Bettmann and White's statistics 10 per cent, died from 
the results of the operation and 31 per cent, were improved. (See Prognosis.) 

When the ulcer is chronic — that is, has lasted a long time — its edges may be so 
indurated and the bloodvessels in its cavity so eroded that little hope of cure by 
natural processes can be entertained, an operation is essential; first, because this 
is the only way to give real relief; second, because the cicatrization process partly 
or completely interferes with gastric motility, and by no means least important 
because some of these ulcers undergo malignant change and such a disaster should 
be avoided. 

Much depends upon the skill of the surgeon. The best have a direct mortality 
of about 2 per cent., the average surgeon 8 to 10 per cent, and the general surgeon, 
to use Lockwood's term, 10 to 15 per cent. In other words, the advice of the 
medical man as to operation must be based on the state of the patient and very 
considerably upon his opinion of the capacity of his surgical colleague. It is also 
to be borne in mind that although a gastroenterostomy may result in the healing 
of the ulcer it does not always mean the recovery of perfect health. As Graham 
says, basing his conclusions on several hundred cases in the Rochester clinic "The 
patient may be, and often is, freed from disease and life prolonged; yet he may 
not be freed from symptoms quite distressing. This is not always the fault of 



GASTRIC ULCER 543 

treatment, but an inevitable result of the pathologic condition, occurring before 
treatment was undertaken." 

In deciding whether an operation is needful in a case which has had an attack 
of gastric hemorrhage, consideration must be given to the character of the ulcer. 
Even those surgeons who are most radical in advising operative measures in these 
cases state that in cases of hemorrhage from acute ulcer medicinal measures will 
usually control that particular bleeding, and, as an immediate second hemorrhage 
is rare, operation at once is not demanded. (See Prognosis.) When the hemorrhage 
does recur and particularly if it be profuse on recurrence, operation is to be consid- 
ered carefully, whether the ulcer be acute or chronic provided the patient's hemo- 
globin is above 60 per cent. The operation of election is gastro-enterostomy, for 
it has been found impossible to find the bleeding spot in most cases because the 
bleeding often comes from several spots, and indeed may ooze from a multitude 
of eroded spots. Needless to say that the gastro-enterostomy is not designed to 
stop a bleeding already in active progress, but is to be performed as soon as 
possible to prevent further bleedings. 

The medical treatment of gastric ulcer consists in restricting the diet, in the 
administration of medicines qualified to improve the state of the gastric mucous 
membrane, and in the institution of rest for the general system as well as for the 
stomach. Foods which are very hot, or very cold, particularly those which are 
very hot, should be carefully avoided, and hyperacidity is to be counteracted by 
the use of calcined magnesia or bicarbonate of soda: 

1$ — Sodii bicarbonatis, 

Magnesise ponderosse, 

Calcii carbonat aa 5j. 

01. menth. piperitse TTtx. 

Sig. — A heaping teaspoonful in half a glass of water when needed. 

In most instances it is wise to insist that the patient remain in bed for a period 
of three or four weeks, during which time the rest cure may be instituted in a 
modified form, since with the improvement in general health, and the cure of anemia, 
healing of the ulcer progresses more rapidly. 

There are two plans of treatment from the stand-point of dietetics which are 
diametrically opposed to one another. The first consists in almost starving the 
patient in the endeavor to give the stomach rest and to decrease to the lowest 
point the secretion of HC1. 

The diet should consist of milk which is predigested by a peptonizing powder 
either before or immediately after it is taken into the stomach. Under certain 
circumstances it may be permissible to give the patient very soft milk-toast in 
small quantities, or to give scalded soda biscuits digested by means of taka-diastase 
or pancreatin. When the ingestion of food increases gastric pain and distress 
it may be necessary to give the patient nothing by the stomach for a period varying 
from one or two days to two weeks, and to nourish him as far as possible during 
this period by nutritive enemata, which should consist of four ounces of peptonized 
milk and one egg, injected three times in the twenty-four hours, the bowels being 
carefully washed out with normal saline solution before each injection in order 
that the residue from the previous injection may be removed. 

For the purpose of relieving thirst, it is often advantageous, when the stomach 
is irritable, to give, daily, normal saline solution by hypodermoclysis. In other 
instances a pint to a quart of normal saline solution may be given high up into the 
colon. 

A number of years ago the late J. M. DaCosta strongly recommended ice-cream 
as a diet for these cases. Care should be taken that the ice-cream does not contain 
too much sugar, as this will cause fermentation and distress. Frozen milk flavored 
with vanilla is better. 



544 DISEASES OF THE STOMACH 

The other plan instituted by Lenhartz, consists in free feeding on the ground 
that it is essential for the healing of the ulcer that the vital resistance of the 
patient shall be raised, that the anemia which is almost constantly present be 
overcome and the general nutrition improved. Further, he claims that the dis- 
tention of the stomach by large amounts of milk taken in twenty-four hours is 
deleterious and that the gastric activity incident to the ingestion of semisolid or 
solid food is not deleterious, or if so is the lesser of two evils. Lenhartz's method 
undoubtedly suits some cases but in those instances in which pain is produced by 
the ingestion of food has to be used sparingly, if at all. The method is as follows : 
Every hour from 7 a.m. to 7 p.m. the patient is fed very slowly 2 drachms of egg; 4 
drachms of milk, which quantities are gradually increased day by day until by 
the sixth day she receives 7 drachms of egg and 14 drachms of milk every hour. 
After the the third day 1 to 2 ounces of sugar are given also every hour. After 
the seventh day one ounce of scraped beef is also given divided into three doses. 
During the first week the bowels are given absolute rest. After this they are 
moved by a glycerin or hot-water enema. Lenhartz asserts that the incidence of 
hemorrhage in his experience before using this diet was 20 in 100 cases, and in the 
next 135 cases only 8 had hemorrhages, and that recovery of health is very rapid. 

The patient suffering from gastric ulcer should receive, in the way of medicine, 
| of a grain of nitrate of silver with J of a grain of extract of hyoscyamus in pill 
three or four times a day and take them an hour before taking food, in order that 
these drugs may act upon the stomach, exercising a healing influence, and preventing 
an excessive secretion of gastric juice. If pain is severe, opium may be substituted 
for hyoscyamus, but there is some evidence that opium does not decrease, and may 
sometimes increase, the flow of gastric juice. In other instances chloretone in the 
dose of from 3 to 5 grains may be given three or four times a day, and it is par- 
ticularly useful if pain is present. In other cases hyperacidity and pain are best 
controlled by 10 to 20 grain doses of bromide of strontium or of sodium. 

The administration of massive doses of bismuth subnitrate has been strongly 
recommended, chiefly by Fleiner. He gives 150 to 300 grains, stirred in 5 or 6 
ounces of warm water, after the stomach has been carefully cleansed by lavage. 
Of course a heavy precipitation of bismuth occurs upon the gastric mucous mem- 
brane. This plan is more suitable for chronic cases than for acute ones. 

In all cases of gastric ulcer it is important that the bowels should be moved 
every day or two by means of one of the alkaline purgative waters, of which probably 
Carlsbad water has the greatest reputation. The Carlsbad and Hathorn spring- 
waters of Saratoga do almost, if not quite as well, as the imported water. The 
advantage of employing these waters is that they not only unload the bowels, 
but tend to correct acidity and relieve chronic gastric catarrh by their favorable 
influence upon the gastro-intestinal mucous membrane. 

Should hemorrhage from the stomach occur, the patient should be put to bed, 
and if not too depressed by the bleeding, a small ice-bag may be placed over the 
epigastrium, and 2 teaspoonfuls of adrenalin chloride (1: 1000), mixed with 2 or 3 
ounces of water may be given by the mouth, with the hope that the adrenalin 
chloride will contract the bloodvessels and arrest the hemorrhage. Where adrenalin 
chloride cannot be obtained, from 5 to 30 drops of Monsel's solution may be given 
in 2 ounces of water. The use of ergot hypodermically, or by the mouth, in this 
condition can scarcely be of benefit, as it will raise arterial pressure in other parts 
of the body and may increase the hemorrhage. The general treatment in these 
cases is, of course, identical with that of profuse hemorrhage occurring from other 
parts of the body, and consists in the use of J of a grain of morphine hypodermically 
to allay mental distress, and hypodermoclysis of normal salt solution. Should the 
hemorrhage be sharp and very profuse, the question of operative interference 
arises. 



CANCER OF THE STOMACH 545 

The surgical treatment of gastric ulcer with perforation is now a well-recognized 
procedure in modern medicine. When perforation occurs operation should be 
resorted to at once, unless the patient is profoundly shocked, when some delay 
is advisable. in order that she may rally. 

The best results are obtained in the cases which are operated on during the 
first twelve hours after the occurrence of perforation. An analysis of these statistics 
shows that the mortality under operation has been progressively reduced : 

In July, 1899, Tinker added 57 cases to Keen's list of 156, and in 1900 he collected 
19 others, which made the total number of 232, with a mortality of 48.81 per cent. 
Later, in the year 1900 Finney made an addition of 36 cases to Tinker's last list, 
thus bringing the number up to 268, of which the mortality was 48 per cent. Of 
163 cases collected since the publication of Finney's paper in 1900, 102 recovered 
and 61 died — a mortality percentage of 37.04. Lund states that 80 per cent, of 
these cases recover if operated upon within twelve hours. English puts the 
recoveries at a little better than 50 per cent, and Moynihan says 35 to 40 per cent. 



CANCER OF THE STOMACH. 

Gastric carcinoma is one of the most common forms of malignant growth. Many 
years ago Welch showed that in 31,482 cases of cancer the disease affected the 
stomach in 21.4 per cent. Startling statistics as to the increasing frequency of 
cancer have been published by several writers, of which one of the leaders has been 
Roswell Park, of Buffalo. In the United States census for 1890, the deaths from 
gastric cancer were placed at 2014 as against 304 from cancer of the rectum, and 876 
from cancer of the liver; whereas, in the census for 1900, there were 4220 deaths 
from cancer of the stomach, 574 from cancer of the rectum, and 1784 from cancer 
of the liver. As a large proportion of cases of cancer of the liver are secondary 
to growths elsewhere, particularly in the stomach, these facts are of great interest. 
In the city of Washington the deaths from cancer of the stomach in the decade 
from 1881 to 1890 were 191, and in the decade from 1891 to 1900, 339, which shows 
an increase greater in proportion than the growth of the city population. So, 
too, Templeton, of Dundee, found that from 1877 to 1902 the death rate from 
gastric and esophageal cancer increased 12.66 per 10,000. 

Etiology. — Gastric cancer is far more common in males than in females. Welch 
states the proportion to be 5 to 4, but in Osier's cases the proportion was 5 to 1. 
Gastric ulcer is the site for the development of gastric cancer in about 50 per cent, 
of cases. But while some patients state that they have been subject to gastric 
disorders for years before the final illness develops, it has been my experience 
that a very large proportion state that hitherto they have had perfect digestion, 
and have never known what it was to have gastric distress in previous years. In 
other words, given a man who complains of grave gastric symptoms and loss of 
weight, who has not cirrhosis of the liver, or dilatation of the stomach, who has 
not used alcohol to excess, and who boasts of his good stomach during the first 
forty years of life, that man will often be found to have gastric cancer. We have 
no knowledge of the etiology of gastric cancer beyond the facts already named. 
Langwill states that gastric cancer is not so much a disease of middle age as is 
commonly believed, a marked percentage of cases occurring under forty years. 

Morbid Anatomy. — Gastric cancer is usually primary, but it may be secondary. 
The most common form is the medullary carcinoma, a form of the spheroidal-cell 
cancer; the adenocarcinoma, the malignant adenoma of German writers, or cylin- 
drical-cell cancer, is second in point of frequency. The scirrhus type is the third 
in frequency. Gelatiniform degeneration occurs in the first and second, and when 
present such tumors are called colloid cancers. 
35 



546 



DISEASES OF THE STOMACH 



The medullary, or spheroidal-cell type, is the most rapid in its growth, usually 
tends to ulcerate early, and is followed by metastasis and direct extension to 
contiguous organs sooner than the other types. 

The scirrhus is a denser growth, infiltrating and indurating the submucosa 
often to some distance, or even all of the organ, diffuse carcinoma under such 
circumstances; the thick, dense, gastric wall has led to the condition being called 
"India-rubber bottle stomach," or "leathery stomach." 

The colloid growths form tumors of greater size, often extending by contiguity 
and matting adjacent organs into a solid mass. On section the clear or grayish 
gelatiniform trembling matrix is found to be enclosed in alveoli, often of macro- 
scopic dimensions. 

The pylorus is the part of the stomach usually affected; next to it in frequency 
is the lesser curvature, but out of Welch's 1300 cases the pylorus was affected 791 
times, and the lesser curvature but 148. 

Moynihan, of Leeds, has investigated the subject of how malignant growths 
spread in the gastric wall, and has concluded : 

1. That malignant disease of the stomach begins in the majority of instances 
near the pylorus, just below the lesser curvature. 

2. That from this point it spreads most rapidly and most widely in the submucosa. 

3. That the rate of growth toward the cardiac orifice is rapid, toward the duo- 
denal side extremely slow. The duodenal extremity of the viscus is rarely affected 
extensively. 

4. That the tendency of the growth is to drift toward the curvatures. 



Fig. 97 




The lymphatic vessels and glands of the stomach: a is the most frequently affected area, b is next, 

and c is the "isolated area." (Moynihan.) 



He found that the lymphatic system of the stomach was comparatively simple. 
There are three chief lymphatic areas of the stomach (Fig. 97). 

1. An area along the lesser curvature (a) from which the lymphatic vessels pass 
upward and to the left into the coronary glands. The coronary glands lie along 
the artery of the' same name. At the celiac axis they become continuous with 
the glands along the upper border of the pancreas. 

2. An area (b) along the greater curvature from which the lymphatic vessels 
pass downward and to the right into the glands lying along the greater curvature. 
These glands are more numerous near the pylorus, and from here pass to the head 
of the pancreas and become continuous with the hepatic group of glands which 
lie along the hepatic artery, and in part along the pyloric artery. 



CANCER OF THE STOMACH 547 

3. In addition to these two areas is a third (c), for which Moynihan suggested 
the name "isolated area." This area comprises the greater tuberosity of the 
stomach, the lower end of the esophagus, and an area along the greater curvature 
as far, approximately, as the limit of supply of the left gastro-epiploic artery. Its 
lymphatic vessels pass downward to the hilum of the spleen. The term " isolated 
area" seems singularly appropriate for this region, for it is very rarely affected by 
growth spreading upward from the pylorus. 

If a cancer of the stomach arising independently of ulcer is examined in its early 
stages it will usually be found covered with mucous membrane, which later ulcer- 
ates. The entire wall of the viscus may soon be involved, but in the colloid form 
the mucous membrane may not be destroyed. 

Fig. 98 




Stomach. Large, ulcerating, fungoid, cylindrical-cell carcinoma, stiuated on the posterior wall near 
the pylorus, which was slightly obstructed by the projecting growth. A glass rod is passed through a 
perforation near the centre of the floor of the ulcer. The cardiac end of the organ is moderately dilated. 
There was secondary enlargement of the lymph nodes behind the stomach, and metastatic nodules in 
the liver. 

The effects of cancer of the stomach upon the shape of this viscus depend largely 
upon the character of the growth, and chiefly upon its situation. The general 
tendency is for the stomach to be decreased in size, but if the growth obstructs 
the pylorus the stomach may be greatly dilated. When the tumor is widely diffused 
the gastric walls are much thickened, and if it be of large size it may displace the 
pylorus very greatly by its weight. 

Perforation of the stomach through the cancerous mass may occur, but this is 
not a frequent complication. 

Symptoms. — The symptoms of gastric cancer may not manifest themselves 
for a long period after the growth has begun, and even when the general nutrition 
is impaired the patient may not complain of gastric disorder. It is a mistake 
to suppose that gastric cancer is usually very painful. 



548 DISEASES OF THE STOMACH 

When symptoms are present they may be divided into the objective and the 
subjective. The objective symptoms are pallor, which becomes well marked; a 
loss of toeight, which is often extraordinary, amounting to a loss of from fifty to 
seventy pounds in a few months, and with this there is usually a rapid loss of 
strength. The anemia is chiefly the result of a marked decrease of hemoglobin, 
although marked reduction and morphological alteration in the erythrocytes may 
yield a blood picture resembling pernicious anemia. Sooner or later leukocytosis 
occurs (see below). 

The symptoms presented by the patient, in the sense that they are complained 
of by him, are loss of strength, gastric distress and "dyspepsia/' loss of appetite, 
nausea, and not rarely vomiting. Vomiting is a far more constant symptom when 
the pylorus is obstructed than when it is free, and the matters vomited may indi- 
cate a feeble digestive power and be colored like coffee grounds due to exuded and 
altered blood arising from the ulcerated growth. Sometimes a free hematemesis 
develops. Care should be taken that the presence of altered bile in the vomit is 
not taken for altered blood. 

Not rarely the patient complains of constant gnawing pain in the stomach, which 
may or may not be increased by the taking of food. The pain is usually more 
severe when the disease is in the region of the pylorus. If the skin over the epigas- 
trium is lightly touched, it may be very sensitive. There may be moderate fever, 
constipation, and edema of the ankles. 

Robson states that pain is present in 86 per cent, of cases, vomiting in 85.3 
per cent., and a tumor is palpable in 76.6 per cent. These figures refer to the entire 
history of the cases recorded, and, as pointed out elsewhere, none of these symptoms 
may be present during the early stage of the disease, when it is most amenable 
to surgical treatment. Such percentages are, therefore, of greater value from a 
statistical than from a diagnostic stand-point. 

Diagnosis. — The pallid, cachectic hue of the patient, combined with a history 
of loss of weight, and with the fact that the patient is usually beyond the fortieth 
year, should make the physician at least suspect the presence of a malignant growth, 
and this suspicion becomes stronger as he is able to exclude other causes of anemia 
and emaciation, such as, for example, diabetes, Bright's disease, and pernicious 
anemia. The presence of cough will usually be a guide to the examination of the 
lungs for pulmonary tuberculosis. It must not be forgotten that abdominal 
tuberculosis produces, as a rule, a dry, harsh skin, instead of the peculiar waxy 
or greasy skin of malignant growth and pernicious anemia. 

In the diagnosis of malignant growth the blood may give considerable information 
and aid us in separating this condition from pernicious anemia, which resembles 
it very closely in some of its objective symptoms. Malignant growth is character- 
ized by a marked decrease in the amount of hemoglobin and in the hemoglobin 
index, a condition the reverse of that in pernicious anemia. When the case is far 
advanced there is usually a diminution in the number of red cells, but this diminu- 
tion is only moderate in early cases. Leukocytosis is usually present in moderate 
degree, averaging, perhaps, 20,000 to 25,000, and it is much more marked if metasta- 
sis, hemorrhage, ulceration, or septic infection occur. The increase in white 
cells is chiefly in the polymorphonuclear neutrophiles. It is a noteAVorthy point 
that these cells may be relatively increased Avithout a distinct leukocytosis being 
present. Normoblasts and myelocytes are sometimes found in limited numbers 
when the disease is far advanced. 

While it is true that in a few cases of pernicious anemia there is a marked diminu- 
tion in the quantity of hydrochloric acid, it is rarely if ever so persistently absent 
as it is in gastric carcinoma. 

Another condition which may give rise to much difficulty in diagnosis is ulcer 
of the stomach, with thickening and induration around it. This condition is 



CANCER OF THE STOMACH 549 

particularly prone to appear in the neighborhood of the pylorus, and it may be 
impossible by palpation to differentiate ulcer and induration from scirrhous cancer. 
In other words, every case in which a mass can be felt in the stomach is not one 
of cancer. (See Treatment.) In such a case the excess of hydrochloric acid in 
ulcer and its absence in cancer are valuable factors in diagnosis. Then, too, ulcer 
is much more frequently present in persons under forty, but cancer is more common 
in persons over forty. 

Inspection of the epigastrium very often gives most valuable information, because 
it may reveal a bulging and undue pulsation due to impulse from the aorta trans- 
mitted by the growth, or the presence of a nodule. A deep breath taken during 
inspection may reveal distinct movements of the mass. If a Seidlitz powder is 
taken in two parts, so that the contents of one paper follow the other, the tumor 
can sometimes be seen to be projected against the abdominal wall by the distended 
viscus. Palpation may reveal a mass which usually presents an uneven surface, 
and this may be distinctly nodular. 

The position of the mass may be varied by the pressure of food in the stomach. 
If a mass cannot be felt, immersing the patient in a hot bath may relax the tense 
belly wall so that the tumor may be demonstrable. Percussion, if it is carefully 
and gently performed, over the mass may give an impaired note. 

Additional signs on palpation consist of a hardening of the gastric walls due to 
contraction of their muscular fibres, and if the patient is thin the mass may be so 
movable that it may be pushed high up under the ribs or far down toward the 
pelvis. The mobility is of some diagnostic value, for if the mass be due to indura- 
tion about an ulcer the gastric wall may be glued to adjacent tissues, and, 
therefore, be made fast. As a rule, tumor at the pylorus is more readily pal- 
pated than one at the middle of the stomach, and a growth at the cardia is 
rarely felt. 

Auscultation may reveal constant, direct, or reversed peristalsis if the growth 
obstructs the pylorus. All the symptoms of gastric dilatation may be present 
if the growth be so situated (see Gastric Dilatation), and as 75 per cent of gastric 
cancer is at the pylorus obstruction is common. A bismuth meal and the .T-rays 
should be resorted to in all doubtful cases to discover obstruction, tumor or 
deformity. 

A very useful and reliable method for the purpose of determining the presence 
of gastric cancer is the determination of the character of the stomach contents. 

If obstruction at the pylorus is present, food remnants are found in the gastric 
contents hours after eating, and if vomiting occurs, the patient may be surprised 
at seeing traces of food taken many hours or even days before. 

If the stomach contents are examined after a test meal there will be an almost 
complete or total absence of hydrochloric acid and an abnormal amount of lactic 
acid present. To determine these facts, we resort to the use of a test meal and 
certain chemical tests, as follows : 

Boas' test meal consists in the use of an ordinary breakfast roll weighing about 
1 ounce, with 10 ounces of water, or of weak tea, which should contain no milk 
or sugar. This is allowed to remain in the stomach for one hour, and then is 
removed by the stomach-tube. The quantity of fluid obtained should equal 
from three-quarters of an ounce to an ounce and a half. It is best to examine this 
fluid microscopically, and then, after filtering it, to apply the tests for hydrochloric 
acid and the organic acids. The two common tests for free hydrochloric acid are 
Giinzburg's phloroglucin-vanillin and Boas' resorcin tests. Giinzburg's reagent 
is composed of: 

Phloroglucin gr. xxx (2 grams) 

Vanillin gr. xv (1 gram) 

Alcohol (absolute) Sj (30 c.c.) 



550 



DISEASES OP THE STOMACH 



This solution should be carefully protected from the light by being kept in a 
dark bottle and should be frequently prepared, as stale solutions are uncertain. 
One or two drops of this reagent are placed in a porcelain dish or capsule, with an 
equal quantity of the filtrate obtained from the gastric contents. The dish is 
then gently heated over an alcohol lamp or Bunsen burner to such a degree that 
slow evaporation takes place. If free hydrochloric acid is present, a typical rose- 

Fig. 99 




Great gastroptosis and dilatation due to cancer occurring in site of an old ulcer at pylorus. The 
greater curvature is as low as the pubes. Above the dark shadow due to bismuth is fluid in the 
stomach and above this is gas in the splenic flexure of the colon. 



red hue develops at the edge of the mixture where it is drying on the dish, or it 
may be less of a pink and more of a bright red. This test is exceedingly delicate 
and very certain. 

Boas' reagent depends upon the fact that resorcin produces a somewhat similar 
reaction with free hydrochloric acid. This reagent is composed of: 

Resublimed resorcin gr. lxxv (5 grams) 

Cane-sugar gr. xlv (3 grams) 

Alcohol (94 per cent.) giiiss (100 c.c.) 



CANCER OF THE STOMACH 551 

A few drops of this reagent are placed in a porcelain dish and an equal quantity 
of the stomach filtrate added to them. Heat is applied as in the previous test, 
and if the acid is present a very perceptible red color appears at the edge of the 
evaporating mixture. The discovery of a hypochlorhydria or absence of HC1 is 
not as pathognomonic a symptom of gastric cancer as was thought at one time. 
Particularly is this statement true when only one test is made. Chronic gastric 
catarrh and disorder of the innervation of the stomach or even the psychic state 
of the patient may greatly influence the secretion of gastric juice. 

The finding of occult blood in the stools is very indicative of cancer, because in 
gastric and duodenal ulcer the hemorrhage is apt to be inconstant. (See Gastric 
Ulcer.) 

Still another point of diagnostic importance is the examination of the stomach 
contents by the microscope, which may reveal blood cells and portions of malignant 
growth. While it is true that the presence of blood may be due to ulcer, the asso- 
ciated pieces of growth are, of course, diagnostic. 

Rommelaere asserts that if a patient over forty years of age with chronic gastric 
disease eliminates less than 180 grains of urea a day, he has cancer. This is 
probably too dogmatic. A better way of putting it is to say that when a patient 
with these symptoms eliminates 450 grains a day he has not gastric cancer. 

It is important to note that a bacillus called the Oppler-Boas bacillus is present 
in the stomach contents of cases of gastric cancer with great constancy. Indeed, 
it is present ninety-nine times in a hundred. This bacillus is a very long, non- 
motile organism, which has the power of converting sugar into lactic acid, and 
lactic acid is present in large amount in this disease. 

Prognosis. — The prognosis is only hopeful in inverse ratio with the size of the 
growth, the ability of the surgeon to remove it, and the general state of the patient. 
Even surgery can offer only temporary relief, for in the majority of cases recidivity 
takes place. Fenwick asserts that if the potassium sulphocyanide disappears 
from the saliva, the patient dies within a month. 

Duration. — This varies greatly. In some instances death comes in a few weeks 
after the disease is recognized. In others it is deferred for months, particularly 
if the growth be scirrhous and involves the pylorus, when gastroenterostomy, by 
relieving obstruction and permitting nourishment, may prolong life for a long 
period. My colleague, Dr. Keen, performed gastroenterostomy in a case under 
my care in which the growth was so great that excision was impossible. The 
patient was greatly emaciated and more than sixty years of age, yet he gained 
nearly thirty pounds in six months, and lived in comfort for two years and a half 
after the operation. 

Treatment. — -Many patients with gastric cancer can be much improved and their 
lives prolonged and perhaps saved by operation, but it is essential that the growth 
shall be limited to the stomach and that it does not involve neighboring parts. 
For this reason it is of vital importance that the diagnosis of the disease shall be 
made at the earliest possible moment. (See Gastric Ulcer.) Indeed, it may be 
said that every patient who develops persistent gastric symptoms after the age of 
forty should be regarded as a possible case of gastric cancer. In the opinion of the 
writer, every case of suspected gastric cancer in any stage should at least be sub- 
jected to exploratory operation, since by this means it may be discovered that the 
diseased area may be excised. Even if nothing more is found than the scar of an 
old ulcer the operation is rewarded in the avoidance of cancer later on. The danger 
of exploratory operation, as compared to the certainty of death if the growth is 
not interfered with, is not to be considered. 

Kronlein has shown that the average duration of life after patients come under 
observation is about nine months. If they submit to operation it is more than 
twelve months. These figures are average figures. If the growth is treated early 



552 DISEASES OF THE STOMACH 

enough perfect recovery may occur and at least from three to five years of existence 
remains. The duration of life is greater in those treated by gastrectomy than in 
those treated by gastroenterostomy, but the surgeon must decide after he opens 
the belly what course to pursue. 

The medicinal treatment of gastric cancer consists first in the administration 
of anodynes if there is much pain. These anodynes may consist of small doses of 
morphine or codeine or cannabis indica. Much of the distress due to so-called 
dyspepsia can be relieved by the use of 8 to 20 drops of dilute hydrochloric acid, 
with 1 or 2 drachms of the fluidextract of condurango, given immediately after or 
with each meal. If starchy foods are taken, takadiastase may be used. 

The use of a stomach-tube for washing out the stomach is usually inadvisable, 
as it may produce a perforation if the growth is soft or the ulceration deep. 

Should vomiting occur and blood be in the vomit, the directions for the treatment 
of hematemesis in the article on Gastric Ulcer should be followed. 

HYPERTROPHIC STENOSIS OF THE PYLORUS. 

Definition. — This condition, as its name implies, is one in which there is thickening 
and overgrowth of the muscular fibres in the pyloric portion of the stomach, with 
spasm and consequent obstruction to the free passage of its contents into the bowel. 

Overgrowth of the tissues about the pylorus may be divided into three types. 
In one the gastric walls become thickened by an overgrowth of connective tissue, 
which not only results in amincreased diameter of the part, but also in a diminution 
of the size of the entire stomach. A second form has been described by French 
authors, which is associated with sclerotic hypertrophic changes in the other 
abdominal viscera, such as the liver, pancreas, and kidneys. The third form is 
that which is known as congenital hypertrophic stenosis, which has no etiological 
relationship to the two forms just described. All three of these forms are quite 
rare, the last being most frequent. 

Etiology. — We have little knowledge of the causes of hypertrophic stenosis of the 
pylorus. In some instances it has been thought that the overgrowth is the result 
of some congenital defect, or, in other words, that it is a primary condition, but 
in others it has seemed to be certainly secondary. It is probable that in the hyper- 
trophic stenosis of adults the underlying cause is chronic gastritis. When it 
occurs in adults hypertrophic stenosis is usually a disease of middle life. 

Morbid Anatomy. — In that form of this disease which arises in middle life and 
which develops as a result of chronic gastritis, notwithstanding the non-existence 
of the obstruction at the pyloric opening, dilatation of the stomach as a secondary 
condition seems to be rare, but this depends somewhat upon how diffuse the over- 
growth of connective tissue happens to be. When it is limited strictly to the pyloric 
region, dilatation ensues because of the obstruction. When it is more diffuse, 
the stomach may be diminished in size. Very rarely does the overgrowth of con- 
nective tissue develop to such an extent as to make it possible to discover any 
mass by careful palpation. 

When the condition is due to some congenital defect, the pathological condition 
is somewhat different. It is found that the organ is larger than normal and that 
its walls are thickened by overgrowth of its muscular fibres. At the pylorus these 
muscular fibres have undergone great hypertrophy, so that this part of the stomach 
feels like a solid mass between the fingers, and on section it is found to be dense 
and firm, the mucous membrane lining the part being thrown into folds which 
lie in the direction of the long axis of the organ. Sometimes one of these folds 
is so much larger than others that it aids in producing obstruction and seems to 
from a large part of the overgrowth. Moynihan has well said that such a stomach 
may appear and feel much like the bladder and prostate when they have been 



HYPERTROPHIC STENOSIS OF THE PYLORUS 553 

removed by dissection. If the duodenum is opened, the pyloric orifice may resemble 
that of the cervix uteri when it is seen through the vagina. The thickening of the 
muscular fibre is not always limited to the pyloric area, but sometimes extends 
into the duodenum. The longitudinal muscular layers are not greatly increased 
in size, and, although there is a general hypertrophy of the muscular element 
throughout the entire organ, it is often so slight at the cardiac end of the stomach 
that it is scarcely noticeable. 

Symptoms. — The symptoms of stenosis of the pylorus in adults consist in a 
sensation of fulness, pressure, and pain in the stomach. There are also evidences 
of motor insufficiency, and when the obstruction to the pylorus becomes marked, 
vomiting may come on to relieve the stomach of materials which cannot escape 
into the intestine. So, too, the patient may lose flesh as the result of interference 
with the digestion and with the retention of proper quantities of food. The hydro- 
chloric acid of the gastric contents is usually diminished, probably because of the 
chronic gastritis which precedes the disease. 

Diagnosis. — Even if a mass be felt in the pylorus the only certain diagnostic 
measure is the bismuth meal and the arrays, which should always be resorted to. 
It may be exceedingly difficult to differentiate hypertrophic stenosis of the pylorus 
in an adult from gastric cancer occurring in this portion of the stomach. In the 
article on Gastric Cancer it was pointed out that many of these patients give a 
history of perfect digestion and no gastric distress until the cancer develops; but 
in hypertrophic stenosis there is usually a history of many years of discomfort, 
with a constant endeavor to find food which would not cause indigestion. The 
absence of cachexia, although the patient may be anemic, also points toward hyper- 
trophic stenosis. On the other hand, if the liver or gallbladder seems to be affected, 
the condition is almost certainly carcinomatous. In some instances it is impossible 
to make a differential diagnosis without operation, and even then it may require a 
microscopic examination to determine that the thickening is not malignant. So 
far as probabilities are concerned, it may be stated that the presence of obstruction 
at the pylorus in a person at or past middle life is very much more likely to be 
carcinoma than hypertrophic stenosis, since the former condition is quite common 
and the latter condition is very rare. 

Difficulty may also be experienced in differentiating hypertrophic stenosis from 
cicatricial contraction due to the remains of an old gastric ulcer. The physical 
signs and symptoms present at the moment of examination may give us no informa- 
tion, but the past history of the case may aid us materially. Thus, when gastric 
ulcer has been present, there may be a history of hemorrhage and severe pain, 
which is absent in cases of stenosis. 

Congenital Pyloric Stenosis. — As already stated, the condition of pyloric 
stenosis, when not due to ulcer or cancer, is met with in the majority of cases in 
very young children, and in such is undoubtedly congenital. In such instances 
the child is born apparently healthy, and after two or three days, or several weeks, 
of life is seized with sudden and persistent vomiting, for which no errors in diet can 
be held responsible. The vomiting is often forcible and often projectile and gives 
the child relief for the time being until more food is taken, when it recurs. The 
time during which the food is retained varies from a few minutes to several hours, 
and in some instances the mere act of swallowing seems to reflexly produce the 
motions of vomiting. In some instances the vomiting is sufficiently prolonged to 
empty the stomach thoroughly; in others a considerable quantity of food may be 
retained. It is a noteworthy fact that even if the vomiting is severe, bile is never 
present in the ejected material, because the closed pylorus prevents it from being 
drawn from the duodenum. The result of the ejection of the food almost as soon 
as it is swallowed, combined with the deficient digestive function of the stomach 
which is nearly always present, is rapid emaciation, exhaustion, and death. Some- 



554 



DISEASES OF THE STOMACH 



times a period of semiconsciousness ensues, and occasionally the child is seized 
with a convulsive attack. 

The duration of life varies from four or five weeks to six months. 

As the disease progresses and emaciation becomes marked, it may be possible 
to see the outline of the stomach in its forcible contractions if the abdomen is 
carefully examined in a good light. If deep palpation can be practised, the thick- 
ened pyloric portion of the stomach can be felt forming a distinct contrast to the 
empty and collapsed intestines, which are prevented from containing their usual 
food and liquid by the obstruction at the pylorus. (See Fig. 100.) 

Fig. 100 




Showing the gastric peristalsis. Note constriction of stomach by passing wave. (Ibrahim.) 



The points which are strongly in favor of hypertrophic stenosis of the pylorus 
in infancy are the causeless and persistent vomiting, the absence of bile from the 
vomit, the constipation, the presence of a tumor in the pyloric area, the collapsed 
intestines and distended stomach, and the fact that gastric digestion is almost 
completely arrested, and, finally, that these symptoms are present in a young 
child. The diagnosis is to be confirmed, if need be, by bismuth and the .T-rays. 

Prognosis. — The prognosis in congenital hypertrophic stenosis depends upon 
the degree of obstruction. It is unfavorable as to recovery. 

Treatment. — The treatment, whether the state be congenital in infants or acquired 
in adults, consists in the use of lavage and in feeding through a rubber tube, so 
that the movements of swallowing are not necessary. In some cases it may be 
possible to prevent the vomiting by gently washing out the stomach before each 
feeding, but this is only of service in those instances in which the stenosis is not 
absolute. When this measure fails, or if the symptoms are exceedingly severe, 
operative procedure must be resorted to before the patient is sufficiently exhausted 
to contra-indicate the operation. The operation in adults should either be pyloro- 
plasty or gastroenterostomy. Moynihan states that anterior gastroenterostomy 
has been performed 9 times, with 5 recoveries and 4 deaths, but 1 of these deaths 
was due to acute obstruction caused by a Murphy button. Loreta's operation of 
pylorodiosis has been performed 9 times, with 7 recoveries. 

It has been generally held in the past that congenital stenosis of the pylorus 
could be relieved only by operative interference. This sweeping conclusion is 
erroneous, since much depends upon the degree of stenosis. If it seems to be 
absolute and improvement fails to take place after the use of lavage and gavage, 
operation must be resorted to before the patient is too exhausted to withstand 



HOUR-GLASS STOMACH 



555 



the shock. There are so many cases now on record in which recovery has occurred 
without operation that medical means should always be given a fair chance to do 
good. The claim that the cases which have recovered without operation have not 
been really instances of organic stenosis but spasm is proved incorrect by the fact 
that subsequent autopsy, when death has been due to other causes, has shown an 
actual hypertrophy to be present. The mortality under operation is about 50 per 
cent., or higher than this if exhaustion is extreme. 

HOUR-GLASS STOMACH. 

Definition. — Hour-glass stomach, sometimes called "bilocular stomach," or 
"Sanduhrmagen," is a condition in which the stomach is divided into two parts 
by a contraction which may exist anywhere between the cardiac and pyloric orifices. 
Very rarely, indeed, a trilocular condition may be present, and, still more rarely, a 
quadrilocular state may exist. 

Fig. 101 




Remarkable hour-glass stomach with perforation of ulcer. The upper dark mass to the right is the 
remains of the fundus. To the left is the barium extravasated into the tissues. Below is the hour- 
glass contraction, and below it is the distended lower half of the stomach, retentive from pyloric 
stenosis. X-ray diagnosis confirmed on operating. 



Etiology. — Hour-glass stomach may be congenital or acquired. There is some 
difference of opinion as to the relative frequency of these two forms of the condition. 
Some authors have maintained that all cases are acquired, while others assert that 
the congenital cases are more common. Fenwick says that about 45 per cent, of 
the cases which have been so far recorded showed no sign of either ulcer or scar 
in the stomach, or if an ulcer or scar were present it was manifest that it was more 
recent than the stricture itself; and again he states that only 1 case of the acquired 
type has been found in the London Hospital in forty years, whereas several instances 
of the congenital type were met with during the same period of time. To those 



556 DISEASES OF THE STOMACH 

who believe in the congenital origin of these cases, Moynihan is strongly opposed, 
and he is undoubtedly correct as modern methods of investigation prove. 

There are three causes of hour-glass contraction: first, perigastric adhesion; 
second, chronic ulcer; and third, malignant disease. The perigastric adhesions 
are most commonly due to ulcer of the stomach or to a nearby inflammatory process 
set up by the presence of gallstone. Chronic ulcer not only produces perigastric 
adhesions, but it may, in healing, cause much contraction and thickening of the 
stomach, so that its wall becomes puckered and its calibre decreased. Associated 
with this contraction, due to the formation of scar tissue, there is also a certain 
amount of muscular spasm, the circular muscular fibres contracting in such a way 
as to resemble a sphincter muscle. This spasmodic contraction accounts for the 
paroxysms of discomfort from which the patient occasionally suffers. 

Pathology and Morbid Anatomy. — On examining a stomach for the seat of hour- 
glass contraction, two sets of thickened muscular fibres, which cross one another, 
may sometimes be seen. These bundles are usually one-half inch or more in 
width, and cross one another at the point of contraction, and it is the shortening 
of these muscular fibres which produces the deformity. That this is not the cause 
in most instances, however, is shown by the fact that these muscular fibres are 
frequently absent, or, at least, are not abnormally developed. When the constric- 
tion is due to the formation of a cicatrix the narrowed band forming the dividing 
septum between the two pouches is composed of fibrous tissue; this may be puckered, 
indicating that it has followed an ulcer. 

Symptoms. — The symptoms of hour-glass contractions of the stomach are by 
no means definite. The diagnosis is practically always made by the use of a 
bismuth meal and the x-rays. 

Treatment. — The only treatment for hour-glass contraction which can afford 
any relief is operative. Thus, a gastroenterostomy may be done from both pouches, 
or gastroplasty or pyloroplasty may be necessary. For these operations the reader 
is referred to books on surgery. 



GASTRIC NEUROSES. 

At the present time several states of the stomach are known to exist which depend 
upon an altered or perverted nerve supply, and are not connected with any patho- 
logical lesion which our methods of examination can detect. Gastric neuroses 
are not commonly met with as conditions independent of true lesions, and the 
physician must not rest satisfied with a diagnosis of gastric neurosis until he has 
exhuasted every possible means of discovering an actual morbid change. In 
some instances the nervous affection of the stomach is a manifestation of disease 
of the central nervous system; in others it is a sign of perverted nervous function 
due to neurasthenia or nervous exhaustion, and in still other cases it may be depend- 
ent upon growths which, being situated in adjacent tissues, press upon the gastric 
nerves and so cause pain or spasm. Finally, it is to be remembered that even 
if the physician can discover no sign of gastric lesion, this does not justify a diagnosis 
of gastric neurosis, because it not rarely happens that disease elsewhere causes pain 
which is incorrectly referred by the patient to the region of the stomach. Thus, a 
child with pericarditis or appendicitis may complain bitterly of epigastric pain. 

True gastric neuroses may be divided for study into three classes, viz., disorders 
of mobility, disorders of sensation, and disorders of secretion, and these in turn are 
divisible into states of excitation and depression. 

Cardiospasm, or cramp of the muscular fibres in the cardiac end of the stomach, 
is a result, as a rule, of irritation of the gastric mucous membrane by superacid 
secretion. Occasionally it may develop as the result of distention of the stomach 



GASTRIC NEUROSES 557 

by gas, and in some instances no direct cause for its existence can be discovered 
save that a state of nervous unrest and instability is present. Cramp of the cardia 
appears in an acute and fleeting form, and as a chronic condition which causes great 
distress and may be serious, in that it exhausts the patient. In the former cases 
pain and spasm seize the patient and then pass away. In the latter it often happens 
that the patient has difficulty in swallowing and expresses the feeling that the food 
cannot enter the stomach, but remains in the esophagus. If the taking of food is 
persisted in, it speedily accumulates in the esophagus, and when this tube is dis- 
tended the patient regurgitates the food undigested and devoid of gastric juice, for 
it has never entered the stomach. The emaciation which follows this inability to 
take food may lead to the belief that a gastric carcinoma is present, particularly 
if the patient is advanced in years. When chronic cardiospasm lasts for a long time, 
dilatation of the esophagus may develop, and even a diverticulum may be formed. 

Treatment. — The treatment consists in the use of remedies designed to prevent 
and counteract excessive gastric acidity, the avoidance of all irritating or stimulating 
forms of food and drink, the use of lavage if there is any evidence of chronic gastric 
catarrh or of fermentation in the stomach, and in feeding through a stomach-tube 
if there is any difficulty in giving the patient a proper amount of nourishment. 
Boas states that in some cases solids are taken more readily than liquids. Seda- 
tives, such as chloretone, the bromides and chloral, may be used. Sometimes 
galvanic electricity gives relief, using for its application an intragastric electrode. 
In some instances the daily passage of a large-sized gastric or esophageal bougie 
produces a cure. 

Pylorospasm. — Pylorospasm is nearly always secondary to lesions, although a 
primary spasm may occur. In pylorospasm a contraction wave may be seen, in a 
thin patient, endeavoring to urge the gastric contents through the closed pyloric 
orifice, and if the spasm is persistent the stomach contents will not only be retained, 
as in pyloric stenosis, but they may undergo fermentative changes as well, so 
that symptoms of chronic gastric catarrh or dilatation may be present. In other 
cases a reversed peristalsis is set up and vomiting comes on, so that symptoms like 
those of hypertrophic pyloric stenosis ensue. The treatment is identical with that 
of cardiospasm. 

Gastric Hyperperistalsis, called by Kussmaul "peristaltic unrest," is a con- 
dition in which the stomach almost incessantly continues to maintain peristaltic 
movement. As a rule, it is most active after meals, but it may be present when 
the stomach is empty, and even persist at night during absolute rest. Although 
marked pain is usually not present, the incessant movement of the stomach causes 
restlessness and gastric discomfort. Often the wave-like movements of the stomach 
can be felt through the abdominal wall, and their progress is from left to right. 
These undulatory movements are not demonstrable, as a rule, unless some gastric 
dilatation is present and the belly wall fairly thin. Three causes are recognized, 
viz., excessive acidity producing irritation, great reflex excitability, and, most 
important of all, stenosis of the pylorus, which obstructs the flow from the 
stomach. 

Treatment. — The treatment consist in the use of sedatives, such as the bromides, 
chloral, codeine, and hyoscyamus, and in the use of counter-irritation over the 
epigastrium. Not rarely an absolute rest cure, with rectal feeding for a week, 
may be needful to cause gastric quiet. Causes which produce nervous exhaustion 
and indigestible foods are to be forbidden and hydrotherapeutic measures should 
be instituted. 

Merycismus. — Merycismus is a neurotic condition in which the patient has 
the ability at will to regurgitate the food from the stomach into the mouth for the 
purpose of rechewing it, as is done by ruminants. It is usually met with in neurotic 
degenerates. 



558 DISEASES OF THE STOMACH 

Nervous Eructation. — Nervous eructation is not a very rare affection. The 
patient is usually very nervous and will often sit for hours "rifting up" gas, which, 
in many cases, is really swallowed air. In other cases the movements of eructation 
are performed without any gas being brought up. This condition is commonly 
seen in hysteria. It is best treated by the rest-cure and the administration of 
tonics or nervous sedatives, such as the bromides, spirit of chloroform, asafetida, 
or chloretone. 

Closely related to nervous eructation is nervous vomiting. 

Hyperesthesia. — Among the sensory disorders of the stomach is hyperesthesia, 
in which the taking of food causes great gastric distress, so that the patient refuses 
to eat enough to maintain nutrition. In hysterical cases the patient may be able 
to eat what she wishes, yet has pain when other articles of food are given to her. 

This condition is to be separated from the hyperesthesia due to gastric ulcer 
since it sometimes develops when this lesion is not present. Sometimes it seems 
to arise from the abuse of alcohol, coffee, ice, or certain drugs, such as quinine and 
the salicylates, or tobacco. In other instances it arises from nervous exhaustion 
due to sexual excess, great mental strain, prolonged lactation, or menorrhagia. 
So, too, it may develop in the course of chlorosis, and while in the majority of 
instances this condition in chlorosis points to ulcer, the possibility of no ulcer 
being present must be considered, in view of our knowledge of the existence of 
this state. 

Symptoms. — The symptoms consist in a sense of fulness and distention of the 
stomach, particularly in the neighborhood of the cardia, with some aching or 
burning, which extends upward under the ribs. Constipation is usually present. 
As the condition advances the disagreeable sensations in the stomach become so 
severe as to amount to pain, and the taking of food usually greatly increases the 
suffering. When fully developed the patient often suffers from vomiting, which 
may occur after every meal. In ulcer, vomiting usually gives temporary relief, 
but in hyperesthesia of the stomach it does not. If the disease persists, there is 
emaciation due to the pain and constant vomiting. The skin over the epigastrium 
is usually hyperesthetic, and the tenderness on deep palpation is diffuse and not 
localized as in ulcer. An examination of the gastric contents usually reveals a 
normal acidity, but in some cases the acidity may be above or below the normal. 

Gastralgia. — Gastralgia, gastrodynia, or gastric neuralgia, may be a cause of 
much severe suffering, for the patient may be seized by a paroxysm of pain which 
seems as violent as a renal or hepatic colic. This pain is felt not only in the epigas- 
trium, but along the edges of the floating ribs to the spine, and it often recurs with 
a peculiar periodicity. It is not rare in hysteria and neurasthenia. The gastric 
crises of locomotor ataxia, the pain of ulcer of the stomach and duodenum, gall- 
stones, and that caused by gas must be carefully excluded before a diagnosis of 
gastralgia is reached; indeed, a diagnosis of simple gastralgia should always be 
looked upon with suspicion, because gastric pain is so commonly due to some organic 
cause. Unlike the pain of ulcer, this form is usually relieved by taking food. 

Bulimia. — A neurosis of the stomach characterized by excessive hunger and 
the ingestion of great quantities of food to alleviate the discomfort is called " Bu- 
limia." It is usually met with in cases of hysteria, in cases of exophthalmic goitre, 
and in cerebral tumor and epilepsy. 

Anorexia Nervosa is a form of neurosis with persistent lack of appetite. 

Nervous Disorders of Secretion. — A form of nervous disorder of secretion con- 
sists in hypersecretion of gastric juice, producing the ordinary symptoms due to 
acid stomach. It is often met with in chlorotic girls, and is usually associated 
with constipation. The excessive secretion may occur in paroxysms or be 
continuous. 

The antithesis of this state is that in which there is an absence of secretion, 



HEMORRHAGE FROM THE STOMACH 559 

sometimes called achylia-gastrica nervosa. This state of absence of HC1 is, of 
course, common in gastric cancer, and it arises also from atrophy of the gastric 
tubules, but there are instances in which, apparently because of disordered nerve 
supply, there is absence of secretion for weeks, months, or even years, yet finally 
it is perfectly re-established. 

Treatment. — The treatment of these disorders of sensation consists in the institu- 
tion of a rest cure for the rehabilitation of the patient's nervous tone; in the use 
of hydrotherapeutic measures and electricity designed to bring about the same 
result, in the prescription of a mode of life which will avoid nervous worry 
and strain, provide a sufficient number of hours of sleep and out-door exercise, and 
prevent the ingestion of articles of food which are difficult to digest or irritating 
to the stomach. For the prevention or relief of painful or disagreeable sensations, 
a number of remedies may be employed. Not infrequently a dose of a drachm 
of spirit of chloroform and a drachm of compound spirit of lavender in a little 
water will dispel gas and distention and act as a sedative to the stomach. In 
other instances \ to 1 grain of menthol may be given in capsule or pill. In still 
others one of the coal-tar products, as antipyrin, acetanilid, or phenacetin, may be 
used, and in some instances much relief will be obtained by the use of chloretone 
in capsule, or tablet, in 3 to 5 grain doses. Where there is a distinct hysterical 
element and it is considered desirable to exercise a mental influence, the stomach- 
tube may be passed once or twice a day. If an excessive secretion of hydrochloric 
acid is present, associated with much nervousness, the bromides may be employed, 
or nitrate of silver and hyoscyamus may be used. 

HEMORRHAGE FROM THE STOMACH. 

Hemorrhage into the stomach is called gastrorrhagia, and when the blood is 
vomited the condition is one of hematemesis. It may result from rupture of dilated 
gastric and esophageal veins, from ulcer of the stomach and duodenum, from 
cancer of the stomach, and from dilatation of the gastric veins in chronic gastric 
catarrh. It has also been known to follow severe injuries over the epigastrium. 
Occasionally the vomiting of blood has been due to an aneurysm which has perfor- 
ated the esophagus and then drained into the stomach. The physician must also 
remember that malingerers sometimes swallow blood for the purpose of deceiving 
their attendants. Sometimes "coffee-ground cancer, vomit," due to the presence 
of altered blood, is met with in cases of gastric cancer, in certain forms of purpura, 
in hemophilia, and in persons suffering from such poisons as phosphorus and car- 
bolic acid. Occasionally, too, in cases of exceedingly severe infectious disease 
such as yellow fever and smallpox, vomiting of coffee-ground material occurs. 
By far the most frequent causes of bloody vomiting, however, are cirrhosis of the 
liver, ulcer of the stomach and duodenum, and cancer of the stomach. When due 
to cirrhosis it is usually met with in males, and when due to ulcer it most commonly 
occurs in females. 

Preble has made a most complete statistical study of gastro-intestinal hemorrhage 
in hepatic cirrhosis, and finds that the great majority of cases occur in the atrophic 
form, although occasionally hemorrhage takes place in hypertrophic cirrhosis. 
In one-third of the cases the first hemorrhage is fatal ; while in the other two-thirds 
the hemorrhage occurs at intervals varying from a few years to several years, the 
longest duration being over a period of eleven years. 

In some instances it is possible to make the diagnosis of hepatic cirrhosis, but 
in other instances the change in the size of the liver is so slow that not for months 
after the hemorrhage occurs is this organ found to be smaller than normal. In 
80 per cent, of the cases, according to Preble, there are varices in the esophagus, 
and in more than one-half of these there are evidences of their rupture. It has 



560 DISEASES OF THE STOMACH 

also been found that fatal hemorrhages may occur in cases which do not suffer 
from esophageal varices. These cases are probably due to the rupture of a large 
number of capillaries in the alimentary mucous membrane. It is interesting to 
note that in only 6 per cent, of the cases which showed esophageal varices was the 
cirrhosis typical in the sense that the ordinary symptoms of this condition were 
present. Very profound hemorrhages may come from a very small opening in a 
bloodvessel, so that at autopsy it may be almost impossible to discover the source 
of the bleeding. 

Aside from the actual vomiting of blood, the symptoms of gastric hemorrhage 
are those of ordinary hemorrhage, namely, pallor, faintness, or actual syncope, and 
sometimes death. The vomited blood, if it has been poured out in large quantities, 
is somewhat venous in color and filled with clots, and if it remains in the stomach 
any length of time it may become brown or granular in appearance, through the 
action upon it of the digestive juices. It must always be remembered that the 
quantity of blood which has escaped from a bloodvessel is not shown by the 
amount vomited, as a very large amount may leak into the stomach before 
vomiting occurs, and the stomach in vomiting may not completely empty itself. 
Care must be taken in determining that the blood comes from the stomach, and 
that the red color is really due to blood. Sometimes a bloody color of the vomit 
may be due to claret or the juice of various berries. A distinction can be made 
by a microscopic examination, by the history of the ingestion of certain articles 
of food, and, if need be, by the use of the spectroscope and the various tests 
which are employed to determine the presence of blood. It must also be borne 
in mind that persons who suffer from nosebleed, in which the leaking vessel is far 
back in the nose, may swallow considerable quantities of blood and then vomit it. 

Hemorrhage from the lungs, or hemoptysis, is to be separated from hematemesis 
by the fact that in hemorrhage from the lungs the blood comes up with coughing, 
and in hemorrhage from the stomach by vomiting, although at times both of these 
symptoms may be present in each class of cases. The characteristic appearance 
of a patient well advanced in tuberculosis will be of great diagnostic aid in such 
cases, and an examination of the chest in the case of hemoptysis will usually reveal 
some lesion; whereas, the lungs will be clear in hematemesis. In a case of hema- 
temesis an examination of the abdomen may reveal an atrophied liver and an 
enlarged spleen, or some other abdominal state, such as the caput medusa, which 
will indicate that there is venous stasis in the abdomen. (See Hepatic Cirrhosis.) 
In hemoptysis the blood is pink and frothy. In hemorrhage from the stomach 
it is dark, has little air mixed with it, and is often acid in reaction; whereas, that 
in hemoptysis is usually alkaline. In hemoptysis no dark, tarry stools are present, 
but they are frequently seen after an attack of hematemesis. A day after an 
attack of hemoptysis the patient may cough up some thickened, bloody mucus, 
but there is no difficulty in separating this from the more fluid, dark blood from the 
stomach. An additional aid in the diagnosis of hematemesis is Boas' test given 
in the article on Gastric Ulcer. 

Notwithstanding the profound mental shock and vital depression which often 
follow a profuse hemorrhage from the stomach, it is worthy of note that death 
very rarely occurs as the immediate result of this loss of blood, unless the patient 
is already devitalized by advanced disease or repeated hemorrhages. 

For the treatment of bloody vomiting see Treatment of Gastric Ulcer. 

CYCLIC VOMITING. 

Under the name of cyclic, periodical, or recurrent vomiting, a condition has 
been rarely met with in which, at certain periods, a child is seized by an attack 
of persistent vomiting, which not only continues while the stomach is being emptied 



DUODENAL ULCER 561 

of its normal contents, but persists for many hours afterward, and in some instances 
ends fatally. The condition in all probability depends upon a form of auto-intoxica- 
tion. The auto-intoxication consists, apparently, in a condition of acidosis, a 
condition in which acetone, diacetic acid and even /3-oxybutyric acid appear in 
the urine as the result of faulty metabolism of fats. The preventive treat- 
ment consists in carefully regulating the diet, cutting down fats and proteids 
and increasing the carbohydrates, exercising care that an excess of* starchy food 
does not cause intestinal disorder. The active treatment consists in administering 
alkalies, 2 or more drachms of sodium bicarbonate by mouth, by rectum, or even 
by hypodermoclysis and the rectal injection of several drachms 'of levulose. 



DISEASES OF THE INTESTINES. 

DUODENAL ULCER. 

Ulcer of the duodenum is a more frequent condition than is generally 
supposed, and in some cases is associated with ulcer of the stomach. W. J. Mayo 
thinks it is three times as common as gastric ulcer. Wilkie, in 490 post- 
mortem examinations, found it 41 times, and in only 6 of these was a 
diagnosis made during life. The proportion given by Burwinkel of gastric 
and duodenal ulcer is 12 to 1. On the other hand, von Wyl found only 
3 duodenal ulcers in nearly 13,000 postmortem examinations, and Kinnicutt, in 
an analysis of 30,000 postmortems, places its frequency at 0.4 of 1 per cent. The 
condition may arise at any period of life, but is most frequent between the tenth 
and fortieth years. Hahn has recorded a case in a child only a day and a half 
old. Such an ulcer must have been antenatal. Holt has collected 95 cases during 
the first year of life and as all but 21 have been reported since 1908 it would appear 
that the lesion is far more common in children than it has been thought. Out 
of 65 cases 70 per cent, occurred between 6 weeks and 5 months of age. 

Unlike gastric ulcer, the great majority of duodenal ulcers are found in men. 
Murphy, of Chicago, quotes Laspeyres as stating that men are affected two or 
three times oftener than women. Krauss, in 64 cases, found the ratio to be 
10 to 1; Lebert, in 39 cases, 4 to 1; Trier, in 54 cases, 5 to 1; and out of 176 cases 
collected by Weir, 144 were in men. 

Wilkie thinks that the sex incidence of duodenal ulcer is explained on anatomical 
grounds. The relatively high pylorus and short fixed duodenum of the male 
allows of its vascular supporting ligament, the hepatoduodenal ligament, being 
exposed to strain, which, in the female with her relatively low pylorus and lax 
duodenum, is borne by the left border of the gastrohepatic omentum and lesser 
curvature of the stomach. 

Etiology. — Among the causes of duodenal ulcer may be mentioned burns, which 
in some unknown way produce ulceration in this portion of the bowel. Renal 
disease, which occasionally results in the ulceration of the large bowel, may also 
cause this lesion in the duodenum. Pulmonary tuberculosis, which produces its 
lesion by infection of a solitary follicle, and diseases of the heart and liver, which 
result in impairment of vitality in the intestinal wall, so that localized infections 
may occur, are also causes. 

As with gastric ulcer, so with duodenal ulcer, a large number of theories have 

been advanced as to its direct causation. Most authorities at the present time 

believe that it is due to erosion produced by the gastric juice, the vital resistance 

of the part having been diminished by inflammation or circulatory changes. That 

36 



562 DISEASES OF THE INTESTINES 

acidity of the gastric contents may so result seems likely, from the fact that ulcer 
most frequently occurs in the duodenum near the pylorus, at a point where the 
acidity of the gastric juice may be but little modified by the alkaline secretion which 
it would meet a few inches farther on in the bowel. 

It would seem probable, however, that a number of factors may produce this 
form of ulcer, acting in some cases together and in other cases singly. These 
factors are well summed up by Murphy and made into four divisions : hyperchlor- 
hydria, local infection, embolism or thrombosis, and foreign bodies. To these 
four divisions Murphy would add a fifth, namely, disorders of the organs of elimina- 
tion, as in burns of the skin or other serious lesions in this part of the body, as 
pemphigus and erysipelas, and in other cases renal disease. 

Not rarely duodenal ulcer is caused by or associated with ulceration or disease 
of the colon or of the appendix. Indeed in many cases of appendicitis inflammation 
of the duodenum is present, which, perhaps, accounts for the epigastric discomfort 
in many cases of chronic appendicitis. 

Pathology and Morbid Anatomy. — Duodenal ulcers are usually single, but they 
may be multiple — 10 to 20 per cent. Sometimes ulcers are opposed to one 
another — the so-called "kissing ulcers" of Moynihan. Out of 233 cases collected 
by Collins, 195 were single. 

Ulcer usually occurs in the first part of the duodenum; within half an inch of the 
pylorus in 85 per cent, of cases. The reason for this is that the first part 
of the duodenum arises from the f oregut, as does the stomach, and thus its mucous 
membrane is free from folds but rich in lymph follicles in which ulcer readily 
develops. This is the reason that obstruction of the stomach or hematemesis 
so often takes place. Out of 149 cases collected by Perry and Shaw, the 
first portion of the duodenum was involved 123 times, the second portion 16 
times, and the third and fourth portions twice. These statistics agree with those 
which have been collected concerning the area and greatest frequency of perfora- 
tion complicating ulcer of the duodenum. In the great majority of cases it is on 
the anterior wall. 

When perforation occurs, it takes place nearly twice as often in the anterior 
as in the posterior wall, still more rarely in the superior wall, and almost never 
in the inferior wall. Perforation occurs much more frequently in ulcer of the 
duodenum than in ulcer of the stomach, if we can rely upon the statistics which 
have so far been collected. Thus, in 404 cases mentioned by Chvostek, Collins, 
and Oppenheimer, perforation took place in 246. On the other hand, it must be 
remembered that a very large number of cases of duodenal ulcer are not recognized 
unless perforation does occur, and it is highly probable that this accident is far 
less frequent in duodenal ulceration than these statistics would indicate, because 
it is a well-known fact that duodenal ulcer is a condition most difficult to recognize 
unless it is found in the course of an abdominal section, further, it is well known 
that these ulcers frequently heal. Thus, Perry and Shaw found evidence of repair 
in half of their cases, and Krug, in 1220 autopsies, met with 30 cases of healing 
of duodenal ulcer. Unlike gastric ulcer, duodenal ulcer rarely undergoes malignant 
change. 

As in perforations of the stomach, so in perforation of the duodenum, a general 
peritonitis ensues, or a localized peritonitis may develop, the extravasated materials 
being walled off from the rest of the peritoneal cavity by an inflammatory exudate. 
As with gastric ulcer, so again with duodenal ulceration, adhesions may take place 
in neighboring organs, and perforation may take place into them. Thus, it has 
occurred that the duodenum has been perforated, and so permitted its contents to 
enter the gall-bladder, the abdominal aorta, the vena cava, the portal vein, the 
superior mesenteric vein, and the hepatic artery; but Murphy asserts that a gas- 
troduodenal fistula has never been found as a result of perforation of a duodenal 



DUODENAL ULCER 563 

ulcer. In some instances perforation of the duodenum has resulted in subphrenic 
abscess. The perforation is very small and may occur just outside the pyloric 
ring. 

Symptoms. — The symptoms of duodenal ulcer, unless the ulceration proceeds 
to hemorrhage or perforation, are too indefinite to make a positive diagnosis possible 
in many cases. Indeed, in fully half the cases in which duodenal ulcers are found 
at autopsy, there have been no symptoms during life which have raised suspicion 
of its existence and in many cases the patient remains well nourished. 

When the symptoms do occur, they so closely resemble those of gastric ulcer that 
a differentiation may be impossible. There is pain and vomiting, and if a blood- 
vessel is ulcerated there may be hematemesis or bloody stools. The pain is usually 
much less severe than in ulcer of the stomach, but at times it may be agonizing. 
There seems to be a general consensus of opinion that it rarely radiates toward 
the back, as does the pain of gastric ulcer, but cases have been reported in which 
pain in the neighborhood of the shoulder-blade has been a pronounced symptom. 
It differs from gastric ulcer in that the taking of food is not immediately followed 
by pain, but by relief; being delayed for several hours after a meal, then developing 
when the food enters the duodenum from the stomach. Occasionally the entrance 
of food into the duodenum causes pain. Moynihan says that the nearer the ulcer 
is to the stomach, the sooner is the pain developed. Not infrequently it causes 
evidence of pyloric obstruction. It has been said that if the cc-rays and bismuth 
meal cannot be used the patient may be given a little partly cooked rice and a 
few raisins at bedtime; and their presence in the stomach contents in the morning 
indicates obstruction (Mayo), but this is a sign of obstruction not necessarily of 
ulcer of the duodenum. 

The hemorrhage, when it takes place, may be sufficiently profuse to cause death, 
or it may be small in amount and be frequently repeated, in which case death may 
ultimately occur from exhaustion. Vomiting rarely occurs except when the stomach 
is overloaded, or when blood enters it from the duodenum. 

Perforation of a duodenal ulcer may be the first manifestation of any lesion 
in this portion of the bowel. According to Schwartz, patients suffering from per- 
foration of the duodenum were healthy in 20 out of 25 instances prior to the accident, 
and in Weir's 51 cases they were without gastric or duodenal symptoms in 25 out 
of 34. So, too, in Perry and Shaw's 151 cases, 91 per cent, presented no evidences 
of disease until perforation or hemorrhage developed. 

While cases of ulcer may recover, the tendency is to a progression of the disease. 
On the other hand, progress does not necessarily mean early death, for Chvostek 
has reported a case in which there had been present symptoms of duodenal ulcer 
occasionally for thirty-nine years. 

Symptoms of perforation of duodenal ulcer are severe epigastric or right hypochon- 
driac pain, followed it may be by collapse; the symptoms resemble, perhaps, acute 
hemorrhagic pancreatitis, and death occurs sometimes as early as twenty-one 
hours after the accident. The symptoms of general peritonitis soon develop, or, 
if the lesion is localized by adhesions, localized peritonitis is found, as already 
stated. Leukocytosis is usually marked. 

Diagnosis. — The tests for minute traces of blood in the stools, which are described 
in the article on Gastric Ulcer, may be used in these cases. 

Duodenal ulcer must be separated from gastric ulcer, if possible. Where there 
is hematemesis with little if any blood in the stools the source of the blood is prob- 
ably but not certainly gastric, whereas a large bloody stool without bloody vomit 
is probably duodenal in origin. In the majority of instances the character of the 
blood in the stool is dark and tarry, owing to its alteration by the intestinal juices. 
If it is bright in character, it probably comes from ulceration of a lower portion 
of the bowel. When duodenal ulcer occurs in infancy there may be no symptoms 



564 DISEASES OF THE INTESTINES 

save intestinal indigestion until hemorrhage or purpura develops. While von Wyl 
admits that it is impossible to make a differential diagnosis in 90 per cent, of the 
cases, he gives us the following points which are of value in differentiation : 

Gastric Ulcer. Duodenal Ulcer. 

1. Usually in women twenty to thirty-five 1. Most frequent in men. 

years of age. 

2. Pain comes on soon after eating. 2. Pain two to four hours after eating, 

and located in right hypochondrium. 

3. Pain lessened by vomiting. 3. Vomiting does not relieve pain. 

4. Vomitus contains, mucus, food remnants 4. Vomiting more rare than in gastric ulcer, 

and often blood. and does not often contain blood. 

5. Severe dyspeptic symptoms usually present. 5. Dyspeptic symptoms slight. 

6. Melena rare. 6. Melena comparatively frequent. 

Estimates of the acidity of the gastric contents are not of much value in differ- 
ential diagnosis since hyperacidity is often present in both gastric and duodenal 
ulcer. 

Gallstone colic is to be separated from duodenal ulcer by the fact that hemorrhage 
does not occur in gallstone colic, and by a previous history of gallstones; but it is 
to be remembered that the absence of a history of jaundice is of little value, for 
jaundice is not a constant symptom in cholelithiasis. As Murphy well points 
out, jaundice was present only 16 times in 400 cases of cholelithiasis operated on 
by him. 

Acute fat-necrosis often cannot be differentiated from duodenal ulcer with 
perforation. As a rule, the vomiting in fat-necrosis is more persistent, and the 
depression or collapse is more prompt and severe. A high-pitched percussion 
note is found in the right hypochondrium in fat-necrosis, but this area is usually 
flat in perforation of the duodenum, unless peritonitis has already progressed to 
the stage of general tympanitic distention. In fat-necrosis there is an absence of 
leukocytosis; in perforation there is a marked leukocytosis. In fat-necrosis there 
is usually no rise in temperature; in perforation there is not infrequently a primary 
rise. 

Intestinal obstruction may closely resemble perforated duodenal ulcer. The 
pain in ulcer is constant; in obstruction colicky; there is hyperperistalsis in ob- 
struction ; there is an absence of peristalsis in perforation ; there is absence of leuko- 
cytosis in obstruction; there is marked leukocytosis in perforation. In both there 
is usually a history of constipation. Perforation of a duodenal ulcer has been 
mistaken for appendicitis of the fulminant type and the correct diagnosis not 
reached even after the abdomen has been opened. Codman says every sixteenth 
case he has operated upon for appendicitis has been a duodenal perforation. 

The ar-rays give us little assistance in duodenal ulcer except that they may show 
stricture (rarely) . It is thought that hurried emptying of the stomach is significant 
of this lesion, the reverse state from gastric ulcer. Much depends on the situation 
of the ulcer. If it is below the pylorus it hurries the food out of the stomach; if 
in the pyloric zone it may cause spasm and retain food. 

As illustrative of how difficult it is to make a correct diagnosis, even when perfora- 
tion occurs, Moynihan tells us that in only 12 out of 51 cases of duodenal ulcer was 
a correct diagnosis made before operation, and that in 49 cases of perforated duo- 
denal ulcer 18 were operated upon for appendicitis. 

Prognosis. — The prognosis, like that of gastric ulcer, is not good for recovery. 
In perforative cases, if operation is not performed, the outlook depends entirely 
upon whether the infective material is walled off by adhesions. If this is the 
case, and a subphrenic abscess is formed, much depends upon the point at which 
this abscess ruptures. If the extravasated material is not confined by adhesions, 
death occurs from general peritonitis. 

When the perforation is recognized and operation is performed, the prognosis 



DIARRHEA 565 

is much more favorable. The difficulty is that in many cases the diagnosis is so 
obscure that operation is not performed until so many hours have passed that 
recovery is impossible. Thus, out of 51 cases operated upon in Moynihan's collec- 
tion there were only 8 recoveries, and in 20 cases collected by Darras only 3 re- 
covered. In 79 cases collected by Weir and Foote the mortality after operation 
was 71 per cent. 

Treatment. — The treatment of these cases consists in absolute rest in bed and 
in dietetic and medicinal measures which are practically identical with those of 
gastric ulcer (which see). If after some weeks no improvement ensues or if relapses 
occur a surgeon should perform a gastro-enter ostomy. If a severe intestinal 
hemorrhage develops the patient should be operated on as soon as he has recovered 
from the immediate effects of the loss of blood lest another hemorrhage prove 
fatal. Whenever a surgeon operates for appendicitis and finds a normal appendix 
he should investigate the duodenum and gallbladder and whenever he operates 
for ulcer and finds it not he should investigate the appendix and gallbladder. 
There is no medicinal treatment that will check hemorrhage from a duodenal 
ulcer. Hypodermoclysis or intravenous saline injections may be used. If perfo- 
ration has taken place and surgery cannot be resorted to, then there is nothing 
left for the physician but to relieve pain by the use of opium and to hope that 
the inflammatory process may be localized. 

DIARRHEA. 

Diarrhea is not a disease, but a symptom, just as headache and dropsy are 
symptoms. It occurs, however, from so many different causes and is so often 
present without the presence of any organic change in the intestinal walls that 
it is best considered as a functional malady, at least in several of its forms. 
Diarrhea is the symptom or condition, above all others, in some cases, but in 
others it is of little significance as compared to the organic lesion which produces it. 

Serous Diarrhea. — Serous or watery diarrhea may arise from the ingestion of 
irritating foodstuffs, which cause the intestinal mucosa to become hyperemic 
and to pour into the bowel the serum of the blood, to dilute the poison, and to 
wash it out of the intestine. In many instances the attack is very brief, and 
even if by an accident an autopsy is possible, no lesion may be found. 

In still other cases the same result may follow sudden exposure to cold and 
dampness, in which case, if the visceral congestion is severe, a secondary catarrh 
of the intestinal mucosa may develop as a later condition. 

In some instances a serious diarrhea seizes persons who are, or who are about 
to be, subjected to a severe nervous strain, as actors at their first appearance, or 
medical students about to go before a severe examiner, upon whose verdict much 
depends. Such a nervous diarrhea is not rarely met with in hysterical persons. 

Finally, in chronic renal disease, patients sometimes are seized by a profuse 
watery purging designed, apparently, to eliminate from the body certain poisonous 
materials that the diseased kidneys permit to accumulate. 

All of these forms of serous diarrhea occur without being accompanied by much 
pain and without the passage of much flatus. (See Catarrhal Enteritis.) 

Treatment. — The treatment depends largely upon the cause of the disorder. 
If it is due to the ingestion of bad food, the patient should receive a moderate 
dose of castor oil (J to 1 ounce), and with it a dessertspoonful of paregoric to pre- 
vent griping. By this means the offending matter is swept out and a secondary 
constipating influence follows, or can be produced by the measures about to be 
referred to. 

Aside from this all cases of serous diarrhea are to be treated by rest, counter- 
irritation in the form of a capsicum or mustard plaster over the abdomen, the 



566 DISEASES OF THE INTESTINES 

application of external heat if the temperature falls, and the internal use of a 
grain of camphor every two hours for several doses, or of a mixture of aromatic 
sulphuric acid and fluidextract of hematoxylon in syrup of ginger every two hours. 
All foods should be forbidden until the diarrhea is to some extent controlled, when 
predigested milk, arrowroot, and broths may be allowed. 

When the purging is an effort at elimination in Bright's disease, care must be 
taken not to check the diarrhea suddenly, lest toxemia develop. 

CATARRHAL ENTERITIS. 

Acute and chronic catarrh of the small intestine are of frequent occurrence? 
and the symptoms produced in the acute form may be very like those described 
under Serous Diarrhea, save that, as a rule, there is more pain and griping in the 
bowels. In both conditions there is present at first an acute hyperemia of the 
intestinal mucosa, followed by a true catarrhal process, in which the glandular 
epithelium becomes swollen and the submucous tissues infiltrated with exudate. 
A careful examination of the mucous membrane reveals slight, if any distinct 
reddening, except at the edges of the valvulae conniventes. If the process has 
been subacute or chronic the intestinal mucosa is boggy and swollen, but not 
reddened, and the lymph follicles, as well as the mucous glands, are enlarged. After 
some days, rarely earlier, and not in all cases, the swollen solitary follicles may be 
the seat of superficial necroses, shown by yellowish, grayish, or grayish-yellow 
erosions surmounting each follicular eminence; such ulcers are rarely of any size. 
When the process has lasted many days the mucosa may be thickened. It is to be 
remembered that in all of these cases the changes are not confined to the small 
bowel, but are also present in the large intestine as well. 

Symptoms. — Aside from the diarrhea and griping pain already referred to, the 
patient suffers from rumbling in the bowels due to hyperperistalsis, from loss of 
appetite, and weakness due to the abdominal discomfort and the serous purging. 
The stools may be light yellow and very fluid, and in the water which is discharged 
will be found particles of undigested food, cast-off epithelium, flakes of bile-stained 
mucus, and myriads of micro-organisms. The pulse is usually quick, and there 
may be fever of moderate degree. 

Treatment. — The treatment is rest in bed, counter-irritation to the abdomen, 
and full doses of bismuth after the bowel has been swept out by castor oil. 

ILEOCOLITIS OF CHILDHOOD. 

Definition. — The ileocolitis of childhood is a state in which symptom of gastro- 
intestinal disorder develops, as manifested by purging, vomiting, and abdominal 
distress. It cannot be distinctly separated from the catarrhal enteritis of adults, 
either from the stand-point of pathology or symptomatology, yet clinicians have 
universally recognized the fact that such a division at the bedside is advisable. 

Etiology. — The ileocolitis of infancy depends chiefly for its existence upon the 
action of micro-organisms and their poisons on the intestinal mucosa. This 
infection may be produced by a large number of organisms, some of which are not 
pathogenic when the child is in perfect health, and which only become competent 
to cause disorder or disease when, by some additional cause, the general or local 
vitality of the patient is reduced. Thus, it not rarely happens that the stools 
contain myriads of streptococci, staphylococci, the Bacterium lactis aerogenes, or 
the Bacillus pyocyaneus, the pathogenic micro-organism which causes green stools, 
and other bacteria. More important than all, the bacillus of dysentery of Shiga 
and that of Flexner is now known to be a cause in a large proportion of cases. (See 
Cholera Infantum and Dysentery.) Shiga's bacillus produces an extracellular 



ILEOCOLITIS OF CHILDHOOD 



567 



toxin and that of Flexner an endotoxin. The character of the organism which is 
chiefly responsible for the illness is an important consideration since the prognosis 
and the treatment depend to some extent upon a knowledge of the type present. 
On the other hand, it is not always the case that the severity of the illness is in 
direct ratio to their number since a virulent strain in comparatively small numbers 
may cause very severe symptoms of profound toxemia. 

Although we cannot separate cases due to different micro-organisms by the symp- 
toms, for these are much alike, it is important to do so bacteriologically from the 
stand-point of treatment. Thus, if Shiga's dysentery bacillus is present a low 
protein diet and an excess of carbohydrate diet is useful. On the other hand, if 
the gas bacillus is dominant carbohydrates are harmful and lactic acid milk is 
useful because its acid and high content of protein is unfavorable to its growth. 

Fig. 102 



AVERAGE MONTHLY DEATHS FROM INFANTILE DIARRHEAL DISEASES 
DURING 10 YEARS, MODIFIED FROM KOBER 


DEATHS 


























105 
100 
95 
90 
85 
80 
75 
70 
65 
60 
55 
50 
45 
40 
85 
30 
25 
20 
15 
10 

5 












































































































































































































































































































































- 































































































- 


- 












































- 














































JAN. 


FEB. 


MAR. 


APR. 


MAY 


JUNE 


JULY 


AUG. 


SEPT. 


OCT. 


NOV. 


DEC. 



The conditions that usually cause these organisms to develop are exposure to cold 
or excessive heat, so that the bowel is congested and its circulation impaired, and 
the use of foods which are unsuitable in kind or have become so by infection or 
chemical change. Winds carrying dust, flies carrying infection, and air carrying 
gases may all aid in impairing the quality of food. At times the condition develops 
as a result of an attack of an infectious disease, such as measles. Heat and humidity 
not only reduce the resistance of the child, but greatly increase the number of micro- 
organisms in raw foods, especially milk, in which they sometimes number as many 
as 100,000,000 per cubic centimetre. (Park and Holt. 1 ) 

Pathology and Morbid Anatomy. — The ileocolitis of childhood affects particularly 
the lower part of the ileum and the colon, the extent depending upon the vital 

1 Those interested in the effect of temperature, season, and milk supply upon infant mortality should 
read a statistical paper by Park and Holt in the Medical News, December 5, 1903. 



568 DISEASES OF THE INTESTINES 

resistance of the child and the virulence of the infection. Even in those cases due 
to the bacillus of Shiga, the most varied lesions are found. The degree of patho- 
logical change varies within wide limits. In some instances there is only a super- 
ficial catarrh, with some infiltration of the mucous membrane, while in others the 
submucous tissues are affected, and in still others areas of mucous membrane may 
slough. In these severe cases the mucous membrane of the entire alimentary canal 
may show more or less catarrh. 

If the mucous membrane of the small intestine is examined at autopsy, its villi 
are found to be soft and swollen, so that the surface of the bowel presents a velvety 
aspect. In mild cases the hyperemia is not intense. A universal congestion is 
present in severe cases, and even punctate extravasations of blood may be seen. 
The solitary follicles are swollen and protrude above the surface in both the small 
and large bowel and at the summits of follicles beginning ulceration, which rarely 
is extensive, is noticeable. Peyer's patches may also be infiltrated, but they are 
rarely ulcerated. In severe or long-continued cases the solitary glands may ulcer- 
ate, but the agminated glands very rarely. An appearance which at first glance 
may be thought to be an ulcerated Peyer's patch will be found to be due to the 
running together of several ulcers of solitary follicles. 

In severe cases a condition of acute membranous enteritis develops, the lower 
ileum and colon being covered by a thin false membrane, which can be seen in 
some cases only with difficulty. This membrane may be of a yellowish-green hue 
and it lies over a part of the bowel which is greatly thickened by an inflammatory 
process which involves its deeper coats. Curiously enough, ulceration of the 
mucous membrane in such an area is unusual. 

Symptoms. — The symptoms of acute ileocolitis in childhood vary greatly in 
their severity and duration. In the mild catarrhal form there is a slight rise of 
temperature of from 1° to 2°, with several loose movements of the bowel each day. 
These stools have a little mucus in each of them and perhaps a few small flecks 
of undigested food. 

If the condition is more severe there is pain in the bowels, with vomiting, high 
fever, and the frequent passage of yellow or greenish stools containing mucus and 
considerable amounts of undigested food, and if the condition persists the mucus 
may become streaked with blood, and tenesmus may be severe. There is little 
flatus and little odor to the passages. The tongue is coated and anorexia is marked. 

Because of the fever, vomiting, and diarrhea, the patient is rapidly prostrated 
and loses flesh with remarkable speed. 

If the course of the colon is palpated through the tumid abdominal wall, some 
tenderness is usually found. As recovery begins the stools become less frequent, 
have a more normal color, the quantity of mucus decreases, and the fever falls. 
If, on the other hand, at the end of a week or two there is no change for the better, 
the more severe state, in which ulceration of the intestinal lining takes place, is 
probably present, and death may ensue from exhaustion and depression, with 
signs of toxemia. 

If recovery takes place it is very slow, a tendency to looseness of the bowels 
persisting for weeks, mucus being seen in almost every stool, and a relapse being 
threatened at each change in weather or in the food. 

In the well-developed ulcerated form the systemic disturbance is profound and 
often sudden in onset, and its very severity may serve to prevent a sharp febrile 
reaction. The stools are often much fewer per day than in the catarrhal form, 
but they contain more mucus and less blood. Unlike the stools in the milder 
type, these passages smell bad. The belly is distended and the general loss of 
flesh is very severe. The mouth and tongue are dry and foul. 

In the membranous form the stools contain mucus and blood and particles of 
false membrane, which are easily discerned if the stools are first mixed with water 



CHOLERA INFANTUM 569 

and then strained through a sieve. The degree of prostration and evidence of 
toxemia in these cases is very severe, and upon the prolapsed rectal mucous mem- 
brane the false membrane may be sometimes seen. At times such cases present 
at onset, or late in the disease, severe cerebral symptoms which may mask the 
intestinal state. 

Diagnosis. — Ileocolitis must be separated from the typhoid fever of infancy. 
In most cases this is not difficult, because in the typhoid fever of children constipa- 
tion is often present, and the rose spots may be found. The chief diagnostic 
points which separate the two affections are that enteric fever is rare and ileocolitis 
common, that in enteric fever the onset is usually gradual; in ileocolitis it is acute. 
In one there is an enlarged spleen and the Widal reaction; in the other neither 
one of these signs is present. If the illness is due to the Bacillus dysenteric, the 
agglutination test may reveal that fact. (See Dysentery.) 

Prognosis. — The prognosis depends upon several facts. Young children fare 
worse than children after the fourth year. City-bred children succumb more 
rapidly than children in the country, particularly if the weather is hot. Children 
who are strong and hearty at the onset have a better prospect than poorly nourished 
weaklings. High fever, many stools, much vomiting, much mucus, marked 
nervous symptoms and signs of toxemia are of evil omen. 

Treatment. — The treatment of ileocolitis consists in the application of mild, 
continuous, counter-irritation over the abdomen by means of a spice poultice, 
which consists of equal parts of powdered nutmeg, allspice, cloves, and cinnamon, 
moistened with warm brandy or vinegar. If this cannot be had a mustard plaster, 
composed of one-quarter to one-half mustard flour and wheat flour, may be applied, 
the idea being to produce continuous, but not severe, counter-irritation. 

The child's diet should be carefully regulated. If it is passing undigested food 
in its stools, those articles which are not being properly dealt with by the digestive 
apparatus should be withheld. If undigested curds of milk are present, milk 
should be stopped, or diluted sufficiently to make its digestion easy, and pepsin 
and hydrochloric acid, or pancreatin with bicarbonate of soda, should be used to 
aid digestion. Beef-juice, may be administered. If the child is not a very young 
infant its nutrition may be greatly increased by giving strained barley or wheat 
gruel. The digestion of these vegetable gruels should be aided by the use of liquid 
pancreatin or taka-diastase. If there are any evidences of inactivity of the liver, 
minute doses of calomel every third or fourth day are advantageous. 

If mucus is present in considerable quantity in the stools a moderate dose of 
castor oil, varying from a drachm to a tablespoonful, may be used once or twice. 
Griping may be prevented by the addition of a few drops of paregoric. 

In some instances small doses, such as 1 or 2 grains of chloride of ammonium 
dissolves in fluidextract of licorice and water, may be given twice or thrice a day. 
(See Cholera Infantum.) 

If the illness occurs in hot weather, it may be impossible to produce a cure 
without the aid of a change in climate. If the child's home is in the city, removal 
to the seashore may be absolutely necessary; whereas, if the condition develop 
while at the seashore, removal to a moderate altitude of 1000 or 2000 feet is 
advisable. (See Cholera Infantum.) 

Antidysenteric serum may be given if an examination of the stools reveals the 
presence of the Bacillus dysenteric 

CHOLERA INFANTUM. 

Definition. — The dividing line between ileocolitis and cholera infantum is in- 
definite and scarcely justified from an etiological or pathological stand-point, but 
clinically it is often looked upon as a separate ailment. Cholera infantum is an 



570 DISEASES OF THE INTESTINES 

acute affection of infancy characterized by profuse watery purging, rapid emacia- 
tion, and profound depression. It is so closely related to that form of diarrhea 
due to catarrhal enteritis in adults and to that met with in the ileocolitis of infancy 
that it scarcely deserves a separate Consideration from the stand-point of etiology 
and pathology, yet its symptom-complex aids us to some extent in making it a 
distinct entity at the bedside. The malady is almost always met with in the hot 
months of the year. 

Etiology. — The causes of cholera infantum are practically identical with those 
of enterocolitis. 

Pathology and Morbid Anatomy. — When a case of cholera infantum comes to 
autopsy the mucous membrane lining the bowel presents a peculiar pallor, which 
is most marked in the ileum. The colon may show areas of congestion. The 
tissues of the body are shrunken because of the profuse purging, the body is wasted, 
the skin wrinkled, and the eyes sunken. The belly may be distended or collapsed. 
If enterocolitis has been present before the severe choleraic character of the purging 
is developed, the lesions described under the discussion of that disease may be found. 

Symptoms. — Cholera infantum receives its name because its chief symptoms 
are like those of Asiatic cholera, in that profuse watery purging, incessant vomiting, 
and collapse soon develop. The pulse rapidly becomes weak and feeble, the extrem- 
ities cold and the face pinched, so that the expression of the child may be shrunken 
like that of a very aged person. This anxious, pinched look, with a peculiar drawing 
down of the mouth, as if the child were about to cry, is very characteristic. The 
fontanelles are depressed. 

At first the child may be exceedingly restless and peevish, but if the attack is 
severe it speedily becomes apathetic, listless, and finally comatose. Although the 
peripheral temperature is low, the rectal temperature is often very high, even to 
105° or 106°. There is often a mottling of the skin, due to the poor capillary circu- 
lation. Thirst is excessive, and cannot be relieved because of constant vomiting. 
The urine is scanty or suppressed. As the end approaches, the patient develops 
irregular respirations, the head is retracted, the temperature is subnormal, and 
the life ends. When the cerebral symptoms are marked, the condition is called 
one of " spurious hydrocephalus/' a most unfortunate and inaccurate name. 

The symptoms are not only those of exhaustion, but of profound toxemia as well. 

Prognosis. — Given a case of well-advanced cholera infantum, the prognosis 
is very grave. It depends upon the vitality of the child, the severity of the purging 
and vomiting, the degree of response to treatment, and the age of the patient, for 
very young infants seldom recover if the disease is once well developed. 

Treatment. — The treatment of cholera infantum consists first of all in the absolute 
prohibition of milk for twelve or twenty-four hours after the patient is first seen. 
It matters not whether the milk be from the breast or from the bottle, it must 
nevertheless be withheld from the child. Indeed, it may be said that there is 
little use in treating these cases medicinally if milk is given. This is particularly 
so when undigested particles of milk are passed in the stools and if this is the case 
2 to 4 drachms of castor oil is the purge indicated. 

During the period in which milk is forbidden, a rump steak may be heated 
sufficiently to start its juices, then squeezed in a meat-press or lemon-squeezer, 
and this juice, pure or diluted with cool water, may be given to the child. When 
these juices cannot be obtained, or when for some reason they cannot be taken, 
whey, barley-water, rice-water, or a water made by boiling and straining wheaten 
grits may be used. If the diarrhea or intoxication is due to the Bacillus dysenteric 
of either Shiga or Flexner a useful form of food is lactose or milk-sugar as this is 
easily assimilated and is unfavorable to the production of toxic materials by the 
micro-organisms. On the other hand, if the diarrhea be due to fermentative organ- 
isms, lactose will probably make the child worse. The use of lactic acid bacilli as 



CHOLERA INFANTUM 571 

in buttermilk made by means of a pure culture, or in the form of the bacilli in 
powder may be useful when putrefactive changes are present. They are particu- 
larly useful when the child is so feeble that temporary starvation is considered 
unwise. A useful preparation is casein milk made by first preparing curds-and- 
whey in the usual form and then filtering off the whey through a cloth. Push the 
curd through a fine sieve and mix it with one pint of water and one pint of good 
buttermilk made from a good culture of lactic acid bacilli. Small amounts of this 
nutritious and therapeutic milk may be given every few hours. If the stools are 
acid in reaction the lactic acid bacilli are contra-indicated. 

Over the abdomen of the child should be applied a spice plaster, composed of a 
tablespoonful each of powdered allspice, cloves, nutmeg, and cinnamon. This 
should be moistened with warm brandy or vinegar, and renewed as frequently as 
it becomes hard or dry. 

The child should receive internally j-q of a grain of podophyllin dissolved in a 
few drops of brandy, and mixed with a little water just before it is taken, every 
hour until three or four doses have been used; or, instead, -g-J-g- of a grain of bichloride 
of mercury may be given in the same manner. If the vomiting is incessant, it 
may be necessary to get the solution of bichloride or podophyllin into the stomach 
by dropping the medicine into the mouth of the child with a medicine-dropper, 
only introducing a few drops at a time. It is of the greatest importance that 
the liver shall secrete and expel bile into the intestine. The appearance of a little 
bile upon the diaper of the child in place of the colorless liquid which has previously 
been expelled is a most encouraging sign, and its absence is correspondingly dis- 
couraging. 

In children, older than six or eight months, good results sometimes follow the 
use of weak sulphuric acid solutions. Thus, 1 minim of aromatic sulphuric acid 
may be given in 4 tablespoonfuls of cool water every two hours. The acid not 
only acts as an astringent, but it probably also aids in destroying infecting micro- 
organisms. 

If there is much distention of the abdomen, some relief to the tympany may be 
given by introducing a rectal tube through which the gas may escape, and if the 
stools are exceedingly fetid and musty it is often advantageous to irrigate the lower 
bowel with normal salt solution once or twice a day, inserting into the rectum along- 
side the nozzle of the fountain syringe a soft-rubber catheter, through which the 
injected material may readily return. The tube attached to the syringe should, 
however, pass up into the bowel for eight inches or a foot; while the tube of exit 
should be just within the sphincter. 

If much tenesmus is present, with a tendency to eversion of the bowel, 1 or 2 
tablespoonfuls of olive oil containing 2 grains of iodoform may be injected once 
or twice a day, or even oftener, for its local anesthetic effect upon the intestine, 
and after this injection the anus should be supported by the nurse's hand, the ball 
of her thumb, covered by a napkin, being placed between the buttocks to aid in 
the retention of the fluid. 

When symptoms of collapse ensue the patient should be surrounded by hot 
bottles, but care should be taken that a peripheral low temperature is not considered 
as representing the temperature of the central portions of the body, which are often 
highly febrile. When the peripheral temperature is low, the central temperature 
high, and the circulation in the peripheral capillaries is impaired, so that the child 
is somewhat livid and its skin mottled, excellent results will often be obtained by 
immersing it several times, for a fraction of a minute, in quite hot water for the 
purpose of producing a certain amount of reaction, relieving internal congestion, 
and bringing the blood to the surface. If marked fever is present and the extremi- 
ties are hot, good results may come from the use of cold sponging with friction. 

Some practitioners have been in the habit of employing minute doses of mor- 



572 DISEASES OF THE INTESTINES 

phine, hypodermically, or by the mouth. In some instances this method of treat- 
ment may be advantageous, but too often it seems to increase the toxemia from 
which the patient is suffering. 

A very valuable method, which should always be recollected in desperate cases, 
is the use of normal salt solution by hypodermoclysis. 



APPENDICITIS. 

Definition. — Appendicitis is an inflammation involving the appendix vermiformis. 

History. — Although inflammation of the appendix vermiformis had been described 
by a number of physicians many years before Reginald Fitz, of Boston, prepared 
his classical paper on this subject in 1886, the importance and frequency of this 
condition was not appreciated until he called attention to it. 

Etiology. — The causes of appendicitis may be divided into two classes, namely, 
those that depend upon the anatomical structure and position of the appendix 
and those that arise as the result of changes in its walls. 

The appendix vermiformis is a vestige of what was a large and important portion 
of the alimentary canal in our early evolutionary ancestry, and, like most vestiges 
of this character, its tissues are possessed of less vital resistance than are those of 
active organs. This is the first reason why severe inflammatory processes so 
often arise in it. Again, it is a sac the neck of which is usually narrower than the 
rest of its cavity, and as a consequence infecting micro-organisms find their way 
into it, and when imprisoned there by swelling of the mucous membrane rapidly 
attack and destroy the epithelial lining of the appendix and migrate into its walls. 
As is well known, nothing is more favorable for the growth of micro-organisms 
that the presence of warmth, moisture, and a condition in which drainage is im- 
possible. Nothing is less favorable to the vital resistance of a part than swelling, 
with pressure upon the bloodvessels and lymphatic channels. Still another anatom- 
ical cause of disease in the appendix is the fact that the mesoappendix is very short, 
and this results in the appendix being curved or drawn on one side. The meso- 
appendix carries the chief bloodvessel which nourishes the appendix, and if from 
swelling, or other cause, the appendix is distorted or twisted, the circulation of 
blood in the nutrient vessels may be so impaired that the vitality of the part is 
greatly decreased. Again, in those cases in which the appendix is very long (for 
it varies in length from one to six inches) the free end may become attached to 
other parts and become greatly displaced, the appendix itself being twisted. 
Finally, the fact that the appendix lies near, or on, the ileopsoas muscle may aid 
in provoking appendicular irritation, and this is probably one of the reasons why 
appendicitis so often follows violent rowing, golfing, and bicycling. 

Among the causes which exist in the appendix itself, in the sense that they are 
present in its cavity, is the presence of fecal concretions (20 per cent.), and rarely 
foreign bodies, of which a multitude have been recovered, such as pins, tacks, seeds, 
and other objects accidentally swallowed. Occasionally intestinal worms, amebse, 
and other parasites have been found. Foreign bodies, however, are comparatively 
rarely found in this viscus (less than 4 per cent.). Primary tumor of the appendix, 
of which a number, mainly carcinoma, have been reported, appears to be at least a 
predisposing cause in some instances. 

In a very large proportion of cases, nearly 85 per cent., the micro-organism which 
is directly responsible for the inflammation is the Bacillus coli communis, which 
is always present in the bowel, and is benign unless the conditions are such as to 
make it malignant, as when it is confined in a swollen and closed appendix. In 
some instances the streptococcus or the staphylococcus is the cause. Any micro- 
organism capable of exciting inflammation upon gaining access to the appendix 



APPENDICITIS 573 

may be the cause. Thus, the pneumococcus, the pyogenic staphylococcus and 
streptococcus, the typhoid bacillus, and even the ray fungus may act in this way. 

Errors in diet may be a productive factor, for in a certain number of cases of 
appendicitis there is a history that the patient has, a few hours before the attack 
or immediately before it, eaten heartily of ordinary or indigestible food. 

The age of the patient is undoubtedly an important factor in the development 
of the malady. Although it is met with in young children and in old persons — 
that is, after sixty years of age — appendicitis is certainly very much more rare at 
these periods of life than in the interval. For this there is no adequate explanation. 
The period of greatest frequency is from the fifteenth to the thirtieth year, and 
Fitz stated that more than half the cases occur before the twentieth year. 

Another predisposing factor is sex. About six times as many men as women 
have appendicitis. This is in part due not only to greater physical activity, but 
to the more frequent causes of intestinal catarrh in males. It also depends in 
part upon the fact that women have a second blood supply to the appendix, at 
least in many cases, namely, an artery which passes from the right ovary to the 
appendix by means of a fold of peritoneum, which has been called the appendiculo- 
ovarian ligament. By this means a greater blood supply enables the part to combat 
infection when the mesenteric vessel is twisted. 

Appendicitis is more frequent in the well-to-do than in the poorer classes, although 
it might be supposed that the greater muscular exertion in the latter class would 
predispose its members to the malady. 

Pathology and Morbid Anatomy. — A knowledge of the pathology of appendicitis 
makes it possible to understand the symptoms which will be described farther on, 
for these depend, to a large extent, upon the severity of the changes in the appendix, 
and upon the extent to which adjacent tissues are diseased. 

Appendicitis may be divided for pathological study into the catarrhal, obliterative, 
ulcerative, gangrenous, and perforative types. 

In the catarrhal type hyperemia and congestion of the deeper layers of the appen- 
dix may be present, but the chief lesion is in the mucous membrane lining the organ. 
This results in a free secretion of mucus and in distention of the appendix, the 
cervix of which is occluded by the swelling of its lining membrane. By this means 
pain is produced and colic ensues, partly as a result of the endeavor of the appendix 
to expel its contents into the colon and partly as a result of colic in the large bowel 
produced by reflex irritation. It can be readily seen that this state may from this 
point proceed to recovery by a decrease in the constriction of the neck of the appen- 
dix and the escape of its contents, or to a far more grave condition dependent upon 
a continuance of the stoppage, a local and general impairment of resistance, and 
the presence of a virulent micro-organism. If the attack has been preceded by 
others, so that the vitality of the part is already greatly impaired and altered, the 
case is even more grave and the appendix speedily becomes gangrenous or 
perforates. 

Even in the mild catarrhal form just described there are usually left behind distinct 
traces of the presence of the acute attack, and this predisposes the patient to another 
seizure. In those cases in which the catarrhal process is severe and in which the 
submucous tissues are much affected, it not infrequently happens that after the 
acute process passes away a subacute or low-grade inflammatory condition ensues, 
which results in round-cell infiltration and in thickening of the mucous membrane 
and submucous tissues. The epithelium lining the appendix is desquamated 
and slight ulceration may occur, with the result that the calibre of the appendix 
may be greatly decreased in several places, or even entirely closed by the adhesion 
of its opposing surfaces. In this manner appendicitis obliterans is developed. 

If considerable quantities of pus, or mucus, are imprisoned back of the constric- 
tion, pain, tenderness, and attacks of appendicular colic, or true appendicitis, are 



574 DISEASES OF THE INTESTINES 

prone to recur. When the inflammatory process is severe enough to affect the 
external surface of the appendix the free end or side of it may become adherent to 
the bowel or other parts, and by this means the appendix may not only be dis- 
torted and held fast, but the infecting germs may pass through its walls and affect 
nearby structures. 

When the ulcerative type is present, there is greater likelihood of the adjacent 
tissues being infected, owing to the fact that the unprotected submucosa, with 
its lymphvessels, and bloodvessels is a fair field for infection. Ulceration is 
particularly prone to occur if a fecal concretion or other foreign body is present 
which may damage the mucosa. Tuberculosis or typhoid fever may cause it. 
Sometimes a foreign body may be the cause of such deep ulceration that per- 
foration occurs, or in other cases the floor of the ulcer is unable to stand the 
stress of accumulated pus or mucus, and the same accident happens. 

The gangrenous type of appendicitis is the most important of all lesions of the 
appendix, not because it is the most frequent, but because it not rarely changes the 
apparently healthy man of one hour into a corpse within two days, and this 
without, it may be, any history of previous attacks which would lead to the belief 
that the appendix was gravely diseased and unable to resist infection. When this 
state is present in its most severe type, the appendix undergoes rapid necrosis, 
its tissues become gangrenous, and it may slough away completely in so short a 
time as forty hours, so that it may be impossible to find it in the pus which is set 
free by the surgeon's knife, only shreds of tissue being present. In other cases 
the process is not so destructive, but the organ is utterly necrotic and decom- 
posed. In many instances the gangrenous process may not involve the entire 
appendix, but occur in one spot, speedily causing perforation and so endangering 
the life of the patient. 

Gangrene of the appendix arises from the invasion of its walls by virulent infect- 
ing germs when its vitality is impaired by some unknown cause, or it follows from 
thrombosis or capillary stasis in its nutrient bloodvessels, whereby the same destruc- 
tion ensues. Gangrenous appendicitis may be rapid, widespread, and fatal, or 
the vital forces of the patient may be sufficiently vigorous in the work of resistance 
to wall off the infected area by lymph, and so confine the morbid process to the 
immediate neighborhood of the part affected. 

The secondary effects of the pathological processes just described are dependent 
entirely upon their severity and the ability of the patient to protect himself from 
general infection. The acute catarrhal form rarely leaves behind it anything 
more than some thickening of the walls of the appendix, with an associated sus- 
ceptibility to another attack. If all the coats have been involved, the tissues 
about the appendix become filled with lymph, and the consequent induration may 
be extreme, the appendix becoming buried in an adherent mass, which may not 
only hide it from view, but form with the adjacent tissues a matrix, which 
prevents the surgeon from finding the appendix if operation is attempted. 

When the inflammation is severe enough to result in the escape of infection into 
the adjacent tissues, we not only have pus in the appendix, but in the surrounding 
parts as well, a perityphlitic or periappendicular abscess, and in those instances 
in which the appendix is perforated either an abscess is formed and walled off from 
the general peritoneum by adhesions or a general peritonitis ensues. 

The situation of the abscess varies with the direction in which the infection 
escapes from the appendix. If the infection escapes anteriorly the site of the 
abscess is often between the navel and the anterior superior spine of the ilium. 
When it escapes on the surface of the iliac fascia or in the pelvis behind the cecum, 
it, of course, lies behind the peritoneum, not in the serous cavity, and retroperi- 
toneal suppuration develops. From here the pus may burrow in as many ways 
as only pus can burrow, upward to the region of the kidney, downward along the 



APPENDICITIS 575 

psoas muscle into the thigh, or it may discharge into the bladder, the rectum, or 
even into the scrotum. 

On the other hand, it must not be forgotten that appendicular abscess may 
develop with very little systemic disturbance and exist for a long time entirely 
unsuspected, being found by accident, it may be, when seeking for some cause of 
distress and discomfort with impaired health. At other times such an abscess, 
after having developed insidiously, produces signs of septic infection the source of 
which at first cannot be traced. 

Finally, attention must be called to the possibility and frequency with which 
infection of the retroperitoneal lymphatics and of the portal vessels may occur 
from disease of the appendix. Attention has been called to this by several writers, 
notably by A. 0. J. Kelly, and by Munro in the Therapeutic Gazette. Not only 
may retroperitoneal abscess be due to perforation of the appendix behind the peri- 
toneum, but organisms passing along the meso-appendix produce pus when they 
reach the connective tissues in the retroperitoneum. Infection of the portal 
vessels and consequent hepatic abscess is not common, but several cases of this 
character have been reported. 

Symptoms. — It must be manifest from the description just given of the patho- 
logical changes that appendicitis is a malady capable of producing very different 
symptoms in degree and' kind. It is not possible, for this reason, to enumerate 
a set of symptoms present in all cases. There are, however, certain symptoms 
which are fairly constantly present. The most 'constant symptom is pain in the 
abdomen. This may be diffuse, or at least the patient may not be able to localize 
it. Not rarely, if the physician repeatedly asks that it be localized, it is described 
as being in the "pit" of the stomach or in the epigastrium. If the epigastrium 
is pressed upon the pain may be increased. This fictitious localization of the pain 
in the early stages of appendicitis may be most misleading. As a matter of fact, 
however, it should be most indicative, and every person seized with pain of this 
character should be suspected of suffering from appendicitis. In some cases the 
pain is referred to the left iliac region, and it is only when the physician applies 
pressure to the right iliac area that the patient appreciates that that is the real 
centre of his suffering, and by manifestations of an unquestionable character shows 
that the source of pain has been discovered. There is one spot called "McBurney's 
point," situated two inches from the anterior superior spinous process of the ilium, 
on a line drawn from this point to the navel, in which pain on pressure can nearly 
always be elicited. McBurney's point corresponds rather with the origin than 
with the tip of the appendix. 

The pain of appendicitis is usually severe and sharp, and in some cases agonizing. 
It is usually sudden in onset, and for this, and the other reasons just given, it may 
be confused at first with renal or gallstone colic. I have seen more than one case 
in which the diagnosis of acute pleurisy had been made. Occasionally cases are 
met with in which the pain is less spasmodic and more dull in character, but they 
are the exception, and if pain is not marked on pressure the presence of appendicular 
tenderness can be exaggerated by pressing on this part while the patient, lying 
down, raises the thigh from the bed with the leg extended. 

Perhaps the most important fact that can be impressed upon the mind of the 
student in connection with the symptom of pain in appendicitis is this, viz., that 
the sudden cessation of pain in a case of appendicitis is not a good sign, but an 
exceedingly bad one in most instances, for it indicates that the distention of the 
inflamed appendix has been relieved by perforation or gangrene. 

When the pain occurs in paroxysms, it is thought to be due to contractions of 
the appendix — appendicular colic. 

Next to pain, the most important symptom in appendicitis is rigidity or fixation 
of the right rectus muscle. Barring voluntary rigidity of this muscle, which can 



576 DISEASES OF THE INTESTINES 

usually be prevented by diverting the patient's mind from his abdomen, it is a 
sign of great reliability, and its degree often measures the severity of the inflam- 
matory process. 

Vomiting is very commonly present in these cases. In some of them it occurs 
so early as to seem to usher in the attack. This is particularly apt to be the case 
if the stomach has been overloaded with food just before the attack. If the stomach 
is empty at the time of onset, vomiting is often absent. 

The febrile movement in a case of appendicitis is rarely very great. The tempera- 
ture varies from 99° to 101°, and occasionally reaches 102° in adults. In children 
it may be higher. 

The pulse is quick, but not very rapid, unless serious abdominal disturbance 
has already developed. It ranges from 90 to 110 per minute. If it goes higher 
than this, general peritonitis is probably present. Distention of the belly with 
gas is usually a late symptom, and if well marked may be indicative of general 
peritonitis, when it is, of course, a very grave symptom. 

After the malady has been present for some days a swelling in the right iliac 
region may appear and be due to pus or to a large protective exudation of lymph. 
The latter formation is, however, usually met with in relapsing cases rather than 
in primary cases. 

Finally, we meet with cases, usually in women, but sometimes in men, in which 
there is present a true mucous colitis with, it may be, a chronic catarrh of the 
appendix. In these persons a tiny discharge of mucopus may daily infect the colon. 
They are to be considered as cases of chronic catarrhal appendicitis and operated 
upon, not because the appendix is so gravely diseased as because it causes disorder 
in the colon. 

Diagnosis. — When the question arises as to the cause of severe abdominal pain, 
an examination of the blood should be made. If a distinct leukocytosis is present, 
the white cells of the polymorphonuclear group being particularly increased, it is 
indicative of an acute inflammatory process somewhere in the body, and probably 
in the appendix, if the symptoms are appendicular. It is, however, a great mistake 
to allow the determination to do an operation to rest upon this sign, for it has at 
times proved a "hollow reed." At best it is to be regarded as collateral and not 
direct evidence of appendicitis. 

Hepatic colic is separated from appendicitis by the presence of a history of 
previous attacks of colic, by the presence of jaundice in some cases, the presence of 
tenderness over the gallbladder, and by the fact that in gallstone colic the pain is 
referred to the chest between the right shoulder-blade and the spine; whereas, in 
appendicitis it is not so referred. 

Renal colic is differentiated from appendicitis by the pain being referred to 
the testicle, pelvis, or the inside of the thigh; by the fact that the urine contains 
blood, if not macroscopically, at least microscopically; there is no excess of pain 
on pressure over "McBurney's point," and there may be a previous history of 
renal stone. Irritability of the bladder is of no value as a differential symptom, 
as it is often present in both renal colic and appendicitis. In neither form of colic 
is leukocytosis marked. 

Ovarian or tubal inflammation may simulate appendicitis, but a pelvic examina- 
tion will usually reveal these states. The possibility of psoas abscess must also 
be remembered. ' 

In some cases of intestinal obstruction the pain may resemble that of appendicitis, 
but the presence of obstinate constipation, the development of fecal vomiting, 
and the discovery of a mass in the belly elsewhere than at the appendix may enable 
the physician to make a differential diagnosis. 

One of the most important differentiations for the physician and surgeon is 
that between appendicitis and early typhoid fever. At first glance this would 



APPENDICITIS 577 

seem to be easy, but those of experience know that it is often difficult, not that 
typhoid fever often develops suddenly, but that appendicitis may develop slowly 
during a mild influenzal infection, or during an attack of gastro-intestinal catarrh 
that has been obscure in its nature. Further than this, the lymphoid tissues of the 
appendix and nearby parts are usually involved in typhoid fever, and may cause 
appendicular symptoms. (See Plate I.) These localized typhoid lesions may 
cause pain and tenderness in the right iliac area. The absence of very severe 
pain, the failure to find the leukocytosis of acute inflammation, the peculiarly 
coated tongue, the presence of tympany, and the later development of rose spots 
and the Widal test will prove the case to be one of typhoid fever. 

Care should be taken that pain and swelling in this area occurring in one who 
has tuberculosis is not taken for appendicitis. It is not rare to find these signs in 
consumptives who are by no means far advanced in their disease. The condition 
is often one of local tuberculous infection of a chronic type. 

The possibility of acute hemorrhagic pancreatitis being present is to a large 
extent excluded by the fact that it is a very rare condition, by the site of the pain 
and the onset of early collapse in this disease. 

Osier has pointed out that in persons subject to the erythematous eruptions, 
severe attacks of abdominal pain may develop which give rise to a diagnosis of 
appendicitis, which may be excluded only after a careful study of the case with 
reference to this state and urticaria. 

Prognosis. — The prognosis of appendicitis depends largely upon the severity of 
the condition. Statistics which show that a certain percentage of all cases get 
well are of interest, but they do not help the physician in an individual case, 
because definite statements as to the character of the statistics are not given. 
A series of mild catarrhal cases will give a recovery percentage of 100; whereas, 
a series of severe gangrenous cases will give a mortality of 100 per cent. That 
recovery frequently takes place is shown by the fact that about one-third of all 
postmortems show signs of the existence of appendicular disease at some time in 
life, yet there may be no history of such an illness. 

The substance of our present knowledge is that the prognosis in an ordinary 
attack of appendicitis is good for recovery from that attack, but that recurrences 
are likely. In the perforative or gangrenous type the prognosis is always grave 
and often fatal. Much depends upon prompt surgical interference. If this is 
delayed, death is the result in the majority of cases of this type. 

If, however, all cases of primary appendicitis of whatever type are considered 
statistically, it is found that the ratio of mortality is only about 15 per cent, 
under medical treatment. (See Treatment.) 

Treatment. — There is perhaps no more difficult point for decision in medical 
practice than that as to the treatment for appendicitis. It is impossible to discuss 
the vast array of arguments for and against early operative interference in this 
brief space. 

Given a case of appendicitis of the acute type, the first thing for the physician 
to do is to call in a surgeon as a consultant, provided a surgeon qualified to do good 
abdominal surgery, if it is required, is obtainable. If none such can be had, the 
patient is far better off without than with operation. As this is one of the great 
medicosurgical problems of practice, responsibility should be divided. If by non- 
surgical treatment the case can be controlled and carried through the acute attack, 
the surgeon should not interfere, for the mortality of operation in the acute stage 
is far greater than it is when the operation is performed in the interval betwen the 
attacks 

The signs, however, which will force the surgeon to immediate operation when 
the patient is first seen, or if he does not improve under treatment, are: great 
rigidity of the rectus muscle, persistent vomiting, a rapid pulse (above 110), an 
37 



578 DISEASES OF THE INTESTINES 

anxious facies, and, perhaps, as an indication of some importance, a very high 
leukocytosis. In such cases the only salvation of the patient lies in immediate 
surgical interference, and each hour of delay diminishes the chance of recovery. 
The whole question is one of severity. If there is reason to believe that the tissues 
are becoming infected and that the local tissues cannot resist the spread of the 
inflammation, then we must operate. 

Many years ago Fitz showed that 40 per cent, die after surgical measures, and 
11 per cent, after medical treatment; but this does not prove that the latter is better 
than the former, but rather that the surgical cases did not get to the surgeon unless 
desperately ill. At present the percentage of deaths in surgical cases is far less, 
chiefly because they are seen early enough or operation is performed at the time 
of election ; but even at a much later date than that of Fitz's paper we find Caley 
(1899) recording 98 medical cases with 3 deaths, and 102 surgical cases with 22 
deaths. When we consider Sprengel's statistics of 516 cases, 232 of which were 
operated on in the interval with 2 deaths, and 284 during the attack with 57 deaths 
and Sahli's 7000 cases treated medically with 90 per cent, recoveries, the value of 
delay, in mild cases, is evident. 

The plan of treatment in mild cases is as follows: The patient is required to 
take absolute rest in bed. No purgatives are given nor pain-relieving drugs are 
to be used unless the pain is excessive, when enough morphine may be used hypo- 
dermically to take the edge off of the agony, but never enough to make the patient 
comfortable or to make him sleep, for such an effect masks the symptoms. No 
food is to be given by the mouth and no drink is to be taken. If need be, liquid 
can be given by hypodermoclysis or by the Murphy drip method. If the case 
has advanced so far that there are signs of general peritonitis the patient should 
be placed in the half-sitting up or Fowler's posture and be given saline solution 
by the rectum by means of the Murphy drip. If the bowels move, a bed-pan must 
be used. Under this treatment the acute inflammatory process may be arrested, 
and the operation can be performed, if need be, after it has subsided. If by the 
end of twelve or twenty-four hours the symptoms are not rapidly subsiding, it is 
necessary to operate at once. Fowler has shown that when operation is done 
within forty-eight hours 83 per cent, recover. When the cases are left to the fourth 
day 60 per cent, recover; to the fifth and sixth days, 58 per cent; to the seventh 
and eighth days, 50 per cent.; and to the ninth and tenth days, only 33 per 
cent. 

This question of deferring operation to the interval between the attacks is still 
under debate. There are some radicals who insist that operation should be resorted 
to without waiting, and, indeed, before the appendicitis is severe. There are 
others who are content to wait till the storm is past, and still others who believe 
that, given a patient who has had but one attack of moderate severity, he may go 
free until another, or a third attack, makes it evident that a recurrence is likely 
to take place at any time, when he should be operated upon in the interval. As 
Dennis well says : " The plan of allowing the simple catarrhal cases which are doing 
well after thirty-six hours to recover without immediate operation, and relegating 
them subsequently to the group known as interval cases, and the prompt operation 
after thirty-six hours when the cases are not doing well, seems to hold out the best 
prospects for recovery. The pendulum has swung too far toward indiscriminate 
operation. But now the introduction of the interval operation has brought the 
pendulum back to swing within the proper limits." (See Peritonitis.) 

It must not be thought that patients who have recurrent appendicitis can 
be promised perfect comfort by operation, for not rarely, while they recover from 
the operation, they continue to have tenderness and pain in the right groin for 
years, but they will be safe from a death-dealing malady. 



INTESTINAL OBSTRUCTION 579 

INTESTINAL OBSTRUCTION. 

Definition. — Intestinal obstruction is a term applied to a condition of the bowel 
in which, by reason of some mechanical impediment or intestinal paralysis, the 
normal movement of its walls and contents cannot take place. In its acute form 
it occurs as the result of no less than six causes: first, congenital malformation; 
second, invagination, or telescoping of one portion of the bowel within the other, 
or so-called intussusception; third, strangulation by bands, diverticula, membranous 
adhesions, or by attachment to other organs, and by the slipping of a coil of intestine 
through an aperture; fourth, as a result of twisting of the bowel, called volvulus; 
fifth, from lodgement of foreign bodies, as gallstones, etc.; and sixth, from intestinal 
paralysis and distention. 

Chronic intestinal obstruction arises from stricture, from tumors in the bowel, 
from tumors external to the bowel, and from the impaction of fecal masses. (See 
Membranous Pericolitis.) 

Under the name of Lane's kink a condition is recognized in which abdominal 
distress is present as the result of fixation by congenital or inflammatory bands 
of the terminal loop of the ileum. 

Congenital Malformation. — Congenital malformations usually consist in closure 
of the intestinal tube by reason of improper development. Such a closure may 
exist at any part of the alimentary canal from the esophagus to the anus. Rarely 
the bowel becomes strangulated or incarcerated or twisted because of some con- 
genital defect. A common congenital defect is imperforate anus and rectum. 
Less frequently there is atresia at the pylorus. Not rarely children born with 
this condition have other congenital defects in the alimentary canal. In the 
statistics collected by Martin and myself, 28 per cent, of such cases showed more 
than one point of obliteration. In cases in which the atresia does not exist in the 
anus or rectum, it is most commonly found near the ileocecal valve, in the duo- 
denum, or in the sigmoid flexure. 

Symptoms. — The symptoms of intestinal obstruction due to congenital causes 
usually appear after food is first taken. There is no passage of meconium from 
the anus, and the vomited materials are often fecal in odor and in appearance. 
Not rarely violent peristaltic waves can be seen through the abdominal wall. There 
is also pain and efforts at defecation. 

Diagnosis. — An examination of the anus or rectum will usually reveal the cause 
of the trouble. If the finger cannot reach the obstruction, a bougie may discover 
it. In other cases, water from a fountain syringe, hung, not over two feet, above 
the patient's buttocks, may be allowed to flow into the bowel to determine its 
capacity. 

Prognosis and Treatment. — The prognosis is, of course, exceedingly unfavorable, 
but if the closure is near the anus a surgical operation may give relief, and, as 
all die without operation, the knife should always be resorted to. Death ensues 
from inanition or exhaustion. 

Intussusception. — The invagination in this condition is composed of three layers 
of bowel. The intussusceptum is composed of the entering and returning layers, 
while the receiving sheath constitutes the intussuscipiens. To the point where 
the entering layer is turned sharply upon itself to form the returning layer, the 
name "apex" is applied. The word "neck" is applied to the ring which results 
from the flexure formed by the returning layer as it merges into the sheath. 

Intussusception may be separated into divisions, according to the severity of 
the condition, or according to the part of the intestine which is involved. Rafin- 
esque makes three divisions, namely, those which are ultra-acute, death taking 
place within the first twenty-four hours; those which are acute, death occurring 
in the first week; those which are subacute, lasting a month and upward. From 



580 DISEASES OF THE INTESTINES 

an anatomical stand-point, intussusception may be divided into the enteric, in 
which the small intestine is alone involved; the ileocecal, in which the ileum and 
cecum, together with the ileocecal valve, are turned into the colon; and the ileocolic, 
in which the ileum is prolapsed through the ileocecal valve, the latter retaining 
its proper position, at least for a time. When the condition is called "colic," 
it involves the colon only. In still other cases, the rectum is solely affected, forming 
the rectal type of the malady. In the great majority of cases the upper segment 
of the gut is received into the lower, but occasionally the reverse condition occurs, 
and when this happens the term "retrograde intussusception" is applied. Double 
and triple intussusception have occasionally been noted. 

Etiology. — The causes of intussusception are not clearly understood, but probably 
depend upon irregular innervation of the intestine, whereby a sudden, spasmodic 
contraction of one portion of the bowel occurs, the adjacent portion being relaxed. 
Intussusceptions of this character are not infrequently met with at the postmortem 
table, having occurred at the time of dissolution. Polyps of the intestine may be 
forced along the lumen of the canal, thereby dragging the wall at the point of 
attachment and causing intussusception. 

Frequency. — In 1652 cases of intestinal obstruction, excluding hernia, collected 
by Leichtenstern and Bryant, 657 cases, or, approximately, 40 per cent., were due 
to intussusception. It is evident, therefore, that this form of obstruction is not 
rare. Intussusception occurs most frequently during the first twelve months of 
life. After the fifth year it becomes comparatively rare until the fortieth or fiftieth 
year, when it again increases in frequency. The ileocecal region is the favorite 
site of invagination at all ages, but ileum invagination is exceedingly rare. If the 
colic form occurs, it is usually at the sigmoid flexure. 

Pathology. — The pathological changes resulting from intussusception consist 
in an extravasation of the blood into the mucous membrane and mesentery of 
the part affected, and in an acute inflammatory process in the walls of the intestine, 
which particularly affects the serous surfaces of the entering and returning layers, 
so that they become glued to one another. Not infrequently, however, this con- 
dition does not arise, and adhesions do not form. As a result of the strangulation 
of the invaginated bowel, it sometimes happens that this portion of the intestine 
sloughs away, and if sufficiently strong adhesions have formed between the neck 
and the upper portion of the intussusceptum, the coming away of this slough may 
result in the recovery of the patient. Very large portions of bowel have been known 
to be passed in this manner. Pampier has recorded one instance in which 124 cm., 
Bottcher another in which 112 cm. were passed. In other instances, however, 
if gangrene of the bowel develops, perforation and general peritonitis ensue. 

Symptoms. — These depend upon the degree of constriction at the neck of the 
intussusceptum. Usually the first symptom is sudden and violent pain. This 
pain sometimes ceases as suddenly as it begins, the patient being in comparative 
comfort. After an interval the pain returns, and the paroxysms become violent 
and prolonged, with shorter intervals of ease. Pressure does not always elicit 
tenderness; indeed, at times it seems to relieve the pain. Vomiting is an even more 
constant symptom than pain, and usually begins early in the attack, but in adults 
it may be absent. Of all forms of intussusception the ileum invagination is the 
one which is most frequently accompanied by early vomiting, chiefly because it 
produces the most complete obstruction. In children a very constant symptom 
is the passage of bloody mucus. Out of 108 cases, analyzed by Martin and myself, 
occurring in the first year of life, this symptom was absent in only 4. 

Tenesmus and bearing down is also commonly met with. In about one-half the 
cases the tumor can be felt through the abdominal wall,* and under the pliable 
abdominal wall of children it should always be most carefully sought for. Such 
a tumor is most commonly found when the ileocecal type is present. Occasionally 



INTESTINAL OBSTRUCTION 581 

in the colic type the invaginated bowel can be felt in the rectum. The movement 
of the bowel may distinctly change the position of the tumor. 

Prognosis. — The prognosis in intussusception is not very good. Treated by 
the expectant method, the mortality is 70 per cent., according to Leichtenstern. 
The statistics of Martin and myself give a mortality of 90 per cent. The mortality 
is greater in infants than it is in older persons. The sloughing and discharge of 
the intussusceptum is always to be considered distinctly favorable, and Martin 
and myself found that in 408 children in whom sloughing had not taken place 
85 per cent, died, while of 149 who passed a portion of the intestine 41 per cent, 
recovered. Sloughing rarely occurs before the second or third week of the disease. 

Treatment. — The treatment consists in the use of a fountain syringe filled with 
normal salt solution, at the temperature of 105°, and this fluid is to be injected 
slowly at the rate of 4 ounces to the minute. The pressure in the hydrostatic 
syringe should not be over two pounds. This method is available only when 
the intussusception occurs in the lower portion of the bowel. If it is in the ileum 
it is valueless. If, after pressure has been continued for the period of a half-hour, 
the tumor does not disappear under gentle manipulation, abdominal section must 
be resorted to at once. The older statistics in regard to this operation were not 
very favorable, most of them being gathered in pre-antiseptic days. At the present 
time operation gives much more favorable results. 

Internal Strangulation. — Internal strangulation by bands is the next most 
frequent form of intestinal obstruction, forming about 36 per cent, of the classified 
cases. The condition occurs most frequently in males between the twentieth 
and fortieth years, and seems to arise in the majority of cases from a former peri- 
tonitis; although occasionally the bowel is strangulated by slipping through the 
foramen of Winslow or through a slit in the diaphragm. Numerous cases of 
obstruction due to a Meckel's diverticulum have been reported. The diverticulum 
may become twisted or by adhesions to neighboring structures form a constricting 
band. 

Out of 151 reported cases the small intestine was involved in 133. 

Symptoms. — The symptoms consist in sudden agonizing pain which is constant, 
although it has paroxysmal increments. The pulse becomes rapid and weak; 
the temperature is abnormal; the vomiting is persistent, and becomes fecal, but this 
condition of the vomit rarely develops before the beginning of the third day. 
Constipation is present, but fecal matter may be passed from the lower part of the 
bowel once or twice. If a large coil of gut is involved, a distinct area of distended 
intestine may perhaps be found. While the presence of this train of symptoms in a 
young child would be indicative of intussusception, in an adult it is indicative of 
strangulation by a band, for intussusception is rare in adults. 

The only method of treatment which is satisfactory is operative. 

Volvulus. — According to Brinton, this condition occurs in 8 per cent, of fatal 
cases of intestinal obstruction; according to Treves, in 2.5 per cent., and according 
to Martin and the writer's statistics, in 4 per cent. Sometimes the intestine is 
twisted for three or four complete turns. The condition occurs most frequently 
after middle life, and occurs more frequently in men than in women. In 18 cases 
collected by Haven, 16 were men. In Martin's and my own table of 100 cases, 
64 were men. The twist is usually about the mesentery as an axis and involves 
the small intestine. Occasionally it may appear in the colon; rarely the stomach 
may be affected. The twisting of the intestine interfers with its circulation, and 
this, combined with the decomposition of the intestinal contents and the resulting 
distention, soon produces peritonitis, and even perforation. The abdomen is 
prone to become immensely distended. 

Symptoms. — The symptoms consist in absolute constipation, vomiting, and abdom- 
inal distention. Meteor ism is constant. The points in favor of a diagnosis of 



582 DISEASES OF THE INTESTINES 

volvulus are the advanced age of the patient, the fact that the disease usually 
occurs in a male, that the pain is not as agonizing as in other forms of obstruction, 
and that the obstructed bowel is greatly distended. 

Prognosis. — The prognosis is much more favorable than in other forms of intestinal 
obstruction. When intestinal obstruction is due to paralysis, the cause is most 
frequently some injury or an operation upon the abdominal contents. The bowel 
is simply dilated or kinked, and the failure in peristalsis is due to paralysis of its 
muscular fibres. This is the type of obstruction which all abdominal surgeons 
greatly fear as a sequence of operation upon the peritoneal contents. 

Treatment. — When the volvulus is due to paralysis after operation it is to be 
treated by the administration of concentrated salines repeated until the bowels 
are moved. When distention has reached a very great degree and vomiting is 
present, salines are no longer useful. The rectal tube should be passed in the hope 
of exciting peristalsis and drawing off gas. Such cases should be subjected to 
operation. 

Obstruction from Foreign Bodies arises from such articles as coins, pebbles, 
knives, and scissors, gallstones and enteroliths. While gallstones are usually 
small, they at times may be very large, and are often greatly added to by concre- 
tions. Thus, Leichtenstern states that one such stone was five inches in circum- 
ference, and he describes an enterolith nine inches in circumference. Such a 
stone is usually formed by concretions about a foreign body, as a cherry-stone. 
Cases of intestinal obstruction of this character are, however, very rare, about 
0.2 per cent, of all cases. The obstruction is usually found in the small intestine, 
sometimes at the ileocecal valve, and occurs more frequently in females than in 
males. 

ENTEROPTOSIS. 

Definition. — Enter op tosis is a condition in which the intestines fall to a lower 
level than that which they normally occupy. Not only the intestines, but the 
stomach, liver, spleen, and kidneys may be displaced downward, the displacement 
being due to stretching or relaxation of the mesenteric and peritoneal ligaments 
and to laxity of the abdominal wall, so that it fails to support the contents of the 
belly cavity. Of the various names which have been applied to this state, other 
than enteroptosis, may be mentioned splanchnoptosis, visceroptosis, and " Glenard's 
disease." When the stomach is chiefly affected it is called gastrop tosis. Entero- 
ptosis is a condition, not a disease. 

Etiology. — Glenard thinks that overloading the transverse colon with feces 
may cause so great a strain upon that portion of the mesocolon which supports 
the large transverse bowel, particularly at its right flexure, that this part may sag 
and so predispose the rest of the colon to drop downward, drawing with it other 
parts. The objection to this argument is that the right flexure of the colon is 
practically never loaded heavily with feces, or, at least, the instances in which 
it is so loaded are far more rare than is enteroptosis. Further than this, the liga- 
ments concerned in the support of the abdominal contents are not the chief source 
of support. Schwerdt states that they do not bear more than one-eighth of the 
weight. The upper organs are buoyed up by the lower ones, provided these are 
retained in a normal position. Although constipation may be a minor factor in 
producing this state, the chief factors are relaxation of the abdominal wall and 
the loss of fat produced by an acute illness or some chronic disease, and occasionally 
by old age. This affection is not uncommon in the insane, particularly when chronic 
constipation, inactivity, and wasting are associated. The relaxation of the abdomi- 
nal wall may also be due to loss of fat and to repeated pregnancies, particularly 
if the woman has, by wearing corsets, weakened her abdominal muscles and then 



ENTEROPTOSIS 



583 



had them subjected to prolonged distention in pregnancy. Occasionally the 
rectus muscles not only atrophy, but separate. (Figs. 103 and 104.) 



Fig. 103 




Fig. 104 




Enteroptosis due to relaxation of the abdominal wall. Hornet's-nest belly. 



584 DISEASES OF THE INTESTINES 

To appreciate the failure on the part of the abdominal muscles in a well-developed 
case of enteroptosis, it is only necessary to stand behind the patient and place the 
palms of the hands upon the lower zone of the abdomen, pressing upward and 
inward, when the entire weight of the abdominal contents may be felt resting 
upon the hands. The complete inability of the abdominal wall to give support 
is then appreciated. 

Enteroptosis is far more frequent in women than in men. Glenard found it in 
women in 306 out of 404 cases. 

Symptoms. — The symptoms in many cases are by no means definite. The patient 
is often regarded as a chronic dyspeptic, as, indeed, she is. There is more or less 
constant discomfort in the abdomen, and the intestines may be in a state of peristaltic 
unrest, so that borborygmi and rumbling are annoying. At times the bowels seem 
hyperesthetic, and the patient complains, not of pain, but of a sense of movements 
which in health are never felt. Some patients describe the sensation as if their 
abdominal contents were "falling out" of them. Some have a distaste for food; 
others crave it, with the hope that it will relieve the sense of emptiness, and then 
regret taking it because its presence in the displaced stomach increases the distress. 
Constipation is usually persistent, and the use of purgatives may serve to cause a 
great increase in rumbling without causing a satisfactory evacuation. The reason 
for this is evident, for the fallen bowel presents sacculations or depressions that 
act like a plumber's trap and prevent free progress of the contents of the intestinal 
tube. 

Associated with these symptoms there is often a good deal of nervous unrest 
and mental depression, and not rarely some vertigo on changing the posture of the 
body. There may also be cardiac palpitation and breathlessness. 

An examination of such a patient will reveal on inspection, provided a certain 
degree of leanness or emaciation is present, that the abdominal wall is thinner than 
normal, that it is relaxed, and that when the patient stands erect its muscles are 
soft and without tone. In health palpation of the abdominal wall reveals some 
resistance, whereas in this state it yields readily to pressure like the side of a partly 
filled water-bag. Inspection not rarely reveals the fact that the zone of the abdo- 
men between the ensiform cartilage and the navel is empty, and that below the 
navel the abdomen is unduly prominent and sags. 

The appearance of such a patient is often noteworthy, for emaciation may be 
so marked as to raise the suspicion of malignant disease, a suspicion which is 
increased by the anemia which is present. Rarely the patient suffering from 
enteroptosis may develop jaundice because adhesions constrict the bile-ducts. 

If the patient with enteroptosis be placed upon the back in a good light, and 
the abdominal wall observed at a distance, peristaltic waves may often be seen 
traversing it. Tapping the knuckles of intestine through the abdominal wall with 
the finger-tip will increase or arrest these movements for a moment. 

Deep palpation may reveal the liver much lower than normal. That this is 
not due to an enlargement of this organ may be proved by the discovery that as 
its lower border passes down into the abdomen its upper border also becomes 
lower, the actual area of liver dulness on percussion being the same as in health. 
The liver is, however, rarely out of place, except in extreme cases. 

Distention of the stomach with gas from a Seidlitz powder, or by pumping air 
into it with an atomizer bulb attached to a tube, will reveal its abnormal position, 
and if it is carefully outlined it may be found that this viscus occupies a more 
vertical position than in health, the pylorus being greatly displaced, while the 
cardiac portion is in a relatively normal posture because it is more firmly suspended. 
The cardia is very rarely greatly displaced, but Steele has reported five such cases 
in a comparatively short time of observation. Ptosis of the stomach is not rarely 
associated with dilatation and with motor insufficiency. (For the measures by 



ENTEROPTOSIS 585 

which the presence of gastroptosis can be determined see article on Gastric 
Dilatation.) 

The spleen is very commonly displaced. It may be well forward in the median 
line, or it may fall more directly downward and be found as low as the pelvic organs. 
Nephroptosis is described in the section devoted to Diseases of the Kidneys. 
During the performance of deep palpation there can sometimes be felt a moder- 
ately firm mass lying transversely in the abdomen in the epigastric area. This 
is said by Glenard to be the colon, but if this be the case the colon is not much 
displaced, and is certainly contracted rather than dilated — a condition opposed 
to that stated by Glenard to be usually present. Ewald believes that this mass 
is the pancreas which has been uncovered by the enteroptosis. 

Auscultation of the belly in these cases often reveals a large number of liquid 
sounds, and if the patient is shaken there may be heard succussion notes and 
sounds which may be called " slopping. " 

While some patients with moderate enteroptosis present many of the symptoms 
just described, it is a fact worthy of note that others with very marked falling 
of the abdominal contents often have no complaint to make of the abdominal 
state, and if they are told of it at once become mentally "centred" on their ali- 
mentary tract, and, if already neurasthenic, speedily drive themselves and their 
medical attendant almost demented by their constant discovery of new symptoms. 

Treatment. — The treatment of enteroptosis is manifestly to be directed to the 
support of the displaced organs and their replacement. Not rarely, if the physician 
stands behind the patient and presses upon and lifts the abdominal contents by 
pressing the hands in front of the abdomen, relief from the sense of abdominal 
relaxation is at once noticed. 

The adjustment of a properly filled abdominal belt or binder is, therefore, a 
valuable aid in this condition. It should be applied every morning before rising 
and not until after the patient, by gentle strokings with her hands, has placed the 
abdominal contents at about the proper level. Its greatest pressure must be 
exercised inward and upward in the zone below the navel. Sometimes the use of a 
broad flannel binder about the lower zone may be sufficient, but the support must 
be upward as well as inward. 

Great care should be taken as to diet. Starches and milk, both of which are 
prone to produce flatulence, should be avoided. If starch is used in an easily 
digested form, as rice and cornstarch, some taka-diastase should be given with it. 
Cheese and beans are absolutely forbidden, and fats are also harmful. Small 
quantities of green vegetables may be taken, and roast or broiled beef and mutton 
allowed at each meal. Eggs are also permissible. The patient should be warned 
against eating heavily at any one time, since an overweighted stomach or colon 
will make the ptosis much worse. If gastric dilatation exists, lavage may be useful. 

In the way of drugs, there are only three which produce much benefit, namely: 
nux vomica in full dose — say, \ grain four times a day; extract of physostigma in the 
dose of | grain four times a day; and capsicum, 1 grain three or four times a day. 
Sometimes it is well to combine all of these in one pill or capsule. 

In the way of digestants, hydrochloric acid and pepsin, or soda and pancreatin, 
and taka-diastase are to be employed. As laxatives, cascara sagrada and aloes 
may be used, 1 grain of the extract of the former and yV grain of aloin being given 
once, twice, or thrice a day, according to the obstinacy of the bowels. The bitter 
fluidextract of cascara given in capsules is the best preparation to employ. 

In cases in which the symptoms are so severe. as seriously to impair health and 
comfort and even the chances of life, operative interference is indicated, the dis- 
placed organs being fixed by suturing. Up to the present time quite a number 
of such cases have been operated on by different methods, Duret, in a case in 
which the stomach came within four inches of the pubis, placed stitches through 



586 DISEASES OF THE INTESTINES 

the lesser curvature of the stomach, then through its anterior wall, and made it 
fast to the peritoneum of the anterior abdominal wall. Recovery followed. In 
other cases the intestines have been raised by taking a reef in the mesentery. 
Rovsing has fastened the stomach by three stout sutures passed through the abdomi- 
nal wall and through the outer coats of the stomach, with the result that the patient 
gained forty pounds in weight. Beyea has taken tucks in the gastrophrenic and 
gastroheptic ligaments, with good results, and Webster has treated a large number 
of cases by excising the tissues between the recti muscles and then stitching the 
edges of these muscles together, thereby affording support for the abdominal 
contents. 

COLITIS. 

Acute Colitis. — This is a very common condition and follows exposure to cold, 
particularly if the abdominal contents have been the parts chiefly deprived of 
warmth. The inflammatory process chiefly affects the lower part of the colon 
and extends to the rectum as well, so that proctitis is developed. The primary 
hyperemia of inflammation is followed by an increasing secretion of mucus, with 
the throwing off of dead epithelial cells mixed with white and red blood corpuscles 
which have escaped from the engorged vessels. If the process is very severe, a 
suppurative state may be developed. In most cases the tendency is to rapid 
recovery, but if the inflammatory process persists, one of two conditions may be 
developed, either small areas of necrosis or ulceration occur, or there is deposited 
in the submucous tissues a considerable amount of connective tissue, which may 
by its contraction impair the function of the glands and perhaps narrow the calibre 
of the bowel. 

Symptoms. — The symptoms consist in severe abdominal pain, with tenderness 
in the region of the sigmoid flexure, and in frequent movements of the bowels, which 
movements soon become very small, so that they finally consist in nothing but a 
little mucus, which is passed with great tenesmus. 

Treatment. — The treatment consists in the use of absolute rest in bed. The 
application of a mustard plaster over the sigmoid flexure and the injection into 
the bowel of 4 ounces of starch-water, with 40 grains of potassium chlorate and 
30 drops of deodorized laudanum, every three or four hours. 

Acute infectious colitis has already been considered in the article on Dysentery. 

Mucous Colitis. — Definition. — Under the name of mucous colitis physicians meet 
with a condition which is, next to dysentery, the most common affection of the 
colon, and in temperate zones is more frequent. It affects persons suffering from 
neurasthenia, in the great majority of cases, and is met with in the overworked 
or overwrought of both sexes, but most frequently in women of from twenty to 
forty years of age. 

The affection is a chronic one, often lasting for several years, and during its 
continuance causing a great impairment of nutrition and much general ill-health. 
Not rarely the irritable state of the colon causes constant abdominal distress. 
Severe colicky pain is also present, and a state of hyperperistalsis of the small 
bowel exists, so that food is often hurried on into the large bowel before it can be 
digested and absorbed; the patient suffering from lienteric diarrhea, not because 
the digestive power is impaired, but because the food does not remain in one part 
of the small bowel long enough to be digested. The stools are not as frequent 
as those of other kinds of chronic diarrhea. 

Mucus in considerable amount is often passed, and this mucus may be so thick 
that it resembles a false membrane, whence the term " mucomembranous colitis." 
Not rarely the patient has excessive peristalsis every time food is taken. 

Blood is almost never passed unless there are hemorrhoids which bleed. There 
is no fever, but profound mental depression. Areas of marked tenderness can 



COLITIS 587 

be found in the abdomen on palpation, and the cutaneous sensibility is often 
increased. 

Treatment. — The treatment of mucous colitis, while it is not capable of producing, 
in the majority of cases, very marked improvement within a short time, is neverthe- 
less successful in a large proportion of patients, provided that it is carefully and 
persistently carried out, and if the patient's mode of life and her diet is arranged 
in such a way as to be favorable in their effects. As the majority of these patients 
have been subjected to nervous stress and are neurasthenic, it is essential that they 
shall be subjected to the rest cure, in order that by re-establishing nervous tone 
and equilibrium a normal intestinal peristalsis and normal digestive functions may 
be established. Without rest in cases of this character other treatment is commonly 
useless. 

. In order that the greater part of digestion and assimilation may be carried out 
in the stomach and duodenum, foods easy of digestion and readily assimilated 
should be given, and should consist chiefly in proteids, that is, broiled or roasted 
meats. Green vegetables and fatty foods should not be allowed. Easily digested 
starches, such as rice and cornstarch, may be given, provided that pancreatin 
or taka-diastase is given with them to hurry their digestion. All vegetable foods 
which leave a bulky residue should be forbidden, as, for example, oatmeal and 
wheaten grits. The patient should take liquids in small quantities frequently, 
rather then in large quantities at long intervals, and should avoid taking liquids 
with her food. She should also avoid taking liquids before going to bed at night, 
as not infrequently liquids taken at this time seem to lie in the bowel unabsorbed, 
and on the assumption of the erect posture by the patient in the morning a morning 
diarrhea is developed. 

Continuous counter-irritation, produced by frequently repeated applications 
of tincture of iodine over the whole abdominal surface, should be maintained, and 
if there is much tenesmus a suppository containing 5 to 10 grains of iodoform 
may be inserted into the rectum in the morning after a movement of the bowels, 
not only for its local counter-irritant effect, but for the beneficial influence of the 
iodine, when absorbed, upon the catarrhal condition of the bowel. In some cases 
where the colon is chiefly at fault, clysters of 1 or 2 quarts of hot normal saline 
solution, or of pure water containing 20 grains of sulphocarbolate of zinc to the 
pint, should be gently given, care being taken that the fluid does not run in so 
rapidly as to irritate the bowel. The patient should lie on the left side until the 
sigmoid flexure is filled, then turn on the back while the transverse colon is filled, 
and perhaps after this turn on the right side with the hope that the fluid will enter 
the ascending colon. 

In those cases in which there is a history of repeated mild attacks of appendicitis, 
or of pain in the right iliac region, appendectomy sometimes produces excellent 
results, the chronic colitis being due to the infection of the colon by small quantities 
of pus which escape from the appendix. Probably the enforced rest which follows 
an operation for the removal of the appendix also is advantageous in producing 
a cure in these cases. When there is relaxation of the belly wall and enteroptosis 
the patient should wear a supporting belt. 

Follicular and Croupous Colitis. — Follicular colitis, sometimes called nodular 
colitis, is a form of inflammation of the colon characterized by marked swelling 
of its solitary glands, or lymph nodes, rendering these structures unusually pro- 
tuberant. After this primary stage of enlargement necrosis and sloughing ensue, 
leaving round ulcers, which are frequently numerous. By the failure of these to 
heal the more chronic state of ordinary ulcerative colitis is developed. 

Ulceration of the colon is, of course, also due, in many cases, to the typhoid 
bacillus, the tubercle bacillus, the Entameba dysenterice, and sometimes to infection 
by Shiga's bacillus. It also develops as a terminal infection in some cases of chronic 



588 DISEASES OF THE INTESTINES 

renal disease. Ulcerative processes in the intestines are very common in the insane, 
and they have been found associated with locomotor ataxia. 

Under the name of croupous colitis, a condition exists in which the mucous 
membrane of the colon becomes engorged and coated with a false membrane, 
and the underlying tissues becoming filled with dead leukocytes and fibrin. As 
in the small bowel, so here, this false membrane may be widely diffused or occur 
in patches. After the formation of the membrane the disease either disappears 
by the exfoliation of necrotic material or the deeper coats of the bowel are affected, 
so that areas of submucous tissue become necrotic and are passed in the stools as 
sloughs. At the site of these sloughs healing by cicatrization develops, or the 
process extends still more deeply to the peritoneum and causes serious secondary 
lesions. In this way is formed a necrotic colitis, the ulcerated areas being gangren- 
ous in appearance and of great size. A large number of pathogenic organisms have 
been found in the bowel in such cases. 

Treatment. — This consists in following a plan identical with that advised for 
mucous colitis, and in addition in giving an injection of nitrate of silver in the 
strength of 40 grains to the quart each evening in place of the normal saline already 
spoken of. This should not be retained. 

Pseudomembranous Colitis. — This is a condition in which not only the large 
intestine, but the small bowel as well is affected by a superficial necrosis, which 
may be diffuse, but is more commonly distributed in patches. The process closely 
resembles croupous colitis, and by some writers the two conditions are held to be 
identical. The false membrane consists of dead epithelium, mucus, fibrin, and 
white blood cells which have passed out of the bloodvessels. In some cases the 
false membrane is almost purely mucin-bearing and quite fibrin-free; the latter 
element is only exceptionally abundant. Not rarely the submucous tissues may 
be infiltrated by serum and leukocytes. 

Pseudomembranous enteritis develops in the course of a number of the acute 
infectious diseases, in pyemia and septicemia, in persons who suffer from chronic 
Bright's disease, and occasionally after the taking of poisons which cause gastro- 
intestinal irritation. It is important to recall the fact that this pseudomembranous 
condition is not diphtheritic in the sense that it is due to the Klebs-Loeffler bacillus, 
and that the proportion of fibrinous exudate is far less than in the membrane of 
that specific disease called diphtheria. Perhaps the most common cause of this 
lesion is the ingestion of poisonous quantities of arsenic, for this drug is eliminated 
by the mucous membrane of the alimentary canal and in the process a necrosis of 
the lining epithelium takes place. 

SPRUE (PSILOSIS). 

Definition. — Sprue (Atrophic Enteritis of the Tropics) is not a distinct morbid 
entity; it is but a terminal condition of many devitalizing and depressing factors. 
Sprue may be defined as a chronic catarrhal inflammation of the entire alimentary 
tract tending ultimately to most extensive atrophy of the gastro-intestinal glandu- 
lar structures, characterized clinically by three cardinal symptoms — sore mouth, 
flatulency, and diarrhea. 

Sprue is a disease of the entire tropical world. The Malayan Archipelago, 
particularly the Philippine Islands, South China, Amoy, Ceylon, Java, and the 
Malayan Peninsula are the regions of its greatest development. 

It is not seen in subtropical or temperate zones, unless in imported cases, with 
the exception of Japan and northern China. It has been known by many names, 
all of them referring to one or another of the peculiar clinical manifestations of 
the disease. Thus, it has been called "diarrhea alba," "aphthse tropica, " "Ceylon 
sour mouth," and "white flux." The name sprue was given to it by the Dutch, 



SPRUE 589 

who found it a veritable plague in their Javanese possession. Since the United 
States has acquired colonies in the sprue region, imported cases have become fairly 
numerous throughout this country, and their consideration is of great interest to 
the general practitioner. 

Etiology. — Extensive studies of the disease have failed to show any specific 
etiological factor. There is some argument whether sprue should be considered a 
specific disease or whether it should be considered as a terminal state following 
other lesions. Sambon maintains the former. Extensive studies by army surgeons 
in Manila show that the latter view is the correct one. The disease commonly 
develops in the tropics, but may lie dormant for years after the return of the colonist 
to his home in the temperate zone. 

The conditions that predispose to the development of sprue are the following: 
The large majority of cases follow chronic amebic dysentery and its sequelae, 
chronic ulceration of the colon and abscess of the liver, with prolonged suppuration. 
Following dysentery the intestinal parasites, and chief of these the uncinaria, are 
common antecedents of sprue. Next is the general deterioration in chronic malarial 
poisoning, and lastly syphilis is a cause. To these must be added the physical 
deterioration incident to prolonged residence in hot climates, even when no acute 
illness is suffered, and the following depressing conditions: childbirth and mis- 
carriage, chronic disease of the kidneys, suppurating lesions anywhere, excessive 
fatigue, long marches, and prolonged campaigns. Some writers report the develop- 
ment of sprue as following the prolonged administration of iodides and mercury. 
Numerous organisms have been described as the cause of sprue and several parasites, 
particularly the strongyloides. Amebse are almost constantly found and various 
bacilli of the typho-colon group, but these must all be considered remnants of the 
preceding pathological condition rather than direct causes of the disease itself. 

Pathology. — Postmortem examination shows complete loss of subcutaneous 
and mesenteric fat. The tissues and cavities are extremely dry; the small intes- 
tine presents extreme thinning of its walls with atrophy of the mucosa and, in 
some cases, entire destruction of the glandular structures. The serous coat is 
normal. Swelling and ulceration of Peyer's patches are seen, and in many cases 
the colon presents the usual appearances of recent or present dysentery. Paren- 
chymatous changes occur in the pancreas, liver, and kidneys, and occasional areas 
of fatty degeneration are present. 

Symptoms. — Sprue is essentially a very chronic disease. The average duration 
is from one to two years, although cases lasting ten years or more are not by any 
means unusual. The patient is emaciated and anemic. The complexion is muddy 
and sallow. There is great lassitude and weakness, and mental irritability with 
pronounced disinclination for physical and mental labor. The disease passes 
through numerous stages of amelioration and numerous recrudescences, but its 
general tendency is always downward. The principal symptoms of sprue are sore 
mouth, diarrhea, and flatulence. 

The mouth lesions of sprue are constant and striking. On examination the 
tongue is found unusually clean. The organ is small, pointed, and somewhat 
yellowish. Along the dorsum of the tongue, along its edges, and on the under 
side, particularly along the frenum, there are numerous, fine, minute ulcers, with 
a thin, aphthous pellicle. These aphthous spots may also be present on the uvula 
and palate. Very commonly the tongue is covered with very superficial erosions 
from one-eighth to one-fourth of an inch in diameter, frequently coalescing and 
resulting in a serpiginous appearance. Where these marked lesions are temporarily 
absent, the tongue still has an unusually clean, dry, glazed appearance, and looks 
very much as though it had been recently varnished. The condition in older 
patients may be very much accentuated and extensive fissures may develop. The 
patient complains of soreness that may be limited only to the tongue, or may 



590 DISEASES OF THE INTESTINES 

involve the palate or uvula, or the entire mouth. He particularly complains 
of burning or a stinging pain on taking salt or highly seasoned food. Occasionally 
the pain is also present on deglutition, and the progress of the food bolus on its 
way to the stomach is indicated by a burning and stinging pain in the gullet, showing 
that the esophagus is in the same condition as the mouth. Nausea and vomiting 
are sometimes present in advanced cases, the vomiting coming on without reference 
to the time of taking food. Eructations and waterbrash are present; the appetite 
is very variable, sometimes being entirely absent, at other times ravenous. 

Flatulence is quite marked. The patient is swollen until the abdomen is tense 
and drum-like. In this condition the appearance of the very much emaciated 
figure, with extremely thin arms and legs, and large, inflated abdomen, is very 
characteristic. The flatulence is always aggravated by taking food and is accom- 
panied by a constant sense of oppression and a gnawing and burning pain in the 
stomach. 

Diarrhea is the most distinctive and constant symptom. There may be only 
one or two movements daily or there may be as many as ten or twelve. They are 
usually passed without pain; they vary very much in their character, but are 
nearly always liquid or semiliquid. They are frothy, white, and have a fetid, 
mouse-like odor. Manson describes them as looking like recently stirred white- 
wash. They are usually remarkably large. Their reaction is commonly acid. 
Microscopically they are found to contain bowel structure, a few red blood cells, 
and intestinal parasites, of which amebse are the most frequent. 

As the disease advances emaciation and asthenia become extreme. The skin 
is dry and scurfy, the patient is unable to assimilate or retain food, and, in many 
instances, he involuntarily abstains from it on account of the severe pain in the 
mouth and throat. In all marked cases there is secondary anemia, the red blood 
corpuscles being reduced as low as 1,000,000, with some degree of poikilocytosis 
and no leukocytosis. 

Diagnosis. — Diagnosis presents no difficulties, when the existence of such a 
disease as sprue is known and its cardinal symptoms are remembered. Incomplete 
cases in which one or the other symptom may predominate or be absent may give 
rise to some difficulties. 

Sprue in particular must not be confounded with chronic dysentery, although 
it is difficult, in cases where sprue develops from dysentery, to definitely mark 
the period where the one disease begins and the other ends. 

Prognosis. — If treatment is instituted before the atrophy of the bowel is too far 
advanced, cure is the rule. If, however, so much of the secreting surface of the 
bowel is destroyed as to make assimilation impossible, death is, of course, inevitable. 

Treatment. — Treatment consists in putting the patient on absolute milk diet. 
He should preferably be kept in bed and milk administered in small feedings. 
The quantity is increased as rapidly as possible, the mouth symptoms and the 
appearance of unchanged milk in the bowel movements being the index as to the 
quantity to be taken. If there be any increase in the amount of soreness of the 
mouth, the milk must be reduced for a time and later gradually increased, until 
the patient is taking from four to six quarts daily. This regimen must be persisted 
in from four to six weeks after the mouth symptoms disappear and the bowel 
movements become solid. Then soft diet should be resumed very carefully. 

Where milk cannot be taken, pure meat diet may be used or an exclusive diet 
of meat-juice. Success has also attended the exclusive use of a fruit diet. Recent 
observations have shown the value of fruit, particularly of berries, in the treatment 
of sprue as well as chronic dysentery. Manson reports the case of a man over 
fifty years of age, at which time of life the prognosis in cases of sprue is exceedingly 
grave. The patient was first treated, with little benefit, with milk diet and other 
special diets; finally the patient was put on a diet of strawberries. The stools 



DILATATION OF THE COLON 591 

at once improved and the patient was soon restored to health. This was not the 
only case in which recovery followed the use of strawberries. Manson considers 
this a decided advance in the treatment of sprue. Medicinally salol and Dover's 
powder may be given for control of the diarrhea. For their tonic and reconstructive 
properties iron and arsenic should be used. These drugs have been shown to be 
of particular advantage in this disease when used by hypodermic injection. 



DILATATION OF THE COLON. 

Hale White places dilatation of the colon in four divisions. The first of these is 
that type of dilatation which is due to acute distention from the accumulation of 
gas. This is not rarely met with in severe infectious diseases, as in the pneumonia 
of drunkards and in severe cases of typhoid fever with toxemia. The distention 
of the colon under these circumstances often interferes with the action of the 
lungs and heart by mechanical pressure against the diaphragm. The zone of the 
abdomen between the umbilicus and the ensiform cartilage, and between the right 
and left hypochondrium is distinctly bulging and tympanitic on percussion. Tym- 
panites of this kind possesses a double significance: first, it is an evil in itself by 
reason of the pressure which it produces, and, second, its presence is evil in that it 
indicates a lowered vitality and an inability of the intestine to expel gas which 
otherwise would not be allowed to accumulate, and which in health would not form. 

The treatment of this form of tympanites consists in the application of a hot 
turpentine stupe over the abdomen and the injection into the rectum of 6 ounces 
of milk of asafetida containing 1 drachm of oil of turpentine, the two fluids being 
thoroughly mixed in order to prevent the turpentine from damaging the bowel. 
In other cases, where it is considered advisable to stimulate the circulation at the 
same time that the gas is expelled, and when it is feared that the turpentine may 
be absorbed and irritate the kidneys, excellent results will follow the use of this 
quantity of milk of asafetida with the addition of \ to 1 ounce of Hoffmann's 
anodyne. Pituitrin may be given hypodermically. A few years ago it was suggested 
by Ogle, and others, that puncture of the bowel through the abdominal wall should 
be performed in those cases in which the gas could not be dislodged and when it 
was causing dangerous pressure. While this advice is theoretically good, practically 
it is of little value. I have tried it in a number of instances, and it has either failed 
entirely or has permitted but a small quantity of gas to escape from a single knuckle 
of intestine, the bowel contracting in such a manner as to prevent most of the gas 
from finding its way to the aspirating needle. If a fine needle is used but little 
gas can escape, while if a coarse needle is employed a sufficiently large puncture 
may be made in the bowel to permit of the escape of gas or liquid into the peritoneal 
cavity after the needle is withdrawn. 

When obstinate constipation is present, and the sigmoid flexure is filled with 
feces, an ordinary soapsuds enema, followed by 1 ounce of sulphate of magnesium 
in 4 ounces of water and 2 ounces of glycerin, may be injected. 

The second group of cases depends upon the accumulation of foreign bodies. 
These are so rare in human beings as to be scarcely worthy of consideration. Occa- 
sionally, however, the dilatation may be due to the presence of enormous gallstones 
which have been still further increased in size by fecal additions. Such cases are 
to be treated by operation. 

The third form is that due to obstruction of the lower part of the colon, so that 
fecal accumulation and secondary ulceration may occur. The obstruction may 
be due to volvulus, to a band or to a coil of adherent small intestine. It is also 
due to stricture or to syphilitic, cicatricial, or neoplastic growths, particularly 
cancer. These cases are very rare, and the treatment is operative. 



592 DISEASES OF THE PERITONEUM 

Finally, in the fourth type we find cases of so-called idiopathic dilatation of 
the colon, which are also exceedingly rare. Many years ago Formad reported an 
extraordinary case of this character, and Hale White has collected several from 
literature. In most of these instances the enormously dilated colon is loaded with 
accumulated fecal matter. 

Treatment can be of little value in the last type of cases, for a congenital defect 
in the muscular and other tissues forming the wall of the intestine is responsible 
for the condition. Relief may, perhaps, be given by making an artificial anus at 
the sigmoid flexure. 

Membranous Pericolitis. — Closely associated with these types of cases are those 
in which much abdominal discomfort arises from membranous pericolitis or Jack- 
son's membrane. Whether this is a congenital defect or the result of inflammation 
is not known. The false membrane runs across the ascending colon to the proximal 
part of the transverse colon. It tends to cause stasis in the ileum as well as in 
the large bowel and often causes acute angulation of the hepatic flexure. Its 
diagnosis can only be made by careful fluoroscopic examination after the taking 
of bismuth or by exploratory operation. 

Adhesions, Displacements, and Redundancy of the Colon. — During recent years 
medical literature has teemed with articles on these conditions chiefly written 
by surgeons. There can be no doubt that adhesions in the neighborhood of the 
caput coli often are the cause of distressing symptoms and if they can be broken 
up by surgical interference, and can be prevented from forming again the patient 
is greatly benefited by operation. This holds true in some cases of adhesion else- 
where. Concerning displacements it may be said it is questionable if they are 
really abnormalities, for the more we study £-ray pictures of the intestines the 
more sure are we that they move about over a wide area without indicating that 
their function is impaired. Little can be done for them surgically although much 
is attempted. (See Enteroptosis) . As to redundancy here again it is questionable 
if surgery should be resorted to. We do not know as yet how many people have 
sigmoid flexure which are longer than they should be without symptoms to justify 
us in operating, because a given patient with abnormal symptoms is found where a 
sigmoid is an inch or two longer than the anatomical average. There is no more 
reason for operating on a sigmoid flexure, because instead of its being eight to ten 
inches long it is found to be twelve inches long, than there is for operating on a 
spermatic cord because in a given case one testicle hangs lower than the other to 
a degree greater than the average. Some cases are benefited by operative inter- 
ference, many cases are not. As my colleague Gibbon has well said, in discussing 
this subject, " A great many things in surgery are easily done that ought not be 
done." 



DISEASES OF THE PERITONEUM. 

ACUTE PERITONITIS. 

Definition. — Peritonitis is a term applied to inflammation of the serous membrane, 
the peritoneum, lining the abdominal cavity and covering in its reflections the 
organs which this cavity contains. 

Etiology. — Within comparatively recent years it was generally considered that 
acute peritonitis was usually idiopathic, but with an increasing knowledge of 
the methods by which infection occurs, we have come to learn that all cases of 
peritonitis are due to an infection which has come to the peritoneum through 
primary disease or the presence of infecting organisms in other organs. Nearly 



ACUTE PERITONITIS 593 

half a century ago Habershon found, in an analysis of 501 autopsies after death 
from peritonitis, that over 50 per cent, resulted from some primary disease not 
involving the peritoneum, and Kelynack, in studying 124 cases of acute peritonitis, 
found that everyone of them developed the disease as a secondary lesion. 

It may be true that exposure to cold and severe strain are productive of peritoni- 
tis, but if this is the case it is only because these influences diminish the vital 
resistance of the peritoneum. 

The two great causes of peritonitis are appendicitis and disease of the Fallopian 
tubes. In both of these instances it is due to the extension of an inflammatory 
process, which in turn arises chiefly from the spread of infecting micro-organisms. 

The method by which pathogenic micro-organisms are enabled to pass through 
the walls of an inflamed appendix has already been spoken of in the article on 
Appendicitis, and it is worthy of note that any cause which seriously interferes with 
the health of even a small part of the intestinal wall may permit the escape of 
micro-organisms into the general peritoneal cavity. Of the micro-organisms which 
commonly produce peritonitis under these circumstances, the Bacillus coli com- 
munis is, perhaps, the most frequent, but a large number of other micro-organisms 
are often present, and there is every reason to believe that they are active in the 
production of the inflammatory process. Next to the Bacillus coli communis 
stands the Streptococcus and the Pneumococcus, the Staphylococcus albus, and the 
Bacillus pyocyaneus. The Bacillus aero genes capsulatus is also not infrequently 
present. Occasionally the Bacillus typhosus seems to be responsible for the 
process. 

When infection takes place by means of the Fallopian tubes, the peritonitis 
may be due to the gonococcus; but in the majority of instances the inflammatory 
process is not due to this organism, but to the streptococci or staphylococci which 
are associated with it; the presence of which, perhaps, enables the gonococcus to 
become pathogenic in this serous membrane. Bumm, however, believes that 
the escape of the gonococcus into the peritoneum is not usually follewed by evil 
results. On the other hand, pure cultures of the gonococcus have beon obtained 
from the abdominal cavity in two cases of acute general peritonitis by Young and 
Cushing. 

Subacute or chronic peritonitis is often due to the Bacillus tuberculosis and acute 
miliary tuberculosis of the peritoneum, which is usually looked upon as a form of 
acute peritonitis, is necessarily the result of the infection by the tubercle bacillus. 
In the acute peritonitis following labor, the so-called septic peritonitis, the strepto- 
coccus is the chief factor. Cases of peritonitis due to the pneumococcus have been 
frequently recorded. 

While we know, therefore, that peritonitis in its acute forms is a secondary 
infection, it must not be forgotten that in a very large number of cases the peri- 
toneum is capable of resisting infection and of destroying micro-organisms which 
may gain access to it. Indeed, the vital resistance of this membrane when in 
health is very remarkable, and a number of investigators have shown that it is 
possible to place in the peritoneal cavity considerable quantities of septic material 
without serious result, provided this serous membrane is not subjected at the same 
time to insult whereby its vitality is decreased. 

Certain diseases which greatly decrease vital resistance greatly increase the 
susceptibility to peritonitis, as, for example, typhoid fever, Bright's disease, and 
advanced arteriosclerosis. 

Peritonitis in children, of course, develops as a result of the causes already 
enumerated. It also is sometimes seen in young infants suffering from congenital 
syphilis, and in those who have intestinal obstruction. In still other cases it 
follows infection of the umbilicus after birth. In still others it is due to an extension 
of infection in empyema, and a few cases are on record in which sewer-gas poisoning 
38 



594 DISEASES OF THE PERITONEUM 

has seemed to produce an epidemic of this character among children exposed to its 
influence. 

Strumpell states that a form of localized peritonitis in the left groin is occasionally 
met with in children, that it is prone to be purulent, and that the pus usually 
escapes through the rectum. 

Pathology and Morbid Anatomy. — The characteristic appearance of the peritoneum 
in primary acute peritonitis is hyperemia, with a diminution in the normal glossiness 
of the membrane involved. This is followed by a more or less copious fibrinous 
exudate, which may be well distributed, or appear chiefly in patches, upon the 
parietal and visceral peritoneum. In many cases there is but little fluid exudate, 
the small quantities present being found in pockets formed by the coils of intestine 
which become agglutinated. In other instances the fluid portion of the exudation 
is very much more copious, and the quantity of fibrin thrown out is also of consider- 
able amount, so that it is not only found well distributed over the surface of the 
membrane, but free flakes may be found floating in the serous exudate as well. 

When the infection is due to pyogenic micro-organisms, and particularly in 
those cases in which the vital resistance of the patient is very low, a septic peritoni- 
tis speedily develops. It is usually very diffuse in such cases, the entire peritoneum 
being involved. The quantity of exudate is moderately large, and is often offensive 
in character, forming what has been called "putrid peritonitis." In other cases 
when the vital resistance is not so depressed, the presence of pyogenic micro-organ- 
isms produces a peritonitis in which pus alone is present. This form of peritonitis 
may be widespread, but is often localized — the so-called loculated or circumscribed 
peritonitis or peritoneal abscess — nature being able to wall off the area of acute 
infection by a plastic exudate, which prevents the infection from becoming well 
distributed throughout the peritoneum. In those cases of septic peritonitis in 
which death occurs early, the physician may be surprised on opening the abdomen 
at autopsy to find that but little change has taken place in the appearance of the 
peritoneum and its contents. Save for some duskiness of the peritoneum and the 
presence of sanious fluid, the abdominal contents may seem to the naked eye to 
be but little altered. 

Occasionally we meet with what is known as hemorrhagic peritonitis, which 
may follow severe septic infection, and in cancerous and tuberculous cases, with 
ulceration, the fluid in the abdominal cavity may be blood-stained. 

Localized peritonitis, such as has already been referred to, is most frequently 
found in connection with diseases of the pelvic organs in women and with cases of 
appendicitis. It may be considered the rule rather than the exception, for the 
disease to be limited by an inflammatory exudate in such cases. Other forms 
of localized peritonitis which are not so frequently met with depend upon an exten- 
sion of infection from the gall-bladder, from perforation or infection through a 
gastric ulcer, and occasionally we find a suppurative peritonitis in the lesser peri- 
toneum as the result of disease of the pancreas or fat-necrosis. In other instances 
this condition arises as the result of renal calculus and nephritic abscess. 

Symptoms. — There are few diseases which, when well developed, produce a 
train of symptoms more characteristic than are those of acute peritonitis. This 
holds true, however, only when the disease is well advanced, and, indeed, is so 
severe that there is grave doubt as to the patient's recovery. In most cases of 
peritonitis, when' the physician is first called to the patient, severe pain in the 
abdomen is the chief condition which is complained of. The pulse is usually 
quick, small, and hard, and the belly wall tender on palpation, and distinctly 
rigid. The face will be found to wear an expression of anxiety, which seems to 
be far out of proportion to the length of the illness and its severity. In many 
instances, even when the pains are exceedingly severe, the patient considers that 
he is suffering from acute indigestion, but acute indigestion is often relieved by 



ACUTE PERITONITIS 595 

pressure, and is usually accompanied by tumidity of the abdomen; whereas, peri- 
tonitis is characterized by great abdominal tenderness and by a flat or scaphoid 
appearance of the belly wall. The pulse is tense and rapid. The fever is usually 
not very high. It often does not go above 102°, and frequently not over 101°. 
Vomiting is frequently present. 

After the pains have been present for a few hours, the exquisite tenderness of 
the abdomen makes the weight of the bedclothes insupportable, and, in order to 
obtain some relief for the abdominal tension, the patient usually lies on his back, 
with the knees up, and supports the bedclothes over his abdomen by his hands, 
looking with dread upon the approach of the attendant lest he touch the abdomen 
or jar the bed. Thirst which cannot be relieved, because of constant retching, 
may add to the patient's distress, and hiccough of a very persistent and exhausting 
character often develops. 

As the disease progresses, the belly, which has been tense and scaphoid, becomes 
hard, not from muscular spasm, but from abdominal distention. In the flanks 
percussion may reveal some flatness due to the accumulation of the exudate in 
these parts. The face not only is anxious in appearance, but rapidly becomes 
pinched and peaked, the eyes appear sunken, the nostrils are thin and drawn, the 
skin pale and livid, and the tongue dry and parched, the typical " Hippocratic facies." 
The pulse at this stage is exceedingly rapid, running, and wiry, and, as the end 
approaches, loses its tense character. A cold sweat may break out about the 
wrists and on the forehead. 

The bowels are usually obstinately confined, but in some instances diarrhea may 
be present, particularly if diarrhea has been a symptom of the case prior to the 
development of the peritonitis. The respirations are usually a little quickened, 
but are shallow and superficial, in order that the abdominal movement may be as 
slight as possible. A remarkable fact in connection with these cases is the preserva- 
tion not only of consciousness, but the development of intense mental activity, 
which in some cases persists up to the moment of death, the patient showing an 
acuteness of mind which is startling. In some instances during the last hours 
there may be a mild delirium, or even slight stupor. 

In septic cases pain is absent in the majority of instances, but the temperature 
in the early stages may be much more febrile than in the ordinary types of the 
disease. Sometimes it is distinctly like that of early septicemia. By the time 
that the septic inflammation is well developed, however, the fever usually falls 
to the neighborhood of normal, and it may reach subnormal. 

Careful examination of the abdomen in cases of well-developed peritonitis not 
only reveals the local symptoms already described, but it may also show localized 
patches of tympany where gas has accumulated in the coils of intestine, which are 
more or less fixed in one position by inflammatory adhesions. These coils, partly 
because of the inflammation and partly because of distention, may soon become 
paralyzed, so that distention increases. 

When the peritonitis is due to a perforation of the intestine or of the stomach, 
the accumulation of gas in the peritoneal cavity may mask the area of liver dulness 
or completely obliterate it. At one time this was considered a very valuable sign 
in the diagnosis of perforation with secondary peritonitis, but we now know that 
in many instances this symptom is absent. 

Complications and Sequelae. — Peritonitis usually runs such a rapid course, either 
to recovery or death, that complications are rarely met. The most important 
and most frequent complication of a serious nature is pneumonia. In 100 cases 
of peritonitis observed in the London Hospital, Treves found that no less than 
17 developed pneumonia or pleurisy after the peritonitis began. Retention of 
urine is frequent. 

As a second intestinal obstruction may develop as the result of adhesions or 



596 DISEASES OF THE PERITONEUM 

by strangulation of the bowel, produced by the slipping of a knuckle of intestine 
through an opening under a band or a false ligament, or by the development of a 
twist of the bowel through interference with its peristaltic movement. 

Diagnosis. — The diagnosis of acute diffuse peritonitis is usually readily made, 
even in its early stages. In its late stages its symptoms, except in the septic 
form, are so characteristic that the diagnosis can be made on a most superficial 
examination of the patient. 

In certain cases of typhoid fever in the early stages, when the inflammatory 
process in the intestines is acute, there may be a good deal of abdominal pain and 
considerable tenderness. The apathetic expression of the face, the higher tem- 
perature of typhoid fever in the stage of onset, the tumid belly, and the coated 
tongue, with red edges, will aid in its differentiation. 

The separation of intestinal obstruction from peritonitis is exceedingly difficult; 
but as they often are coincident, the one following the other, and the treatment 
of such cases the same, differentiation is unnecessary. The rapid onset of severe 
pain of a cramp-like character, the complete absence of any movement of the 
bowels, the presence of intestinal unrest, and in intussusception the palpation of a 
mass may make the diagnosis possible. 

Certain cases of hysteria at times present symptoms so characteristic of peritonitis 
that even the most skilful may be misled. Every symptom may be presented, 
yet the patient always recovers. 

Acute hemorrhagic pancreatitis may also so closely resemble peritonitis that a 
diagnosis is impossible, but this malady is exceedingly rare. In it there may be a 
preceding history of gallstone disease, whereas in peritonitis, unless perforation 
of the gallbladder has occurred, there is no such history. 

The pain of gallstone colic and renal colic is so localized that much difficulty 
in diagnosis does not exist, as a rule. 

In cases of perforation of the stomach with secondary pyopneumothorax sub- 
phrenicus, the differentiation may be exceedingly difficult, save that swelling in 
the epigastrium and a history of gastric ulcer may be present. 

When perforation of the stomach has occurred without the formation of abscess, 
so that the gastric contents and gas escape into the peritoneum, great tympany 
and modification of the area of liver dulness is found. Not infrequently in sub- 
phrenic abscess a pleural effusion exists, so that serum may be drawn from this 
level and pus from the level below the diaphragm. 

Occasionally, in children suffering from pleurisy, pericarditis, and pneumonia, 
violent pain is complained of in the abdomen, which may mislead the physician, 
if he be not on his guard. 

A high leukocyte count indicates only an inflammatory process somewhere in 
the body. 

Prognosis. — The prognosis in every case of well-developed acute diffuse peritonitis 
is distinctly unfavorable. If the physician has reason to believe that the peritonitis 
is localized, the outlook becomes more promising. A good deal depends, too, upon 
the cause of the peritonitis, and upon the character of the infecting micro-organism. 
Thus, if is follows perforation of the stomach or bowels, and it is not walled off 
from the general peritoneal cavity, and again, if a skilful surgeon is not at hand to 
operate at once, the prognosis is hopeless. When the infection after perforation 
is localized, the mortality is not so great, but this form of localized peritonitis is 
far more fatal than that form which is due to appendicitis. 

The duration of life in fatal cases of peritonitis varies very greatly. Death 
may come as early as thirty-six or forty-eight hours, or may be deferred for a 
week or ten days, or even longer. 

Treatment. — The treatment depends so entirely upon the cause of the peritonitis 
that it behooves the physician to study the case most carefully. If seen shortly 



ACUTE PERITONITIS 597 

after the onset of the malady, the physician should at once consider the possibility 
of perforation of some portion of the alimentary canal being responsible, and should 
examine carefully into the history of the patient as to the possible presence of 
gastric ulcer or intestinal ulcer due to typhoid fever or dysentery. If the patient 
is an adult, careful consideration of the possibility of extension of inflammation 
from the gall-bladder should be followed. It is hardly necessary to state that as 
appendicitis and diseases of the Fallopian tubes are the most common causes of 
peritonitis, the condition of these two parts should be most carefully inquired into, 
both as to previous history of the patient and as to the physical signs which may 
be present. If the peritonitis is diffuse and has followed perforation or strangula- 
tion, the salvation of the patient depends upon immediate surgical interference, 
unless, perchance, shock prohibits operation, when it is permissible to wait two 
or three hours, in the hope that by the use of external heat and stimulants the 
patient may be enabled to better bear surgical measures. If, on opening the belly, 
a diffuse general peritonitis is found, it would seem best, in the majority of cases, 
to resort to the plan suggested by J. B. Murphy, namely, to remove the appendix 
if it can be reached, close the perforation if it exists, introduce a drainage tube into 
the pelvis, place the patient in a semirecumbent posture and give a quart of normal 
saline solution by the rectum every two or three hours. 

When it is due to appendicitis, the age and general physical condition of the 
patient must largely influence the decision as to operative interference. I agree 
with McCosh, who states that in aged persons, particularly if they have been 
dissipated, medical treatment gives better chances than surgical interference, 
while the reverse holds true in young persons. If a surgeon of experience cannot 
be obtained, medical treatment will always give the best results. 

The question as to the procedure which should be followed if the cause lies in 
the appendix has already been discussed in the article on that disease. 

The profession has passed through three periods of fashion in regard to the drug 
treatment of peritonitis itself. Forty years ago it was extensively taught that 
general peritonitis should be treated by the administration of massive doses of 
opium, which were not only sufficient to relieve pain completely, but also to produce 
mental quiet. Under the leadership of Alonzo Clark, of New York, enormous 
doses were sometimes given, as much as 258 grains of opium being given in a day; 
and while it is undoubtedly a fact that patients with peritonitis are able to take 
large doses without being poisoned, this plan of treatment received its death-blow 
with the discovery that nearly all cases of peritonitis are due to an infection, and 
that the source of infection must be discovered, and, if possible, removed or drain- 
age at least established. The use of opium has therefore become obsolete because 
it masks the symptoms, and is thought to have no definite influence upon the prog- 
ress of the disease, save that it diminishes the suffering of the patient. It is prob- 
ably safe practice to administer a sufficient quantity of morphine or opium to 
diminish agony, but not enough to mask the symptoms or make the patient so 
comfortable that he will refuse operative interference when the physician thinks 
it advisable. 

Soon after the infectious nature of peritonitis was recognized, the profession 
went to the extreme of purging with saline cathartics, and even with vegetable 
cathartics, all cases in which symptoms of acute peritonitis were manifest. There 
is no doubt that this method was used to excess, and at the present time we know 
that it is unnecessary and probably harmful. 

Counter-irritation applied over the abdomen in the shape of a large number of 
leeches may be useful in sthenic cases. In other instances a light mustard plaster 
may be used for relief. In still others an ice-bag has been employed. It is useless. 
Thirst may be relieved by the use of small pieces of ice, or, better still, by rinsing 
the mouth with glycerin 1 part and water 3 parts, to which has been added a few 



598 DISEASES OF THE PERITONEUM 

drops of lemon-juice. Liquids should not be swallowed, as they increase the ten- 
dency to vomiting. If thirst is excessive, fluid may be supplied to the tissues by 
hypodermoclysis or by the rectal drip method. As a rule, the patient does not 
live long enough in well-developed peritonitis to make the question of feeding an 
important one. If the focus of infection is removed by operation, the feeding 
is that used after all abdominal sections. 

CHRONIC PERITONITIS. 

Chronic peritonitis occurs in four forms, namely: a local adhesive process; a 
diffuse process; one characterized by a proliferation of inflammatory material and 
connective tissue; and in a hemorrhagic form as a complication of severe disease in 
adjacent organs or malignant disease of the serosa. 

The local adhesive type is often found in the neighborhood of such organs as the 
liver, spleen, and stomach, when, as a result of an acute inflammatory process 
in the visceral peritoneum covering the organ, an adhesion takes place, and, per- 
haps, thick fibrous bands develop. In many of these cases this condition is not 
even suspected during life. In the neighborhood of the pelvic organs this type 
of peritonitis is exceedingly common, and is, perhaps, the most frequent peritoneal 
lesion met with by the gynecologist. Sometimes intestinal obstruction results 
from a slow, chronic, inflammatory process, which glues a knuckle of intestine 
to the omentum or the anterior wall of the peritoneum. 

In the diffuse but chronic type of peritonitis a condition closely resembling that 
of fibrous tuberculous peritonitis develops, so that the peritoneal cavity is prac- 
tically obliterated, and the coils of intestine are often matted together so that it 
is impossible to separate them. The parietal layer of the peritoneum is greatly 
thickened, and all the abdominal organs seem to be constricted and drawn by the 
cicatricial process. 

Closely allied to the last type is the proliferative form, in which the changes are 
not very different, except that there is, in addition, a considerable quantity of 
serum in the abdominal cavity. Sometimes this may be present in such quantities 
that the belly is greatly distended. The omentum is rolled up as a window-shade 
is rolled up, and extends across the upper zone of the abdomen in a round mass. 
The intestines may, or may not, be adherent to one another, the presence of the 
fluid serving to separate them and to prevent dense adhesions taking place. At 
times some of the fluid may be divided off into pockets by the adhesions. This 
form of proliferative peritonitis is usually due to tuberculosis, and not infrequently 
complicates alcoholic cirrhosis of the liver, but it is generally believed that in some 
cases it may arise from other causes than tuberculosis. Even if the cause is not 
tuberculosis the condition may, however, very closely resemble it on palpation, 
because nodules may be found. (See Tuberculosis of the Peritoneum.) 

In cases of carcinoma of the viscera a chronic form of peritonitis associated with 
the exudation of blood-stained or hemorrhagic serum is occasionally met with. 
Indeed, the obtaining of such serum from a case of ascites is always to be considered 
as indicative of that form of peritonitis depending upon malignant growth. As a 
rule, the chief lesions are found in the pelvis, or there may be present a general 
carcinomatosis of the peritoneum. In other cases the pelvic viscera may be 
coated with fibrinous exudate, which undergoes connective-tissue changes, and 
becomes highly, vascularized. 

Friedreich has described a form of chronic hemorrhagic peritonitis which follows 
repeated resort to paracentesis abdominis, the entire peritoneal surface being 
granular, reddened, and dotted with extravasations of blood. 

Chronic Adhesive Sclerotic Peritonitis. — This is a very rare state, apparently met 
with more frequently in Germany than in the United States. It was described 



ASCITES 599 

by Virchow in 1853, and in more recent times by Riedel. It consists in an extensive 
subperitoneal fibroid infiltration or sclerosis, without ascites and without serous, 
or serofibrinous, or purulent fluid in the abdomen. In other words, it is rather a 
disease primarily involving the subperitoneal connective tissue than a true chronic 
peritonitis. This hyperplasia results in a sclerotic process, which in turn produces 
contractions and retractions, and, by the formation of adhesions, fastens organs to 
the abdominal wall. The symptoms are those of the chronic fibroid type of tuber- 
culosis peritonitis already described, but the condition is not due to tuberculosis. 
Wetherill states that the peritoneum shrinks so that when abdominal section is 
performed it is impossible to approximate its edges on closing the wound. 

For a description of the so-called "iced liver of Pick" see Adhesive Pericarditis. 

MORBID GROWTHS OF THE PERITONEUM. 

Cancer of the Peritoneum. — This is an exceedingly rare condition as a primary 
lesion. In all probability when it does occur, it is an endothelioma rather than an 
epithelioma. 

Carcinoma and carcinomatosis of the peritoneum are usually if not always 
secondary to cancer of some contained viscus. The primary growth may be 
so small as to escape superficial examination even at autopsy, and is commonly 
in the stomach, pancreas, or biliary passages, or, less frequently, in the rectum; 
in the female the pelvic organs are by far the commonest site of the prirr ary growth. 
On account of the pervious nature of the diaphragmatic lymphatics, the pleura?, 
pericardium, and peritoneum may be simultaneously affected, or invasion of one 
may be quickly followed by extension to the others. 

The symptoms of either the primary or secondary carcinoma of the peritoneum 
are emaciation, ascites, and, it may be, the discovery of nodules, or of a furled 
omentum, such as occurs in certain types of peritoneal tuberculosis. The fact 
that the fluid is often hemorrhagic has already been referred to. In the colloid 
cases the peritoneum may be filled, not with fluid, but with a jelly-like substance, 
which is so firm that it will not fluctuate. 

Other Growths of the Peritoneum. — Hydatid cyst of the peritoneum is occasionally 
found, although, as a rule, it develops in the abdominal organs rather than in the 
peritoneum itself. A cyst the size of an orange has been reported by Jones as 
occurring in the mesocolon. It was successfully removed. Rein has reported a 
multiple hydatid cyst occurring in the omentum of a woman in the third month 
of pregnancy. She was operated on and recovered. Other instances have been 
reported by various clinicians, the largest number of cases collected being those of 
Moneger, who has reported 32. He tells us that such cysts are nearly always 
secondary to rupture of cysts in neighboring organs, and there is usually a history 
of violent pain at the time of rupture. Perhaps the most extraordinary case is 
that reported by MacDonald, who has reported the case of a man with thirty 
hydatid cysts of the peritoneum. Other cysts of the mesentery are chylous, 
dermoid, serous, and sanguineous. 

Very rarely sarcoma and cystic adenoma affect the peritoneum. 

ASCITES. 

Definition. — Ascites is a symptom, not a disease. The term ascites is applied 
to the accumulation of serous fluid in the abdominal cavity. In some cases the 
quantity of fluid is very small, but in others it amounts to several gallons. 

The fluid in ascites is usually of a light straw color, and does not coagulate 
when exposed to the air. 



600 DISEASES OF THE PERITONEUM 

Etiology. — The intra-abdominal causes of ascites, as just stated, are atrophic 
cirrhosis of the liver, tuberculous peritonitis, and morbid growths, which, by 
pressure upon bloodvessels, or by producing changes in the peritoneum, result 
in a transudation of fluid. A thrombophlebitis, or other form of venous obstruc- 
tion, may also cause ascites. Thrombosis, tuberculosis, or neoplastic invasion 
of the thoracic duct, or its obstruction by parasites (filarise), or other causes, and 
also wounds of the duct or of the receptaculum, or larger lymph-vessels or chyle- 
vessels may produce an ascites the fluid of which contains chyle. In cases of 
chronic Bright's disease of the parenchymatous type, ascites is often present as 
part of the general anasarca. 

Symptoms. — When the abdomen of a patient suffering from ascites is exposed, 
it is seen to be greatly enlarged, this enlargement being chiefly in the lower and 
lateral zones, although if the intestines are by chance distended by gas the upper 
and middle zone may be much enlarged. The line of the ribs is usually sharply 
defined, by reason of the fact that they do not yield readily to the pressure and 
are held in place by the diaphragm. 

If the ascites be due to hepatic cirrhosis, the venules about the navel will often 
be found engorged (see Cirrhosis of the Liver), and in all forms of ascites due to 
venous obstruction the veins under the skin in the right and left hypogastrium 
and groins may be surcharged with blood in an endeavor to establish a collateral 
circulation, and so relieve deep pressure in the venous trunks. 

The signs of fluid in the abdominal cavity are dulness on percussion in the flanks, 
and in the suprapubic region when the patient is semirecumbent, with tympany 
over the anterior and middle zone of the abdomen extending upward to the epigas- 
trium, owing to the intestines being floated up against the anterior abdominal 
wall by the fluid beneath. If the hand of the nurse is placed with its ulnar edge 
upon the middle line of the abdomen, the left hand of the physician placed on the 
right flank, and the right hand used to lightly strike the left flank, distinct fluc- 
tuations will be felt by the left hand, the impulse being transmitted by the fluid 
from one side to the other, the hand of the nurse being used to prevent the trans- 
mission of this impulse by way of the abdominal wall. Changing the patient's 
position from the recumbent to the erect posture will change the area of dulness 
on percussion and the shape of the abdomen, owing to the alteration in the position 
of the fluid. Palpation will reveal fluctuation if the belly is not too tense. Per- 
cussion will give a tympanitic note in the epigastrium when the patient is sitting 
up and flatness below the navel and at the sides of the abdomen. 

A patient who has ascites to any considerable degree is usually unable to lie 
with the head low, because if this attitude is assumed the pressure of the fluid 
against the diaphragm is such that breathing is interfered with. For this reason 
he usually sits propped up in bed or in a reclining chair. The face, which is usually 
thinner than in health and somewhat haggard, forms a striking contrast to the 
large abdomen, which is "aldermanic" in appearance, and if the legs be dropsical 
as well, the massiveness of the lower half of the trunk, as compared to the upper 
half and to the neck and face, presents a striking picture. Not rarely the face 
bears the expression known as the " abdominal fades." 

Dyspnea may not be noticeable when the patient is at absolute rest, but it not 
rarely happens that so slight an exertion as conversation will develop this symptom, 
particularly if, in addition, there be some tendency to edema at the bases of the 
lungs. As a rule, men are more uncomfortable when suffering from ascites than 
are women, because their respiration is naturally more diaphragmatic than that 
of women, whose respiratory movement is chiefly costal. 

Diagnosis. — Ascites must be differentiated from distention of the abdomen 
due to a large ovarian cyst. This can usually be accomplished by palpation, 
percussion, and vaginal examination. Inspection of a case of a cyst will usually 



ASCITES 



601 



reveal somewhat greater distention of one side of the abdomen than the other. 
The area of dulness on percussion will not be in the lower zone of the abdomen 
alone, but will extend upward toward the ribs and will include part of the area in 
the anterior and middle zone of the belly, which in ordinary ascites is tympanitic. 
Change of posture with cyst does not greatly change the area of dulness. Further 
than this, a large ovarian cyst of this character will usually be tense and will 
offer more resistance when the abdomen is palpated with both hands. 

Fig. 105 




Case of enormous ascites due to atrophic hepatic cirrhosis. 

From enlargement of the spleen in chronic leukemia ascites may be differentiated 
by reason of the fact that in this disease the area of dulness is chiefly in the upper 
zone instead of in the lower zone of the belly, that tympany is usually not present 
in the middle line if the spleen extends so far, and that the edge of the spleen can 
be readily palpated. In some cases, however, in which the spleen is enlarged 
in leukemia, ascites is also present, and it may be impossible to feel the edge of the 
spleen until some of the fluid is -removed. This removal may be more difficult 
than in an ordinary case of ascites, because the spleen may be so close to the anterior 
abdominal wall and may extend so far down toward the pubis that ordinary para- 
centesis cannot be readily performed without danger of puncturing the spleen. 
Ascites must also be separated from great enlargement of the liver, as in hyper- 
trophic cirrhosis. Here, again, the presence of dulness in the right upper zone of 
the abdomen and the ability to feel the lower edge of the large liver will aid mate- 
rially in the differentiation. In both enlargement of the spleen and enlargement of 
the liver the area of dulness and of tympany is not materially altered by changing 
the posture of the patient as it is in ascites. 

Treatment. — The treatment of ascites depends to some extent upon its cause. 
If it is due to interference with the circulation by pressure, as in atrophic hepatic 
cirrhosis, little can be done except to remove the fluid by paracentesis, for the 
purpose of giving the patient relief from distention. If it is due to cardiac disease 
an improvement in the condition of the heart by the use of digitalis and rest, and 
the- judicious administration of saline purges, may remove the fluid. In renal 



602 DISEASES OF THE LIVER 

disease the use of purgatives may also be of value, but paracentesis has usually 
to be resorted to if the fluid is present in large amount. In peritoneal tuberculosis 
paracentesis may be of value, but the best method of producing cure is to resort 
to abdominal section, permitting the fluid to escape through the incision, and then 
maintaining drainage. 

Before performing paracentesis abdominis the patient should be made to evacuate 
his bladder, in order that by no possibility can it be punctured by the trocar. 
If the patient be a woman, great care should be taken that an ovarian cyst is not 
punctured. Puncture of a papillomatous cyst not infrequently results in the 
early death of the patient. 



DISEASES OF THE LIVEE. 



INFLAMMATION OF THE LIVER. 



Acute Hepatitis or Hepatic Abscess. — Definition. — Acute exudate hepatitis is a 
state of inflammation of the liver in which, after a stage of hyperemia with 
exudation, the area involved undergoes necrosis, and abscess results. 

Etiology. — Inflammation of the liver, severe enough to result in suppuration, 
may arise from injury, from inflammation of the portal vein or of the bile-ducts, 
or from adhesions to neighboring organs which are infected and from which infection 
may spread, as, for example, in cases of gastric ulcer. 

Suppuration within the substance of the liver beneath its capsule or in the bile 
passage occurs under many varying conditions. 

Traumatic Abscess. — Liver abscess may result from traumatism. The trauma- 
tism may be a severe blow or contusion, or a penetrating wound in or near the 
liver from a bullet, knife, or other weapon. Traumatic abscess of the liver is 
usually single. When it occurs as a result of contusion in the absence of direct 
infection, the injury acts by lessening resistance and permitting colonization of 
pyogenic bacteria brought to the organ by the portal vein or hepatic artery. 

Pyemic Abscesses. — Pyemic abscesses are v as a rule, multiple. One group 
of cases arises from pyogenic embolism of the portal vein. There is phlebitis 
or thrombophlebitis of the portal trunk or its branches, the infection being due 
to ulcerations in the colon and rectum, or to appendicitis, ulcerations and suppura- 
tive processes about the neck of the bladder, and typhoid fever. Another group 
of cases arises from embolism of the hepatic artery, as in ulcerative endocarditis 
and other pyemic conditions. Infection may also reach the liver through the 
lymphatics. Abscess may also arise from the direct extension of infection from 
the gallbladder and the biliary ducts. Ascarides, liver flukes, echinococcus, and 
the Balantidium coli may also cause abscess of the liver, and it has also been 
observed as a sequel to measles, epidemic influenza, and ulcer of the stomach. 

Amebic Abscess of the Liver. — In the consideration of the etiology of tropical 
abscess, we find predisposing and direct causes. As a predisposing cause, the 
passive congestion of the liver which exists, to some extent, in a large proportion 
of colonists in the. tropics, must be remembered. Other predisposing factors in 
the production of tropical abscess are malaria and exposure to cold and wet. Abuse 
of alcohol is probably an important predisposing cause. In Waring's careful 
study of the subject of abscess of the liver, he found a clear history of the abuse 
of alcohol in 65 per cent, of the cases. 

The direct cause of tropical abscess is the entamehoz dysenteric which may or 
may not have previously excited intestinal lesions. Various observers have found 
that tropical abscess of the liver has been preceded by dysentery in from 72 to 



INFLAMMATION OF THE LIVER 603 

97 per cent, of all cases. Woodward, in 3680 dysentery autopsies, found liver 
abscess in 779, or 21 per cent. Boston collected data of 2430 autopsies, with 
486 abscesses, or 20 per cent. Legrand, of Alexandria, found that in 109 cases of 
hepatic abscess which occurred in children 31 were due to dysentery. Hepatic 
suppuration may develop very shortly after the dysentery, or may be delayed for 
years. (See Dysentery.) 

Pathology and Morbid Anatomy. — Abscess of the liver usually occurs either in 
one or two large purulent collections or in a number of small abscess cavities. 

The single large abscess is usually the result of dysentery, and the infection 
reaches the liver through the veins, which closely anastomose with the hemorrhoidal 
plexus. If the cause be dysentery of the amebic type, the ameba is found in the 
wall of the abscess, and less constantly in the abscess contents. In still other 
cases an examination of the pus reveals the presence of the Bacillus coli communis, 
or the Streptococcus pyogenes or a pyogenic staphylococcus. In still other cases, if 
the abscess be very chronic, the pus may be sterile. 

In tropical abscesses the lesion is solitary in about 60 per cent, of the cases; 
it is single, from coalescence, or double in about 15 per cent, of the cases, and 
the remainder are multiple. The abscesses vary in size from a pigeon's egg to a 
cocoanut. 

The single abscess may be very large, and may fill an entire lobe of the liver. The 
right lobe is usually affected, and as the abscess gradually nears the surface of the 
organ it may burst through the capsule into the peritoneal cavity, or, as is far 
more common, the advancing inflammatory zone causes the surface of the liver to 
become adherent to adjacent structures, so that when rupture takes place the pus 
breaks into the bowel, as in a case recently under my care, or through the diaphragm 
into the pleura, or even into the lung, so that the pus from the liver escapes by 
the respiratory tract. 

Accumulations of pus, in burrowing a way for escape, often cause extraordinary 
effects, and cases are on record in which the pus from one of these abscesses has 
escaped into the pericardium, and even into the pelvis of a kidney. Still other 
instances have occurred in which the pus has found its way into the great veins 
of the abdomen or into the gallbladder. Rupture externally is not common. 

The pus from such an abscess is often very offensive, and it generally differs 
from ordinary pus in appearance, being thin instead of creamy, reddish instead of 
yellow, and oftentimes it is quite green from the presence of bile. Sometimes, 
however, the pus is quite like that commonly found in abscesses. 

The lining of the abscess cavity is shaggy, because of the pieces of dead hepatic 
tissue which hang upon it (Fig. 106). In abscesses of long standing more or less 
imperfect encapsulations of the pus may occur. 

Large multiple abscesses are sometimes met with as the result of suppuration 
about an echinococcus cyst. 

Small multiple abscesses are usually pyemic — i. e. f of metastatic origin. Septic 
emboli, or micro-organisms, from septic foci elsewhere are carried by the blood 
into the liver and cause multiple areas of necrosis and suppuration. The liver 
therefore presents not one large abscess, but a large number well distributed 
through its tissues. These abscesses vary in size. Several small necrotic cavities, 
which may hold several drachms of pus, may be present, or a number may coalesce 
to form one large abscess. Although each abscess seems isolated, it is usually in 
communication through a branch of the portal vein with others, so that by this 
vascular pathway the whole gland is riddled with pus. The pus may vary from 
foul, reddish, or greenish material to the character of what used to be called, in 
preantiseptic days, "laudable pus." 

When the infection takes place along the bile-ducts, as the result of the entrance 
of micro-organisms, the introduction of which is facilitated by the presence of 



604 



DISEASES OF THE LIVER 



gallstones, it is often found that the pus is not only distributed widely through 
the organ, but, in addition, that the gallbladder is full of pus as well, so that the 
entire biliary tract is involved in the suppurative process. 



Fig. 106 




Liver, amebic abscess of right lobe; case of dysentery. Note the shaggy necrotic wall and that the 
abscess has approached the superior surface of the organ. 



Fig. 107 



LEUCO- 
CYTES 


TEMP. 


NOV. 

30. 6 


7. 131 


4. 20 


21. 2 


DEC. 

7128. 4 


5. 12. 


32,000 


108° 














30,000 


107° 














28,000 


106° 














26,000 


105° 














24,000 


104° 














22,000 


103° 


f 


a ■ * 


T ' ' 




i 






20,000 


102° 




1 


5 




1 


zl 

\\\f\ 








18,000 


101° 




J 

< 








16,000 


100° 


1 






If 


Hi 

ft 1 






14,000 


99° 




J 


iuM, 




12,000 


98°- 










iwlU— 












vyw * 


10,000 


97° 














8,000 


96° 





























Chart showing septic fever and marked leukocytosis in case of hepatic abscess. Fall in leukocj-tcs 

after abscess is drained. (Bassett-Smith.) 

Small multiple abscesses may be due not only to the ordinary organisms of 
suppuration, but to infection by the Entameba dysenteries. 



INFLAMMATION OF THE LIVER 605 

Symptomatology. — The symptoms of hepatic suppuration are usually marked. 
In some cases, however, even with the existence of large abscesses, the lesion is 
latent, and the disease is not suspected until rupture of the abscess occurs. The 
chief symptoms are fever, sepsis, enlargement of the liver, and pain. 

The pain is felt not only in the right hypochondrium, but in the region of the 
right shoulder-blade, and, as the abscess approaches the surface and causes inflam- 
mation of the peritoneum, the pain may be sharp and even severe. 

There is loss of weight and strength and pronounced feebleness in muscular effort. 
Dyspeptic symptoms become marked. There is anorexia, nausea, morning vomiting, 
with a heavily coated tongue. The patient becomes anemic and gradually takes on 
a peculiar subicteric color. The fever begins early and is the most constant symp- 
tom. At first it does not run high, but later an evening temperature of from 
104° to 105° is not uncommon. The fever is irregular or intermitting in type. 
It is preceded by a chill and then followed by a sweat. These sweats are very 
severe and contribute greatly to the depression and exhaustion of the patient. 
They follow the fastigium of the fever and are prone to come on during sleep, 
whether it be by day or night; so that they may be properly called sleeping sweats 
rather than night sweats. 

Enlargement of the liver is constant. It is symmetrical, 'and in extreme cases 
may reach as high as the third rib in front and may extend as far down as the crest 
of the ilium, or over as far as the umbilicus. The right hypochondrium may appear 
full and bulging, and there may be an apparent fulness or sleekness of the right 
side, and in marked cases obliteration of the lower intercostal spaces. 

When pus approaches close to the surface it is always preceded by an edema 
of the skin overlying the abscess, and in cases with large abscess fluctuation may 
be present. Auscultation over the liver may reveal peritoneal or liver friction. 

Occasionally sharp pain is felt in the esophagus, when a food bolus passes the 
level of the diaphragm. A dry, hacking, unproductive cough is very commonly 
present and frequently leads to error by directing attention to the lungs rather than 
to the liver. 

The decubitus of the patient is characteristic. He lies on his right side with 
that shoulder drawn down and knee drawn up to relieve the tension on the 
abdominal muscles. 

Jaundice is not common and only appears when the enlarged liver or abscesses 
make pressure on the bile-ducts. Pressure on the portal vein may cause a moderate 
degree of ascites. 

Pneumonia of the right base often occurs when the abscess is high up in the 
dome of the liver. 

Diagnosis. — The condition which in all probability most closely resembles hepatic 
abscess is infection of the gall-duct or gallbladder, produced by the presence of a 
stone or stones, for here, too, there is septic absorption, high fever, chills, sweats, 
and tenderness about the liver, although pus may not be actually present. In 
this condition, however, there is a history of gallstone colic in some instances, and 
of jaundice. Further, the emaciation and anemia are not so marked, nor is the 
liver so generally increased in size. A marked leukocytosis is present in either 
case. 

The absence of marked swelling of the spleen, of any history of malarial infection, 
and the lack of the malarial parasite in the blood, combined with the fact that 
the fever does not yield to quinine, all go to prove the febrile state not malarial. 
The blood condition may also aid in the diagnosis. There is usually a marked 
leukocytosis, which ranges from 12,000 to 53,000. Unfortunately, this symptom 
is not constant, but when it does occur it makes a clear distinction between this 
disease and malaria. Other conditions that simulate liver abscess are hepatic 
colic with fever, suppuration in and about the gallbladder, suppuration in or near 



606 DISEASES OF THE LIVER 

the right kidney, subdiaphragmatic abscess, empyema or pneumonia of the right 
base, and ulcerative endocarditis. 

An empyema or pleural effusion on the right side can be excluded by the decrease 
in vocal resonance and vocal fremitus caused by that state, and by the presence 
of Skodaic resonance just above the area of dulness on percussion. 

It is important to remember that amebic abscess may be present without diarrhea 
or dysentery, the amebse, nevertheless, being present in the stools and in the liver. 

In all obscure cases attended by the signs of hepatic disease and sepsis, an effort 
should be made to establish the condition of the liver by exploratory operation. 

Prognosis. — The prognosis of abscess of the liver depends on two factors, the 
number of abscesses and the time when the case is brought to operation. 80 to 
90 per cent, of single abscesses brought to early operation should recover, but often 
operation is postponed too long. In cases of spontaneous rupture into the colon 
50 per cent, recover. The prognosis is not so good where rupture takes place into 
the lung or pleura. Recovery occasionally takes place when two and three abscesses 
are present. 

In 162 fatal cases of hepatic abscess the mortality is given as due to the following 
causes: severity of the accompanying dysentery, 125 cases; bursting of abscess 
into the peritoneum 12 cases, into the pleura 11 cases; gangrene of the abscess 
wall, 3 cases; rupture of adhesions, 2 cases; pneumonia, 2 cases; and rupture into 
the pericardium, 1 case. The prognosis in multiple abscess is hopeless, for manifest 
reasons. 

Treatment. — The treatment of hepatic abscess consists in sustaining the patient's 
strength by good food and by iron and arsenic, and, if the abscess is single, by 
opening and draining it as soon as its existence is determined unless it be due to 
the Ameboe dysenterice, when it is to be punctured, aspirated and injected with 
quinine solution or one of emetine without drainage (see Dysentery). 

Exploratory puncture should not be practised unless the surgeon is prepared 
to go ahead and operate at once. If ordinary pus be found, puncture may spread 
infection by permitting a leak along the wound. This is especially a danger with 
large needles, and large needles must be used on account of the thickness and 
viscosity of the abscess contents in some cases. 

CIRRHOSIS OF THE LIVER. 

Definition. — Cirrhosis of the liver is a state in which there is an overgrowth 
of connective tissue of the gland. In some instances this overgrowth results in 
an atrophy and shrinkage of the organ (atrophic cirrhosis); in others the liver 
becomes greatly enlarged (hypertrophic cirrhosis). 

Recently Kretz, MacCallum, Kelly, and others have called attention to regenera- 
tive changes in the liver cells as being a prominent feature of cirrhosis. They do 
not regard the normal liver as made up of distinct lobules but as consisting of 
continuous mantles of cells surrounding the bloodvessels. In cirrhosis, following 
degenerative changes, these cells regenerate and rearrange themselves and, accord- 
ing to Kretz, cirrhosis is consequently to be regarded as a focal recrudescent chronic 
atrophy of liver cells modified by parenchymatous regeneration and not as a disease 
entity. He believes that practical extension of our knowledge on this subject 
is to come from investigating the causes of degeneration of liver cells rather than 
from attempts further to differentiate and classify so-called types of developed 
cirrhosis. 

Cirrhosis of the liver derives its name from the Greek word typpot;, meaning 
yellow or tawny. The term cirrhosis was first applied by Laennec, because the 
liver, when cirrhotic, is yellow or tawny in color. Cirrhosis is an unfortunate term, 
in that it in no way describes the pathological state which is present. Further 



CIRRHOSIS OF THE LIVER 607 

than this, the word cirrhosis is now applied to pathological states of other organs 
in which no yellow hue is seen. 

Atrophic Cirrhosis. — The liver in cases of atrophic cirrhosis is often enlarged 
in the early stage of the disease, but after this primary change it undergoes a 
diminution in size, so that eventually it is much smaller than normal. This primary 
enlargement, which does not always occur, is perhaps due to hyperemia, cellular 
infiltration, and edema. The characteristic picture of atrophic cirrhosis is, there- 
fore, that of a small, contracted liver, tawny in hue, and possessing a roughened 
surface, which in some cases may be so irregular as to be called " hob-nail" liver, 
because of its resemblance to a rough shoe, the sole of which is filled with hob-nails 
(Fig. 108). 

Atrophic cirrhosis of the liver is a not uncommon malady in adults, and it is by 
far the most frequent of all the types of cirrhosis which affect this organ. 

Fig. 108 




^■Km 



A 
Liver, advanced cirrhosis; typical hob-nailed organ. A, gallbladder. 

Etiology. — The causes of atrophic cirrhosis of the liver are chronic alcoholism 
and other chronic intoxications, of which lead is certainly one of the most important. 
There is good reason to believe that prolonged gastro-intestinal indigestion and 
disorders of nutrition, such as gout and its allied states, may exert a similar effect. 
Experimental cirrhosis has been produced in animals by acetic, lactic, butyric, 
and valerianic acid, all of which are present in cases of gastro-intestinal disorder. 
Syphilis may cause it (see Syphilis of the Liver), and hepatic cirrhosis has been 
known to develop after severe infectious fevers. Cardiac disease, with great and 
prolonged hepatic congestion, may also produce cirrhotic changes, and it is a 
noteworthy fact that cirrhosis may be present as a part of a general fibroid process 
involving the bloodvessels and the kidneys. Mallory summarizes the etiology 
under five types of cirrhosis, namely, toxic, infectious, pigment, syphilitic, and 
alcoholic. 

Pathology and Morbid Anatomy. — In cirrhosis of the liver the dominant lesion 
is an increase in its connective tissue. This overgrowth varies very greatly in 
different cases. Although the fibrous overgrowth may penetrate the lobules, it is 



608 DISEASES OF THE LIVER 

principally increased at the periphery of these structures. Again, it may be 
equally distributed throughout the entire liver or affect certain areas very much 
more than others, and, finally, the overgrowth of fibrous tissue may be so great 
that bands, both large and small, may traverse the liver substance, separating 
it into masses of compressed glandular tissue. 

The fibrous tissue formed in this process, like fibrous tissue formed elsewhere 
in the body, undergoes cicatricial contraction, and by this means fatty degeneration 
or atrophy of the liver cells composing the lobules is facilitated. These changes 
are due, not only to the pressure exerted on the lobules, so that their cells are 
flattened and deformed, but also to the effects produced on the circulation of blood 
in the liver. 

It will be recalled that the hepatic artery carries to the liver the blood which 
is to nourish its cells, just as the bronchial arteries carry the blood which is to 
nourish the lungs. The blood from the branches of this vessel in performing its 
nutritive function pass through the so-called interlobular vessels, and from these 
into the intralobular vessels, which carry blood from the digestive organs. 

The overgrowth of fibrous tissue in the interlobular spaces, in the fibrous sheath 
of the interlobular veins, and sometimes even between the cells about the intra- 
lobular veins results in obstruction to the flow of blood. The arterial supply is 
little affected, but the venous flow is interfered with, and in this manner the cells 
suffer, not only from the pressure of the fibrous tissue, but from the pressure in 
the vessels. Nor is this all, for the fibrous tissue obstructs the smaller bile-ducts 
and so prevents the escape of bile, with the result that atrophy takes place from 
retained secretion, and the tissues of the liver become bile-stained. 

Many pathologists adhere to the view that the destruction of the parenchyma 
of the organ takes place first, and that the overgrowth of the connective tissue 
already described is secondary to this change. 

The remote effects of the interference with the circulation of blood in the liver 
is catarrh of the stomach and duodenum, due to the obstruction of the blood in 
the portal veins. This state, finally, may cause varicosities in the gastric or 
esophageal vessels, and hematemesis may ensue, or it may cause fatal hemorrhage 
from the bowels because of similar varicosities in the intestinal wall. The marked 
portal obstruction leads to transudation from the peritoneal vessels, constituting 
the ascites of hepatic cirrhosis. 

Not rarely in well-developed cases of hepatic cirrhosis the veins of the abdominal 
wall will be found enlarged in an endeavor to supplement the deep abdominal veins 
in the transfer of blood from the portal area to the vessels of the thorax. Still 
another state, called the "caput medusa?," is the development of a bunch of enlarged 
veins about the umbilicus. This has been generally considered as due to the stasis 
in the paraumbilical vein or in the umbilical vein, which has not closed, as it usually 
is after birth. As a result a collateral circulation is established by an anastomosis 
with the internal mammary, epigastric, and cutaneous veins. 

From the description which has just been given of the effect of cicatricial con- 
traction, it is easily seen why the liver presents upon its surface so many excrescences 
or projections (the so-called "hob-nail liver"), for parts of the gland are pressed 
out of place, and other parts pulled in, by the ever-growing fibrous bands. (See 
Fig. 108.) 

The atrophy of the parenchyma of the liver in the true atrophic form causes a 
very great diminution in the size of the organ, so that the organ may be less than 
one-half its natural dimensions. 

The spleen is usually enlarged, and arteriosclerotic changes are often present. 
Secondary fibroid changes in the pancreas have also been described. 

In the so-called fatty cirrhosis, in which the deposit of fat is more pronounced 
than the cicatricial contraction of fibrous tissue, the gland may not be decreased 



CIRRHOSIS OF THE LIVER 609 

in size, and it may be much larger than the normal. Such a liver is rarely hob- 
nailed, but smooth, or but slightly roughened. 

Peritoneal and pleural tuberculosis is a not uncommon complication of atrophic 
cirrhosis of the liver. 

Symptoms. — The symptoms of atrophic cirrhosis of the liver are, to a large 
degree, dependent upon the obstruction to the circulation of blood in the intra- 
lobular and interlobular vessels, and if the effects of this obstruction are relieved, 
or prevented from developing, by the establishment of an efficient collateral circula- 
tion, there may be no symptoms at all for many months, or, indeed, for years. 
Occasionally we meet with cases in which an extreme degree of atrophy of the 
liver seems to be present with no symptoms of any importance, and yet the patient 
is taking far more alcohol than is good for him. It is scarcely conceivable that the 
establishment of a collateral circulation can be responsible for the absence of all 
systemic disturbance, but there is no other explanation for it. 

When obstruction to the flow of blood in the portal vessels is produced gastric 
catarrh develops, and this causes indigestion and distress in the epigastrium, with 
morning nausea and vomiting. Usually the patient loses strength and is prone to 
become spare and lean if previously stout. 

The occurrence of hemorrhage from the stomach, and bowel has already been 
mentioned when discussing the secondary lesions of the disease, as has also the 
presence of enlarged abdominal veins and the caput medusce on the abdominal wall. 
Thayer has called attention to the fact that in some cases a distinct venous hum 
or thrill may be heard or felt in the epigastrium just above the umbilicus. In 
some cases these signs are even more marked in the space just below the xyphoid 
cartilage. Where anemia is marked, another murmur or venous hum, due to the 
state of the blood, is heard to the right of the navel over the inferior vena cava. 
(See also the article on Hematemesis.) The skin of the trunk is often more sallow 
and yellow than normal, but it is rarely discolored by a true jaundice. At times 
the temperature may be subnormal, and at others slightly febrile. 

In some cases which have manifested few or none of these symptoms, the patient, 
with little warning, develops a state of delirium, which is often of a noisy and 
joyous type, but he soon sinks into a state which proceeds to coma, and then to 
death. To this state the term " hepatic coma" has been applied. It was thought 
at one time to be due to cholesteremia, but this view has now been cast aside 
without any satisfactory explanation of the state being offered. I have so often 
seen this condition follow free drainage of ascites that I believe this operation 
predisposes to its development. 

The physical signs of atrophic cirrhosis consist in an inability to palpate the 
lower margin of the liver by ordinary effort, and in the small area of hepatic dulness 
on percussion. In those cases in which ascites is marked, it is often impossible 
to discover the state of the liver until the fluid is withdrawn. 

Some have held that the ascites is really the result of an associated low-grade 
peritonitis. 

Hess has lately directed attention to obliterating endophlebitis of the hepatic 
veins as producing symptoms almost identical with those of cirrhosis. Most of 
the 23 cases on record, as also the one he reports, were diagnosed cirrhosis of the 
liver. The signs leading one to suspect obliteration of the hepatic veins are absence 
of the history of a cause of cirrhosis, pain over the hepatic area or localized in the 
upper abdomen, and rapid swelling of the liver and development of ascites. 

Prognosis. — The prognosis as to the duration of life depends entirely upon the 
degree of obstruction to the circulation and upon the severity of the patient's 
symptoms. If ascites is well developed and the emaciation marked the outlook 
for more than a few months of life is bad, yet there are cases on record in which 
repeated tappings have resulted in the prevention of recurrence of ascites and in 
39 



G10 DISEASES OF THE LIVER 

the apparent recovery of the patient. Probably in these cases the ascites was 
not due to the cirrhosis, or the relief of pressure has permitted the establishment 
of a collateral circulation. The occurrence of hemorrhages is always a most grave 
omen, yet patients often live for months after severe bleedings. 

Treatment. — The treatment consists in removing the cause of the disease, if it 
be alcohol, and in an endeavor to prevent intestinal fermentation and disorder 
by mild purgatives, digestive stimulants, acids, and antiseptics. Each morning 
the patient should have the bowels well moved by a glass of hot Hunyadi or Carlsbad 
water, and while this is acting he should receive a few drops of Fowler's solution 
for the nausea and lack of appetite at breakfast. During breakfast, luncheon, and 
supper he should take a capsule made up as follows: 

1$ — Pancreatin, 

Taka-diastase, 

Sodii bicarbonat aa gr. ij. — M. 

S. — Take with each meal. 

In some cases the catarrhal state of the stomach and bowels is benefited by the 
use of small doses of iodide of potassium, 5 grains three or four times a day, or of 
ammonium chloride in the same amount. 

Within the last few years it has been proposed by Talma and others that an 
endeavor be made to relieve the obstructive symptoms of atrophic cirrhosis by 
establishing a collateral circulation by surgical procedure. The anterior surface 
of the liver, of the spleen, and of the parietal peritoneum and intestines are rough- 
ened by being rubbed with surgical gauze, and the omentum is attached to the 
parietal peritoneum of the anterior abdominal wall by sutures. By this means 
it is hoped to cause adhesions through which the collateral circulation may be 
established. The operation is not devoid of danger because of the malnutrition 
of the patient and seems to have lost popularity. 

Ascites should be treated by tapping. (See Ascites.) The use of violent hydra- 
gogue cathartics, in the hope that the quantity of fluid will be materially decreased, 
is not very successful, as a rule, and may weaken the patient. It is, however, 
important to keep the bowels opened freely to avoid distention and pressure. 

Hypertrophic Cirrhosis. — Definition. — Hypertrophic cirrhosis is a condition 
in which the liver is very much enlarged, its surface is smooth, jaundice develops, 
but ascites is absent. It is called by the French cirrhose hypertrophique avec ictere, 
or hypertrophic cirrhosis with jaundice. 

Etiology. — The causes of this malady are unknown. Alcohol is not a factor. 
In the cases I have seen a history of severe and prolonged malarial infection has 
been present in several instances. It is a disease of young adult and early middle 
life, but cases occur in children of tender years. 

Pathology and Morbid Anatomy. — An essential difference between atrophic and 
hypertrophic cirrhosis is that in the former the connective tissue which is developed 
undergoes contraction, whereas in the hypertrophic form it remains more cellular 
and does not contract. The second difference lies in the fact that in hypertrophic 
cirrhosis there is a very considerable increase of connective tissue about the biliary 
ducts (biliary cirrhosis), with comparatively little or no increase of this tissue 
about the bloodvessels. For these reasons we do not find any marked decrease 
in the blood supply of the gland, but we do find jaundice because the biliary ducts 
are obstructed. In the atrophic form, therefore, venous obstruction causes ascites; 
in the hypertrophic form biliary obstruction causes jaundice, but there is usually 
no ascites. Between these two types of cirrhosis intermediate cases develop, in 
which sufficient overgrowth of connective tissue about the bloodvessels may be 
present to cause ascites, for in hypertrophic cirrhosis there is an overgrowth of 
connective tissue about the interlobular vessels, and even between the cells of the 
lobules. 



CIRRHOSIS OF THE LIVER 611 

Although the liver is enlarged, it does not present the hob-nailed appearance 
of atrophic cirrhosis because contractions do not occur. On cross-section it 
presents a firm surface of a yellowish-green hue, and strands of connective tissue 
can be seen traversing it. 

It has been shown that in some instances hypertrophic cirrhosis is a secondary 
condition arising from disease of the bile-ducts, and that in others it is a primary 
state without connection with any direct cause yet discovered. As a consequence, 
some writers have divided this disease into two types and have asserted that these 
are separate entities. The pathological changes in the two cases are so nearly 
identical that this separation is not justifiable. To the primary form the term 
"Hanot's cirrhosis" has been applied. In this form there is pigmentation of the 
skin in addition to jaundice, there is usually more pain than in the commoner 
variety, and the spleen is usually very large. It is better to call such cases 
instances of Hanot's type of hypertrophic cirrhosis. 

Symptoms. — The predominant symptom of this disease is enlargement of the 
liver, which often extends to a lower level than that of the navel and far to the 
left of the middle line. When the liver is palpated it is found to be hard and its 
surface fairly smooth, its edges rounded, and its movement heavy and difficult 
when it is pressed upon. Percussion reveals the fact that it not only extends 
downward, but upward far above the ordinary hepatic level, and laterally even to 
the sixth rib, pushing the diaphragm and lung before it. The spleen is usually 
considerably enlarged. Jaundice is generally present and varies from a faint 
lemon-yellow to a dark olive hue, but it is a noteworthy fact that the stools are 
not without bile, as in ordinary jaundice. The urine, of course, contains bile. 
At times attacks of severe hepatic pain develop, and the liver may seem more 
enlarged than usual at these periods. Pruritus is often a most persistent symptom, 
and xanthoma may be developed to an extraordinary degree. In a case now under 
my care the yellow xanthomatous patches about the eyes formed a striking contrast 
to the dark olive hue of the rest of the face. More or less disturbance of digestion, 
due to gastric catarrh, from an impaired circulation in the stomach, is nearly 
always present. 

Diagnosis. — An enlarged liver, like that seen in hypertrophic cirrhosis, is also 
seen in leukemia, but the association of profound anemia and pallor of the skin 
separate it from the condition now under consideration. Great enlargement 
of the liver also occurs in heart disease from hepatic congestion, and in cases of 
adherent pericardium. The state of the heart makes the diagnosis possible in 
these instances. Malignant growth of the liver can often be differentiated by the 
presence of a primary growth in the gallbladder or stomach, and by the nodules 
felt in the liver substance. 

Prognosis. — The prognosis as to cure is hopeless. As to duration of life, it 
varies from one to ten years. Death comes from some terminal infection, from a 
hemorrhage into the bowel or stomach, or from an ever-increasing feebleness. 
At times coma develops. 

Treatment. — There is no treatment for the disease itself. The digestion should 
be kept in good order by the line of treatment outlined for this function under 
Atrophic Cirrhosis. 

Syphilitic Cirrhosis. — Syphilis may produce, in its inherited form or tertiary 
stage, a remarkable degree of cirrhotic change in the liver. The overgrowth of 
connective tissue in this type projects itself everywhere between the lobules and 
between their cells, or forms large bands which, as they contract, produce extra- 
ordinary irregularities in its surface, so that the organ appears to be as well covered 
with knobs as a tuberous root is covered by projections: a polylobed organ. (See 
Syphilis.) 

Because of the frequency of syphilis, this form of cirrhosis is not very rare. 



612 DISEASES OF THE LIVER 

The importance of recognizing it lies in the fact that while we cannot cure the 
state already developed, by active antisyphilitic treatment we may be able to 
arrest or delay its progress, and in this sense the prognosis is better than in the 
non-syphilitic type. In some cases, however, this peculiar nodular formation 
does not occur, and the course of the disease may be identical with ordinary atrophic 
cirrhosis. Sometimes tumors due to the formation of gummata can be felt. The 
symptoms differ in no way from those of ordinary cirrhosis, except when gummata 
are present. 

Treatment. — The treatment of syphilitic cirrhosis, while it presents greater 
opportunities than are offered by therapeutic measures in ordinary cirrhosis, cannot 
be expected to produce very remarkable alterations in the liver. Wonderful as 
are the effects of the iodides, salvarsan, and mercury in the treatment of syphilis, 
they cannot regenerate tissues which have been destroyed, and the most that we 
can expect from them is that they will do something to arrest the progress of 
the disease, and, perhaps, cause a removal of some of the cells which have been 
proliferated, but which have not as yet become organized tissue. In those cases in 
which there are any evidences of active syphilis, it is hardly necessary to state that 
specific treatment should be carried out most thoroughly. (See Syphilis.) 

PERIHEPATITIS (CAPSULAR CIRRHOSIS). 

Inflammation of the capsule of the liver and of the tissues immediately beneath 
it, when it occurs in a chronic form, may be associated with chronic peritonitis 
and with hepatic cirrhosis. More rarely it develops as a result of chronic pleurisy 
on the right side. The thickening which ensues may, by its contraction, result in 
deformity of the surface of the liver. This effect is increased by the fact that 
abnormal projections of connective tissue dip downward from the capsule into the 
liver substance and divide it into masses of parenchyma, which undergo atrophy 
from pressure. The condition is, therefore, in some cases, at least, not very different 
from that' met with in ordinary atrophic syphilitic cirrhosis. 

The condition is very rare and is thought by Hale White to be due to, or a 
sequence of, contracted kidney. Unlike most instances of chronic contracted 
kidney, the patient often has marked ascites because of the state of the liver. As 
already stated, it sometimes happens that the capsule of the liver is secondarily 
involved in cases of chronic peritonitis, particularly in cases of adherent peri- 
cardium and chronic inflammatory changes in the mediastinum. (See Adherent 
Pericardium and Mediastinitis.) 

AFFECTIONS OF THE HEPATIC BLOODVESSELS. 

These consist, aside from those already considered when discussing the subject 
of cirrhosis, in three chief changes. 

Hyperemia occurs physiologically whenever the liver is actively engaged in 
disposing of foodstuffs. Pathologically, it probably takes place when an extra 
amount of stimulating food and irritant drink are taken. Neither condition is 
capable of being diagnosticated. 

A much more important state is the congestion due to cardiac disease, or to other 
causes which retard the egress of blood from the gland. We find, therefore, that 
all the causes which tend to result in interference with the free flow of blood in 
the inferior vena cava above the liver may cause hepatic congestion. Insufficiency 
of the tricuspid valves of the heart, pulmonary emphysema, fibroid lung, bronchiec- 
tasis, and valvular disease of the left side of the heart, with secondary obstruction 
in the right side, all produce it. 

The congestion is, of course, due not to an increase of blood in the portal vein 



AFFECTIONS OF THE HEPATIC BLOODVESSELS 613 

but in the hepatic veins. As a result of this, the centre of each lobule is congested, 
and its periphery contains relatively less blood. Frequently the cells in the areas 
of greatest congestion are pigmented. As a result of this, the homogeneous hue 
of the normal liver is altered, and it presents what is called a " nutmeg" appearance, 
particularly if the cells at the periphery become still paler from fatty changes. 
In some cases, however, nothing more than the appearance of intense congestion 
is present. When the continued pressure by the excess blood and the consequent 
malnutrition causes atrophy of hepatic cells, the condition is known as " red atro- 
phy" of liver. 

During life the congested liver is usually much larger than normal, and may 
attain enormous dimensions, but not rarely, when the congestion has lasted for a 
long time, it grows smaller than it is in health, and its surface may be roughened, 
so that it may somewhat resemble the roughened surface seen in early stages of 
atrophic cirrhosis. In fact the connective tissue is usually increased. 

A third vascular lesion is thrombosis of the portal vein. The formation of this 
thrombus may be due to pressure on the vein produced by a tumor, by gallstones, 
by traumatism, and in some instances it may arise from septic infection. When 
the thrombus forms from pressure, and is not infectious, it may become organized 
and gradually close the vessel permanently. This does not necessarily work 
much havoc in the liver, because the nutrition of this organ is carried out by the 
branches of the hepatic artery, which speedily enter into anastomosis with the 
neighboring vessels. While the liver itself may not suffer very greatly, the abdomi- 
nal circulation is usually much disturbed by obstruction of the portal vein, and 
the spleen, the kidneys, and the veins of the entire abdominal network become 
engorged, so that ascites usually occurs and hematemesis or bloody stools may be 
produced. 

If the thrombus is infectious (suppurative pylephlebitis), the pathological and 
clinical picture is quite different, for in this case the clot does not act as a mechanical 
obstruction alone, but as a source of septic infection. Necrosis and suppuration 
take place in the wall of the infected vessel and in the hepatic tissues around it. 
The thrombus may break down and minute pieces of the infected mass pass into 
smaller divisions of the portal vein, and so spread the disease until multiple abscess 
of the liver develops. 

The sources from which such septic infections arise are found in ulcer of the 
stomach and bowels, appendicitis and suppuration of the lymph nodes in the 
mesentery. Another origin is suppurative angiocholitis. (See Abscess of the 
Liver.) In infants infection may take place by way of the umbilicus. 

Symptoms. — The symptoms of congested liver consist in finding its lower margin 
below the ribs to an abnormal degree and distinct tenderness on pressure, particularly 
in the epigastrium. Pain in this region is often complained of by the patient even 
when he is at rest. If tricuspid regurgitation is present, the liver may have systolic 
expansile pulsation, which must not be confounded with movement of the liver 
due to direct transmission of the impulse of the apex beat of the heart. In some 
cases distinct evidences of gastro-intestinal catarrh develop, and the congestion 
of the gastric vessels may be so great as to cause rupture and hematemesis. Ascites 
due to the interference with the venous return in the lower parts of the body, and 
edema of the legs from the same cause may be present. 

Treatment. — The treatment consists in unloading the gastroduodenal and hepatic 
glands and bloodvessels by a full dose of the blue mass (10 grains), followed, by 
a saline purge. This is to be followed by the use of digitalis to support the heart, 
and, if the arterial tension is high, by the administration of nitroglycerin, to lower 
the arterial pressure and so relieve the heart of work. (See Valvular Disease 
of the Heart.) 



614 DISEASES OF THE LIVER 



AMYLOID LIVER. 



Amyloid disease of the liver occurs as the result of severe and prolonged suppura- 
tive changes in other parts of the body, as in chronic bone disease, in pulmonary 
tuberculosis, and in syphilis, particularly if the latter disease has caused suppuration 
over a long period of time. The liver is usually very large and may be easily felt 
far below the ribs, presenting a smooth surface. Occasionally an amyloid liver 
is small. When it is cut across it is found to be hard and infiltrated by amyloid 
material, which stains a mahogany hue when it is touched with a watery solution 
of iodine. 

Symptoms. — The symptoms are not typical. Indeed, it may be said that the 
changes in the liver produce no manifestations that call attention to hepatic disease, 
for there is no jaundice and no pain, neither is there any ascites. The presence 
of enlargement of the liver, with a smooth surface of the gland, and the presence 
of a suppurative focus, combined with an absence of any of the signs of hypertrophic 
cirrhosis and morbid growth, make the diagnosis easy. 

Treatment. — There is no treatment for amyloid liver, except the removal, if 
possible, of the suppurating area, which is the underlying cause of the disease, and 
in the maintenance of as great a degree of health as possible by the use of fresh air, 
sunshine, iron, arsenic, and good food. 

FATTY LIVER. 

Fatty liver, like fatty heart, occurs in two forms, namely, as a true fatty degenera- 
tion of the hepatic cells and as an infiltration of fat between the cells. The true fatty 
degeneration without cirrhosis is rarely met with, except as a result of the ingestion 
of some poison, such as phosphorus, antimony, iodoform, sulphate of copper, 
or carbolic acid. A similar change is present in acute yellow atrophy of the liver. 
In uncomplicated fatty infiltration the liver is enlarged and smooth. On autopsy 
it is pale and yellow and renders the incising knife greasy. Its specific gravity 
is so low that the organ may almost float in water. No distinctive hepatic symp- 
toms are present. 

Often fatty infiltration is part of general obesity, and the large deposit of fat 
in the abdominal wall and in the tissues near the liver make a diagnosis difficult. 

Large, fatty, cirrhotic livers have been recorded, and fatty liver accompanying 
alcoholism, severe anemia, and cachexia, as in tuberculosis, also occurs. In such 
cases the change is thought to be due to faulty oxidation. 

TUMORS OF THE LIVER. 

The most important morbid growth in the liver is carcinoma. It is rarely primary. 

Secondary carcinoma is quite common and is nearly always due to metastasis 
from the alimentary viscera, as from carcinoma of the gallbladder, of the stomach, 
of the pancreas, or of the intestines. In rare instances the metastasis is from more 
distant organs, as the uterus or mammary gland. 

Carcinoma of the liver rarely occurs as a solitary nodule. Usually it is in the 
form of multiple growths, which vary in size from a small seed to an orange. When 
these growths are immediately subcapsular they appear as large protuberances 
on the surface of the organ, which may be felt as nodules through the belly wall, 
or they lie buried in the tissue of the liver and present a disk-like surface upon the 
level of the capsule, so that they may be felt in thin persons as a slightly flattened 
or umbilicated elevation. The nodules are sometimes very hard, at other times 
quite soft, and in the centre softening may take place, so that an apparent cyst is 
formed (Fig. 109). 



TUMORS OF THE LIVER 



615 



The liver is sometimes enormously enlarged and may extend far below the navel, 
thereby causing great distention of the belly. A very rare form of hepatic cancer 
is that in which the liver diminishes in size with the development of the growth. 

Sarcoma of the liver is rarely encountered. 

Cavernous angiomata have been described, and cysts, single and large, or multiple 
and small, have been found in this organ. The latter are congenital, the so-called 
"cystic disease of the liver." (See also Hydatid Disease.) 

Symptoms. — The evidences of tumor of the. liver may be so easily observed in 
many cases that there is no difficulty in making a diagnosis, particularly if emacia- 
tion, anemia, and profound cachexia are present. In other cases the fact that 
the patient is still well nourished, and the growths deeply situated, may render it 
impossible to discover the existence of a mass by palpation. In some instances there 
is present nothing more than a vague sense of distress in the hypochondrium, with 
loss of weight and strength. In still others, if the gall-ducts are obstructed, 
jaundice may come on, and if the pancreas is involved, fatty stools may be present, 
or glycosuria is found. Pain may be severe, but usually it is not. At times the 
veins of the leg on the right side may be obstructed by a thrombus, or a phlebitis 
may be present. Moderate fever may occur. 



Fig. 109 




Liver, secondary carcinoma. Even the smaller nodules show more or less umbilication, which is 

marked in the larger masses. 



Diagnosis. — The diagnosis requires that we exclude hypertrophic cirrhosis, 
which can be done by the more rapid development of the enlargement of the liver 
in carcinoma, and by the presence of cancerous cachexia. From echinococcus 
cyst it must be separated, by the fact that the cyst usually fluctuates, or, at least, 
is not so hard as is nodular cancer. From gumma of the liver other tumors can 
be differentiated only by the history of the patient and the response to antisyphilitic 
treatment. 

Prognosis. — When the growth is malignant, the outlook is, of course, hopeless 
as to recovery. 



61G . DISEASES OF THE LIVER 

Treatment. — If the growth is a gumma, antisyphilitic treatment is of great value. 
(See Syphilis.) If it is a cyst or non-malignant, surgical interference is a possible 
source of relief. If it is malignant, no efficient treatment except the relief of pain 
can be instituted. 



ACUTE YELLOW ATROPHY OF THE LIVER. 

Definition. — Acute yellow atrophy of the liver is a condition characterized by 
marked fatty degeneration of the organ and violent headache and delirium. It is 
a very rare disease. 

Etiology. — The causes of acute yellow atrophy are unknown, but it occurs more 
frequently in women than in men, and has been associated in many instances 
with the puerperal state. A micrococcus has been found in the liver in some cases, 
but the suspected bacterial origin of the disease has not been proved. Some 
pathologists regard it as a local state representing a general infection, and others 
as a distinctly local disease, but its toxic nature is generally admitted. 

Pathology and Morbid Anatomy. — The changes which take place in the liver are a 
rapid decrease in its size due to necrosis, fatty degeneration, and cellular fragmenta- 
tion. So rapid may be the process that after three or four days the organ is not 
one-half its normal size. The gland is soft and its capsule shrivelled, as if it were 
too large for the organ. If an incision is made into the viscus the lobules will be 
found almost destroyed, and the cut surface is mottled, softened, and gray, red, 
or yellow, according to the stage of the disease. In the gray areas the forms of 
the hepatic cells are recognizable, and their protoplasm is granular in appearance. 
In the yellow areas the cells are more or less filled with fatty globules and yellow 
pigment, and in the red areas the cell outline may be lost, and only cell debris, 
or the remains of broken-down cells, may be found. The spleen is usually enlarged, 
the kidneys are the seat of parenchymatous degeneration, and the heart muscle 
is also degenerated. Hemorrhagic extravasations may occur, not only in the liver, 
but in the stomach, bowels, bladder, and kidneys as well. When death has been 
long delayed, evidences of universal tissue degeneration may be found. 

If the urine is examined, it will be found loaded with bile and an excessive quantity 
of leucin and tyrosin, or, perhaps, only one of these products. Leucin appears in 
round disks, and the tyrosin in needle-shaped crystals, which are usually bunched 
together. 

Symptoms. — The symptoms of this malady are jaundice, severe headache, vomiting, 
and finally delirium, fibrillary muscular tremors, convulsions, and death. As a 
rule, there is little or no fever, but cases with high temperature have been recorded. 
Petechial spots and large hemorrhages may develop beneath the skin. 

Diagnosis. — The development of what might be called fulminating jaundice 
in a woman during the puerperium should awaken a suspicion of this disease at 
once, but such an onset does not necessarily prove the presence of acute yellow 
atrophy, unless there is marked decrease in the size of the liver, and leucin and 
tyrosin are present in the urine. Even these additional signs are not pathogno- 
monic. Particular care must be taken that the coma of hypertrophic cirrhosis 
is not taken for acute yellow atrophy of the liver, for sometimes hypertrophic 
cirrhosis belies its name, in that the liver is not greatly engorged, and acute yellow 
atrophy may occur without the liver being greatly decreased in size. 

Prognosis. — Death nearly always occurs. A few cases are said to have recovered. 

Treatment.— Beyond the use of mild purgatives, diuretics, and stimulants there 
is no treatment for this malady. 



ACUTE CATARRH OF THE BILE-DUCTS 617 



DISEASES OF THE BILIARY TRACT. 

1. Acute Catarrh of the Bile-ducts, Acute Cholangitis or Catarrhal Jaundice. — 

As its name indicates, this is a condition in which the mucous membrane lining the 
gall-ducts becomes inflamed and swollen, and its secretion thick and tenacious. 
These two conditions produce partial or complete occlusion of the ducts, which in 
turn results in biliary stasis and jaundice. In the liver itself marked pigmentation 
also occurs, because of the accumulation of pigment granules in its cells. When 
the inflammatory process affects the gallbladder, it is called catarrhal cholecystitis. 
Acute catarrh of the bile-ducts is the cause of most attacks of jaundice which last 
for a few days. 

Etiology. — This condition nearly always arises from a primary catarrh of the 
duodenum, which extends to the common bile-duct. It may follow exposure to 
cold, particularly if the exposure follows heavy eating and drinking. It usually 
accompanies the presence of gallstones if they arise in or enter the common or 
hepatic duct. It also is a result of infection in many cases, as in influenza, or more 
rarely in pneumonia. Still more rarely jaundice occurs after a severe fright or a 
paroxysm of intense anger. Any cause which interferes with the circulation in the 
liver and duodenum may also indirectly produce this state, as, for example, mitral 
stenosis. 

In nearly all cases the inflammation does not extend beyond the lower part of 
the large ducts. 

Symptoms. — The symptoms vary very greatly. In some persons a well-marked 
jaundice develops, with such slight general symptoms that the patient does not 
know he is ill until he sees his reflection in a glass or a friend remarks upon his 
yellow hue. In other cases the patient may feel and seem wretchedly ill, probably 
because he has in the intestine certain substances which, in the absence of bile, 
develop toxic materials which the torpid liver does not destroy. Headache is 
often marked, and profound weakness may be felt. The stools are putty color 
because of lack of bile, and the urine is the hue of porter, because of the presence 
of this secretion in excess. The color of the skin varies from a faint lemon to a 
much deeper hue, but the deep olive-green jaundice of chronic hepatic disease 
is not met with. The pulse and respiration are remarkably slow, owing to the 
pathological action of the retained biliary salts. The temperature may be sub- 
normal, but if the condition is due to an acute infection it may reach 102° or more. 
The liver on palpation and percussion is usually found to be moderately enlarged, 
about two to three fingers' breadth below the ribs, and it is often tender on pressure. 

Catarrhal jaundice usually lasts from a few days to several weeks. After the 
patient has been ill for some days he usually loses weight very rapidly. There is 
no mild, brief acute illness which causes a greater loss of weight in a few days than 
this affection. 

Diagnosis. — The development of jaundice in persons under forty without any 
signs of grave disease renders a diagnosis of acute catarrh of the bile-ducts probable. 
In older persons, particularly if the jaundice develops gradually, the possibility 
of malignant growth being present must be excluded. In other cases when jaundice 
comes on suddenly, the cause may be gallstones, and in such instances a history 
of colic may be given. If distinct enlargement of the gallbladder is present, the 
probability of carcinoma is great. (See Tumors of the Gallbladder.) 

Prognosis. — In cases of acute catarrh of the simple form the prognosis is always 
good. 

Treatment. — In acute catarrh of the bile-ducts the treatment consists in placing 
the patient in bed, and in the application of hot compresses over the liver, renewing 
the compresses as rapidly as they become warm. In some instances it is ad van- 



618 DISEASES OF THE BILIARY TRACT 

tageous to wet the compresses with hot water which contains a drachm of dilute 
nitromuriatic acid to the pint; or, in other cases, for the purpose of producing 
counter-irritation, a turpentine stupe may be employed. 

The kidneys should be kept acting freely by the administration of large quantities 
of Vichy water, or in other instances Poland water, if Vichy water is not to be had. 
In some instances, if the kidneys are inactive, it is advantageous to add to the 
water 10 grains of bicarbonate of potash in each glass. 

If the bowels are at all confined, as they are prone to be, they are best moved 
by one of the saline purgatives, of which sodium phosphate is usually considered 
most advantageous. This may be given in quantities varying from 20 grains to a 
drachm in half a glass of hot water every two hours until the bowels are thoroughly 
moved. 

The administration of calomel in the early stages of catarrhal jaundice is not 
rational. The object of the physician is to re-establish biliary flow, and the 
difficulty which exists is that the liver is unable to get rid of the bile which it 
secretes. To stimulate this gland to a greater secretion of bile by calomel, when 
its ducts are blocked, is manifestly not good therapeutics. 

After the acute stages of jaundice have passed by, it is often advantageous to 
give broken doses of calomel, in order to overcome the natural inactivity of the 
liver after acute inflammation in its bile-ducts, and these should be followed by 
the doses of phosphate of sodium, already named. 

Patients with jaundice frequently insist upon getting up and going about. This 
is not a safe thing for them to do, as it is entirely possible for them, if the cause 
be gallstones, to convert an attack of acute catarrhal jaundice into one of acute 
cholecystitis. 

In regard to diet, the patient had better subsist upon nutritious broths, thickened 
it may be with barley or rice, partly digested with pancreatin, and well flavored 
with salt. Milk is usually not well digested by patients suffering from this con- 
dition, particularly if it contains any considerable quantity of cream. All fatty 
articles of food should be avoided, as the emulsification of fats in the intestines 
in the absence of bile is imperfectly carried out. 

2. Chronic Catarrh of the Bile-duct. — This state rarely arises as a sequence 
of the acute type just described. More commonly it is due to obstruction of the 
common duct caused by the presence of gallstones, growths, or stricture. Two 
results ensue from such a state, depending upon the degree of obstruction. When 
the duct is totally blocked, we find on opening it that it is not filled with bile, but 
with clear or slightly tinged mucus which is devoid of bile, and that the mucous 
membrane is not much affected, for it remains smooth. Such patients present 
marked and persistent jaundice, the skin often being olive-green in hue. When the 
duct is not quite occluded, the retained mucus is bile-stained; it is cloudy, not 
clear, and it may contain micro-organisms from the bowel. Because of the infection 
of this mucus from the bowel marked fever may be present, characterized by sharp 
intermittency, and associated with fever and sweats, just like those met with in the 
suppurative type about to be described. 

Treatment. — Chronic catarrh of the bile-ducts cannot be materially modified 
by medicinal measures. Prolonged counter-irritation in the form of tincture of 
iodine over the liver may be tried, but it must be continued for long periods of 
time before any possible influence can be expected from it. If constipation exists, 
the bowels should be relieved, preferably by saline purgatives, of which the phos- 
phate of sodium, Hunyadi water, or some similar mild purgative, are considered 
the best. 

The diet should be composed of easily digested meats and easily digested starches, 
the digestion of which should be aided by the use of pancreatin and taka-diastase. 
Milk and fatty foods are usually not well digested by such patients, and are prone 



OCCLUSION AND CONSTRICTIONS OF THE BILE-DUCTS 619 

to cause fermentation and distention of the bowels by gas. The best treatment 
for these patients is operative interference, for the presence of fever indicates infec- 
tion and hints at the existence of pus. 

3. Suppurative Inflammation of the Bile-ducts. — When infection of the mucous 
membrane results from the growth of the Bacillus coli communis, or more rarely 
the Streptococcus pyogenes or other pyogenic organisms, suppuration occurs. It 
is sometimes called "suppurative cholangitis/' The solution of continuity in the 
mucous membrane which permits infection may be due to gallstones. In some 
cases typhoid fever, pneumonia, typhus fever, or pyemia may be the cause. 

This form of inflammation extends much farther into the smaller biliary passages 
than the acute catarrhal form, and by this means the liver may become generally 
infected, the ducts containing pus and the gallbladder also being filled with the 
same material. In some cases the suppurating ducts may cause small abscesses 
in the liver substance outside their walls, and these again may grow large enough 
to communicate, and so abscesses of considerable size develop. When the process 
is severe the ducts may be perforated, and the pus and bile escape into the peritoneal 
cavity, causing peritonitis, or fistulous tracts may communicate with the bowel 
or the exterior of the body. 

Symptoms. — The symptoms are usually so sharply developed that there is little 
difficulty in deciding that pus is present in the liver. The fever ranges from high 
to low, as in sepsis; the liver is enlarged and very tender; the gallbladder may be 
palpable, and jaundice is also well marked in some cases, but slight in others. The 
presence of pus in so vascular and important an organ causes profuse sweats and 
rapid loss of flesh, but pain is usually not severe. 

Diagnosis. — Suppurative cholangitis is to be differentiated from abscess of the 
liver, if possible, and, more important than all, from severe catarrhal cholangitis 
without the formation of pus. 

In hepatic abscess there will be found, on careful examination of the patient's 
history, that at some time in the near or remote past there has been an attack 
of dysentery or of an infection in some part of the body from which pyogenic 
micro-organisms have been carried to the liver. Very rarely there may be a history 
of trauma. While such a history may be found in a case of suppurative cholangitis 
it is much more indicative of abscess. A history of gallstone colic is indicative 
of cholangitis, and it must be recalled that only moderate attacks of pain in the 
hepatic or gastric region may be present in cases of gallstones. In other words, 
every person that has passed a gallstone does not give a history of severe colic. 
Finally, the presence of jaundice is a sign of cholangitis, for this symptom is 
usually absent in abscess. In both cases the liver is enlarged and there is a distinct 
leukocytosis. 

From severe catarrhal cholangitis suppurative cholangitis is separated by the 
facts that in the former state the leukocytosis is not so marked as in the suppurative 
type, there are no marked chills, sharp fevers, or sweats, nor is there so much 
tenderness and enlargement of the liver. 

Treatment. — There is no medicinal treatment for this condition. The same 
rule holds good in regard to pus here as for pus elsewhere; whenever it is present, 
the safety of the patient demands that it should be given an exit, but if the suppu- 
rative process is diffuse this, of course, cannot be done. 

4. Occlusion and Constrictions of the Bile-ducts. — Occlusion of the bile-ducts 
sometimes takes place by the entrance of an intestinal worm, by the impaction 
of a gallstone, or by the pressure produced by an aneurysm, a carcinoma, or other 
growth, such as enlargement of the lymph nodes, enlargements or tumors of the 
head of the pancreas, inflammation and fibroid changes around the ducts, and 
twisting or angulation, caused by hepatoptosis or other changes in the visceral 
relations. If the cystic duct is obstructed the gallbladder is greatly enlarged, 



620 DISEASES OF THE BILIARY TRACT 

but no jaundice is present, but if the common or biliary ducts are closed, intense 
jaundice is developed. (See Tumors of the Gallbladder.) 

Congenital occlusion of the ducts sometimes is met with. When it is complete 
death occurs within a few weeks after birth. Hemorrhages from the navel and 
other parts of the body are usually present in these cases. 

Symptoms. — The symptoms are those met with in chronic catarrh of the bile- 
ducts and vary as these vary with the degree of obstruction and the degree of 
infection. Cases occur, however, in which life is prolonged for long periods if 
the ducts are not completely closed and infection does not take place. A remark- 
able instance of this character has been reported by Cocking, of Sheffield, in which 
a woman was jaundiced for fifty years from her third week of life, yet was in perfect 
health otherwise. 

Treatment. — The treatment is surgical. 

ACUTE CHOLECYSTITIS. 

Definition. — This is a state in which the gallbladder suffers from an acute inflam- 
matory process, which varies from catarrh of the mucous membrane to suppuration, 
and even to phlegmonous change in the walls of the viscus. The process may be 
catarrhal, pseudomembranous, gangrenous, or suppurative. It may be restricted 
to the lining mucosa and submucosa, or extend to all the coats. When the over- 
lying serosa is affected the process is called pericholecystitis or paracholecystitis. 

Etiology. — Cholecystitis arises from the presence of gallstones, which, by injuring 
the gallbladder, permit infection to occur, and by the entrance of pathogenic 
organisms, which, by reason of lowered vitality of the patient, or other causes, 
are able to produce more or less severe inflammatory changes by their presence. 
The time at which the micro-organism enters the gallbladder and that at which it 
makes its presence felt may be widely separated; for while it is true that bile is 
antiseptic in its influence under certain conditions, the germ may remain alive but 
quiescent for months or even for years, and produce its effects only when some 
illness or other cause offers an opportunity for it to develop. This period of inac- 
tivity, so far as inflammatory action is concerned, may be utilized in the formation 
of gallstones about the nucleus formed by those bacilli which have become agglu- 
tinated. (See Cholelithiasis.) The organisms found in the gallbladder are very 
numerous as to kind. The typhoid bacillus, the tubercle bacillus, the Bacillus 
subtilis, the streptococcus, the staphylococcus, and the colon bacillus have all 
been found here, although it is probable that the latter does not remain active, 
except for a short time. 

Morbid Anatomy. — The gallbladder is found to be filled with dark, mucopurulent 
material, in which, if the wall of the gallbladder is seriously involved, there may 
be traces of blood. Occasionally the distention of the gallbladder is due not only 
to blocking of the cystic duct by a stone, but the canal is closed by the intense 
inflammatory process. Perforation of the gallbladder or gangrene of its walls 
may develop if the inflammation is very severe, and it not rarely happens that 
adhesions form between it and the nearby tissues. 

Riedel states that such adhesions develop in no less than 75 per cent, of cases 
of cholecystitis. These adhesions are of importance because as a result of their 
formation a gallstone perforating the gallbladder may find its way into adjacent 
organs.* (See below.) Riedel also states that the adhesions depend as to their 
location to a large extent upon the position at which the stone exists. Thus, if 
it be in the gallbladder the adhesions are between this viscus and the colon or the 
omentum. If it be in the cystic or common duct the adhesion is to the stomach, 
in the region of the pylorus. These adhesions are also of importance because they 
may cause pain or obstruction of the pylorus or duodenum. 



CHOLELITHIASIS 621 

Symptoms and Diagnosis. — The symptoms are those of acute inflammation in 
the hepatic area, varying in severity from a slight discomfort and soreness to violent 
and alarming pain and collapse. There is tenderness, particularly about the region 
of the gallbladder, and this speedily may amount to exquisite pain on pressure. 
The point at which the greatest tenderness is felt is where the lower third of a line 
drawn from the navel to the ninth rib joins the middle third. With these symptoms 
there is fever, often ushered in by a chill. When the development of the condition 
is sudden, as it very frequently is, the patient may be seized with nausea and 
vomiting, threatened collapse, and other symptoms of fulminant abdominal disease. 

The pulse is rapid; the belly is distended and its walls rigid. 

Diagnosis. — Unless the pain is so localized as to aid materially in diagnosis, 
and unless the physician is provided with a history of gallstone colic, or of an inflam- 
mation in the gallbladder after one of the acute fevers, as typhoid fever, the symp- 
toms may mislead him into a diagnosis of intestinal obstruction or acute appendici- 
tis ; for paralysis of the bowel may be present, on the one hand, and in appendicitis 
the pain is often referred to the region of the epigastrium or liver. In certain 
cases of appendicitis, with a history of recurrent attacks or of a recent attack, the 
physician must also recall the fact that pain in the hypochondrium may arise 
from a septic focus, carried there from the appendix by the lymphatics. So, too, 
a gastric ulcer with perforation and subdiaphragmatic abscess may simulate 
acute cholecystitis. When palpation reveals an elongated gallbladder projecting 
below the edge of the liver, which is very tender on palpation, the diagnosis is 
readily made. Jaundice may or may not be present. It is often absent. It is 
important to bear in mind the fact that attacks of hepatic colic may occur in cases 
of cholecystitis without any gallstones being present. 

But in hepatic colic an examination of the blood will not reveal leukocytosis 
of polymorphonuclear cells, which will be notably increased by the presence of 
an acute inflammatory process in or about the gallbladder. In questioning the 
patient as to the possible presence of gallstones it should be remembered that 
mild attacks of pain in this region may be as indicative of the passage of these 
bodies as a history of typical gallstone colic. Acute cholecystitis is rarely character- 
ized by the suddenness of onset of pain and abdominal tenderness which are met 
with in acute pancreatitis or perforation of the stomach due to ulcer. If these 
symptoms are present they may, however, be due to perforation of the gallbladder 
due to chronic cholecystitis arising from gallstones. (See Cholelithiasis.) Some- 
times when there is an infection of the gallbladder, as in the third or fourth week 
of typhoid fever, the onset of cholecystitis may be as severe as that of perforation. 
Occasionally during the course of acute ulcerative endocarditis with secondary 
cardiac failure the liver becomes enlarged and tender and chills and fever are met 
with. Pyopericardium must also be excluded if possible. 

Treatment. — The treatment in all cases in which the symptoms are severe is 
prompt operative interference. Temporizing measures consist in the use of rest 
in bed, counter-irritation over the region of the gallbladder, and the use of gentle 
saline purges to unload the bowels. 

CHOLELITHIASIS. 

Definition. — The term cholelithiasis is applied to a condition in which the gall- 
bladder or the other parts of the biliary passages contain one or more gallstones. 

Etiology and Pathology. — The predisposing causes of gallstone formation are 
all conditions which produce catarrh of the stomach and duodenum and biliary 
passages. A sedentary life with high living is a factor. So, too, enteroptosis 
may aid in its development. The condition is commonly met with after forty 
years of age, but cases have been seen in childhood and even in the newborn. More 



622 DISEASES OF THE BILIARY TRACT 

than 75 per cent, of all cases occur in women, and 90 per cent, of these women have 
been pregnant one or more times . 

Biliary calculi are formed as the result of the deposit of certain of the ingredients 
of the bile, chiefly cholesterin, about a nidus, which we now know is often, if not 
always, an accumulation of micro-organisms. The presence of these infecting 
agents has already been discussed in the article on Cholecystitis, but it is particu- 
larly important to bear in mind the fact that typhoid bacilli are frequently the 
origin of stone, probably because they often remain in the gallbladder for years, 
and because, when they agglutinate, they form with epithelial cells a good nidus 
for the deposition of biliary materials. That micro-organisms play this part 
is now proved not only by many observations on man, but by experiments on 
animals. As Moynihan has cleverly expressed it, every gallstone is a tombstone 
erected to the memory of the germs that lie dead within it. 

The mere presence of micro-organisms, however, is not sufficient for the formation 
of stone. It is necessary that a catarrhal state of the mucous membrane be present, 
since in this condition three ingredients of the stone are excreted by the walls of 
the gallbladder, namely, mucus, cholesterin, and a substance called "bilirubin cal- 
cium." Healthy bile prevents the deposition of bilirubin calcium, but if albumin 
is present this action is arrested and the deposit is made. When inflammation 
is present enough albumin enters the bile from the diseased mucous membrane 
to permit of this effect, and the small quantity of cholesterin present in normal 
bile is also much increased. It is evident, then, that for the deposit of the materials 
forming a gallstone an unhealthy mucous membrane is primarily essential. 

The view that inflammation of the biliary mucous membrane is essential to 
gallstone formation is combated by Aschoff and Bacmeister who believe that 
obstruction to the flow of bile is the chief factor. They also insist that the choles- 
terin is derived from the bile and not from the mucous membrane. As a matter 
of fact stones are developed in both ways. 

The stones are single or few in number and have a radially arrayed centre with 
a laminated exterior rich in calcium when non-inflammatory in origin. The in- 
flammatory stones are not radially centred and are usually faceted and numerous. 

Gallstones when composed chiefly of cholesterin are transparent or slightly 
tinged by bile. If broken, such a stone appears crystalline, with radiating lines. 
In other cases the stone is composed not only of cholesterin, but of biliary pigment 
and salts of magnesium and calcium. Such stones are usually dark in color, brown 
or green. They may be round or marked by facets, due to attrition, where they 
have rubbed against other stones. In these stones also a radiating crystalline 
formation is present on fracture. These dark-faceted stones are the ones commonly 
found. More rarely stones of small size are found, composed almost entirely of 
bile pigment. Calcium carbonate stones are still less frequently met with. 

In size gallstones vary from fine gritty sand to masses as large as a small banana. 

In the vast majority of cases of cholelithiasis biliary calculi are formed in the 
gallbladder. Very rarely small particles of biliary sand form in the bile-ducts 
of the liver itself. The large stones found in the cystic and common duct have 
formed in, and then slipped from, the gallbladder. 

The number of stones found in the gallbladder may vary from one or two to 
several thousand, if the tiny, sand-like pieces are counted. When the number is 
large, they usually show signs of lateral pressure, but sometimes several may 
exist without facets being developed. 

If a gallstone lodges in the common gall-duct so as to completely occlude it, 
there is usually found at autopsy a condition of dilatation of this duct, which is 
filled with a clear, mucus-like fluid. (See Occlusion of the Bile-ducts.) If the 
obstruction is not complete and infection of the duct takes place, the state is one 
of cholangitis, already described, or even of suppurative angiocholitis. 



CHOLELITHIASIS 623 

When the cystic duct is completely obstructed by a stone, the gallbladder 
may be greatly enlarged and filled with clear fluid or with other gallstones. If the 
gallbladder is infected suppurative cholecystitis develops, and perforation may 
occur. (See Symptoms.) In other cases the gallbladder undergoes atrophy, 
and may be so shrunken as to be nothing but a small mass of fibrous tissue the 
size of a large nut, hidden in the hollow naturally occupied by the gallbladder. 
Less commonly a process of calcification is developed, and the gallbladder becomes 
coated or infiltrated by lime-salts. 

Symptoms. — It is important to bear in mind the fact that the mere presence of 
gallstones in the gallbladder does not necessarily cause any symptoms whatever. 
The records of autopsies in Germany, in particular, show that a very large propor- 
tion of all women who come to autopsy in the later years of life have gallstones, 
and yet there has been no suspicion of their existence prior to death. Only about 
5 per cent, suffer from distinct symptoms due to this cause. On the other hand, 
if the biliary tract becomes infected, or if an acute congestion of its mucous mem- 
brane occurs, more or less severe symptoms may be at once produced and fever 
may develop; or if a stone becomes dislodged from the gallbladder and slips into 
the cystic or common duct, this mechanical difficulty may at once produce biliary 
colic. 

The symptoms of biliary colic may consist in severe pain, which amounts to an 
agony in many instances. Sometimes, however, the pain is very moderate, and 
is thought to be due to indigestion. The patient often vomits and sweats profusely 
during the pain. The pain manifestly originates in the gallbladder, but is radiated 
to the right shoulder-blade and to the epigastrium. The facial expression is one 
of anguish and anxiety, and the color of the skin is pallid. 

After the attack has lasted for some hours, or on the day after an attack, a 
moderate degree of jaundice may appear, but it is rarely well marked unless the 
attack lasts for several days or the obstruction is persistent. If the stone is in 
the cystic duct, no jaundice occurs unless the neighboring mucous membrane 
in the common, or hepatic duct, becomes swollen and inflamed, or unless the stone 
is so placed in the cystic duct that it presses upon the hepatic duct. The presence 
of jaundice in a case which suffers from severe pain in the region of the gallbladder 
is a positive diagnostic sign of much value, but the absence of jaundice does not 
in the slightest degree negative the view that gallstone is present. Kehr states that in 
720 cases operated on for gallstone, 80 per cent, showed no jaundice. 

The urine, if the stone is in the common duct, may soon show the presence of 
bile, and not rarely albumin is found in it. In still other cases red blood cells may 
be found in the urine, and this may lead us into the belief that the pain is due to 
renal colic. 

An attack of biliary colic lasts, as a rule, for but a few hours, but occasionally 
the patient suffers from a prolonged seizure lasting over several days and marked 
by temporary remissions, which are, perhaps, due to exhaustion of the irritated 
gallbladder or to temporary restoration of biliary flow. 

The presence of a stone or stones in the common or cystic duct produces not 
only symptoms of biliary colic in some cases, but other signs as well, which may 
be of use in diagnosis. If the stone blocks the common duct completely, the jaundice 
which develops is persistent and well marked, and further attacks of colic may 
never occur, or, indeed, there may not be a single attack in the patient's history. 
Febrile movement is usually absent, because the complete obstruction of the duct 
prevents infection from the intestine. The gallbladder is usually not distended. 

When the common duct is not completely closed, and in the majority of cases 
it is not occluded, the attacks of biliary colic are more frequent, and the degree of 
jaundice varies. This is due to the fact that at times, when the mucous membrane 
surrounding the stone is not acutely inflamed or congested, bile is permitted to 



624 DISEASES OF THE BILIARY TRACT 

escape into the bowel, so that the pressure is relieved and the stools become bile- 
stained. Such a condition of repeated attacks of colic with varying degrees of 
jaundice may also be due to the stone becoming so fixed in the ampulla of Vater 
that it forms a ball- valve, which sometimes permits the passage of bile and some- 
times prevents it. In rarer instances the stone becomes encysted in the wall of the 
duct, and so acts as a valve, and in still other cases it may become lodged at the 
junction of the cystic and hepatic duct, and by pressure cause symptoms character- 
istic of obstruction in both the cystic and common duct. 

These cases of partial obstruction differ from those of complete obstruction, 
in the fact that they not rarely develop fever, owing to infection of the common 
and hepatic duct by micro-organisms from the bowel. The febrile attacks which 
ensue may be so irregular or so intermittent in type that they closely resemble 
those of malarial fever, but they are in reality septic fever, the so-called " intermit- 
tent hepatic fever of Charcot/' Such attacks may persist for years with no more 
serious changes in the ducts than a chronic catarrh with thickening and the pro- 
liferation of an exudate about the parts. 

In some cases, however, the degree of infection is so severe that suppuration 
takes place, not only in the common duct, but in the hepatic duct as well, and 
even in the gallbladder, producing suppurative cholecystitis and suppurative 
angiocholitis. (See Suppurative Inflammation of the Bile-ducts and Acute 
Cholecystitis.) 

The additional symptoms, to those of biliary colic, which arise when the cystic 
duct becomes the lodging-place for a stone are chiefly enlargement of the gall- 
bladder from distention and the negative, but nevertheless valuable, evidence of 
absence of jaundice. The size of the gallbladder in cases in which the obstruction 
is complete is sometimes marvellous. Instances have been recorded in which 
the enlarged gallbladder has been mistaken for an ovarian tumor, and not rarely 
the enlarged, pear-shaped mass can be felt near the median line of the abdomen. 
(See Diagnosis.) On the other hand, the facts in regard to atrophy of the gall- 
bladder, already named in the discussion of the pathology of this affection, should 
be recalled; in other words, the absence of a large gallbladder does not exclude 
obstruction to the cystic duct. 

If the gallbladder, which is distended by retained bile and gallstones, can be 
palpated, it may be possible to produce what is called "gallstone crepitus" by the 
rubbing of the stones one upon the other. 

Complications and Sequelae. — A stone may perforate the gallbladder, and, by 
way of the adhesion, gain the cavity of the duodenum and escape with the feces. 
In still other cases the perforation takes place through an adhesion to the colon, 
but very rarely does the stone escape into the small bowel below the duodenum. 
In other instances the gallbladder becomes adherent, by an inflammatory exudate, 
to the abdominal wall, and the stones finally escape from the fistulous opening. 
I had a case in my clinic at the Jefferson Hospital some years since in which the 
patient passed almost daily a little pus and a little bile with one or more stones 
through such an opening, yet seemed in excellent health, probably because nature 
had established free drainage. More commonly the perforation takes place so 
that the stone enters the peritoneal cavity and then the associated infectious material 
causes fatal peritonitis. When the gallbladder becomes adherent to the diaphragm 
and perforation ensues, the stone with pus and bile may escape into the pleura 
or into the lung. In the Transactions of the Association of American Physicians 
for 1897, Graham, of Toronto, reports 10 cases of cholelithiasis perforating into 
the lung, and in 4 of them the stone passed through an adhesion which existed 
between the gallbladder, the diaphragm, and the pleura. The spitting of bile, 
with a distressing cough, and dulness on percussion in the area just above the 
liver, where pulmonary resonance is usually present, make the diagnosis certain. 



CHOLELITHIASIS 625 

Gallstones have been carried far away from the gallbladder by suppuration 
after perforation, and have even been found in the urinary bladder as a result of 
this process. Perforation of the gallbladder with fatal syncope has been reported 
during an attack of biliary colic. 

Diagnosis. — When the symptoms are classical a diagnosis is easy, but they are 
very often not classical. It should be remembered that when a patient has repeated 
attacks of epigastric pain with distention and vomiting and these symptoms 
are unrelieved, or only temporarily relieved, by medical measures and if these 
symptoms develop in a patient who has had typhoid fever, or in a woman who has 
had many pregnancies, the presence of gallstones is to be suspected, even if palpa- 
tion reveals no enlargement or tenderness of the gallbladder and even if there is 
no jaundice but there is hyperacidity. The conditions to be differentiated from 
cholelithiasis are appendicitis, diaphragmatic pleurisy, gastric ulcer, gastralgia, 
the gastric crisis of ataxia, acute pancreatitis, and renal stone. Appendicitis 
is detected by finding even greater pain on palpation in the appendicular area; 
pleurisy is excluded by careful auscultation to reveal a friction sound. In gastric 
ulcer there is a history of pain immediately after the taking of food, and perhaps 
of hematemesis; and the patient is usually a young woman, whereas gallstones are 
usually present in women past forty years of age. A person with an ulcer is usually 
poorly nourished and anemic, whereas the patient with gallstones is usually plump 
and possessed of a thick abdominal wall. Hyperchlorhydria is present in ulcer, 
and may be present in cholelithiasis. In those cases, however, in which there are 
adhesions between the gallbladder or its duct and the pylorus or duodenum, these 
differential signs may fail because pyloric obstruction causes pain after taking food 
and produces hyperchlorhydria. An attack of gastric crisis in ataxia, while often 
associated with vomiting, can be detected by the history of an ataxic gait and by 
the presence of an Argyll-Robertson pupil or other signs of that disease. In pan- 
creatitis the swelling and centre of greatest pain is usually a little lower and nearer 
the middle line than in gallbladder disease or gastric ulcer and the condition of 
the patient is more prone to be that of collapse and shock. Often, of course, the 
pancreatitis is the direct result of the cholelithiasis. Renal stone causes pain to be 
radiated to the inside of the thigh and to the testicle. Movable kidney may, by 
dragging or pressing upon the common biliary duct, cause obstruction, and so 
produce an attack of biliary colic and jaundice not due to stone. Further, the 
pain due to twisting of the ureter in such a case may simulate hepatic colic. The 
finding of a floating kidney clears up the diagnosis. A new growth may produce 
similar symptoms, and it may be impossible to differentiate the obstruction from 
that due to gallstones. In none of these states is the greatest degree of pain on 
pressure over the gallbladder. 

It is essential that attention be paid to one very important differential point, 
which must always be borne in mind, the so-called " Courvoisier's law," namely, 
that an enlarged gallbladder with jaundice is a sign of malignant growth of the 
gallbladder rather than that of obstruction due to stone. 

In a certain proportion of cases, however, a correct diagnosis before operation 
is impossible even by the most experienced physician. As Lund has well said: 
"Who of us is not familiar with cases in which we have made a diagnosis of gallstone 
disease, on a basis of irregular attacks of pain in the right hypochondrium, with 
localized spasm and tenderness, the pain radiating over the abdomen and perhaps 
into the right shoulder, only to find on operation an ulcer of the pylorus, requiring 
a gastro-enterostomy for its relief ? We have also operated for relief of a dilated 
stomach, with constant vomiting and emaciation expecting to find a cancer or 
chronic ulcer of the pylorus, and found a gallbladder full of pus with a stone 
impacted in the cystic duct, obstructing the pylorus by involving it in a mass of 
adhesions and requiring gastro-enterostomy as well as a cholecystectomy." The 
40 



626 DISEASES OF THE BILIARY TRACT 

proper thing to do in these cases is to explore because be the lesion what it may the 
condition demands surgical interference. On the other hand Richardson has 
well said the tendency is toward hasty, imperfect and inaccurate diagnosis, because 
operative diagnosis is so easy and unmistakable. This tendency is surely a per- 
nicious one, and one to be resisted with all our might. Whenever time permits 
the proposed operation should be based upon the most careful and exhaustive 
study of the patient; or, still better, no operation should be performed until that 
operation, by a positive diagnosis, has been found necessary. Every lesion should 
be regarded as one not demanding or justifying operation until, in the particular 
patient, that demand has been completely justified. The exploratory laparotomy, 
for example, should be reserved for those cases in which security of the patient 
demands certainty of diagnosis, and those in which there is everything to gain, 
and little to loose by exploration. 

Treatment. — The treatment of biliary colic, like that of renal colic, consists in 
the administration of a hypodermic injection of J of a grain of morphine, with 
Y^-o" 0I " atropine, and yiro °f a grain of nitroglycerin, to relieve pain and to relax 
spasm. If the first injection does not give relief at the end of fifteen or twenty 
minutes it may be repeated, the atropine being left out. After the attack is over 
the patient should rest quietly in bed for two or three days, in order to hasten the 
disappearance of the inflammation of the mucous membrane, which is usually 
associated with the attack, and thereby decrease the danger of a subacute or chronic 
inflammatory process developing in the gallbladder or common duct. 

No medicines have any effect upon the gallstones which are already formed, 
but a number of remedies may be given to patients who suffer from gallstones, with 
the object of preventing the formation of others, and with the hope that by their 
use catarrh and irritation of the mucous membrane lining the gallbladder and the 
common duct may be materially diminished. These remedies consist in the mild 
saline purgatives, such as the various imported purgative waters, which are gentle 
in their action, and which may be preferably taken hot in the dose of one or two 
teacupfuls before breakfast. Chloride of ammonium, in the dose of 5 td 10 grains 
three times a day, is useful for its effect upon mucous membranes, and is, perhaps, 
best given in equal parts of fluidextract of licorice and water. 

Until within recent years the physician was content when a case of cholelithiasis 
escaped month by month from a return of biliary colic, deeming it inexpedient 
that any radical measure of relief should be instituted. With our present knowl- 
edge, however, it cannot be doubted that the question of operative interference 
must be carefully considered in every case in which a positive diagnosis of chole- 
lithiasis can be made. The time for operation is, of course, during a period of 
quiescence, since at the time of an attack the acute inflammation which exists 
in and around the gallbladder may seriously complicate the work of the surgeon. 

The question as to how frequently the patient should be allowed to suffer from 
gallstone colic before operative interference is urged is one which varies with each 
individual case. If the jaundice which is present with the first attack is not severe 
and lasts but a very short time, and if the temperature of the patient is not dis- 
turbed, or returns to normal within a period of twenty-four hours, and if, again, 
palpation in the neighborhood of the gallbladder some days after the attack 
fails to reveal evidence of a low-grade inflammation, as manifested by tenderness 
or pain, it is then permissible, and, indeed, advisable, that the patient should not 
be operated upon. Even when as many as two or three such mild attacks have 
occurred at long intervals, the condition may not be such as to require that the 
physician should strongly recommend surgical aid. When, however, the attack 
of biliary colic is violent or repeated, when the jaundice persists for a long period, 
and when distinct evidence of persistent cholecystitis continues, then operation 
should be resorted to, particularly if a mass, caused by the gallbladder being 



MALIGNANT GROWTHS OF GALLBLADDER AND BILIARY PASSAGES 627 

distended by stones, can be distinctly felt. To delay operation in a case of this 
kind until frequent attacks have resulted in the formation of a large amount of 
inflammatory material about the gallbladder is very unwise. By this means 
cases which would offer under ordinary circumstances no surgical difficulties may 
become almost inoperable, and what should be an easy convalescence may be 
instead a difficult and prolonged illness, testing the skill of both the physician 
and surgeon to the utmost. 

The Mayos have performed, up to October 25, 1914, 848 operations for uncom- 
plicated gallstone, with a mortality of only 0.7 per cent. Grouping together all 
cases complicated by the presence of stones in the common or cystic ducts, cases of 
cholelithiasis in which infection occurred, cases of biliary infection and malignant 
disease, their mortality is 2.4 per cent, in 7014 cases which they have operated on. 
They believe these figures to be a strong argument in favor of early operation 
in cases of cholelithiasis, to which view I assent provided a first-rate abdominal 
surgeon is to operate. 

MALIGNANT GROWTHS OF THE GALLBLADDER AND BILIARY 

PASSAGES. 

Etiology. — The cause of the development of morbid growths in these parts is 
unknown, and only some of the predisposing causes are recognized. 

In the case of carcinoma of the biliary ducts and the gallbladder, there can be 
no doubt that age has a very distinct influence. The growth usually develops later 
in life than does carcinoma in any other part, namely, about the fifty-sixth year; 
whereas, the period of greatest frequency of cancer of the mammary gland is, 
according to Kelynack, about the forteith year. It would also seem probable 
that gallstones very distinctly predispose to the development of carcinoma in 
these parts, for they are found present in from 90 to 95 per cent, of all cases; whereas, 
the frequency of gallstones in persons dying from other diseases than cancer of 
these parts is from 6 to 12 per cent. (Kelynack). On the other hand, it has been 
claimed that the presence of carcinoma of the gallbladder leads to the rapid forma- 
tion of stone. Probably the pathological condition of the mucous membrane which 
aids in the formation of stone (see Cholelithiasis) also predisposes to the develop- 
ment of a morbid growth, and this effect may be increased by the irritation produced 
by the stones after they are formed. 

In women carcinoma of the gallbladder is far more common than it is in men. 
Musser, in his classical paper upon this subject, found that out of 98 cases 75 were 
in women and only 23 in men, and other clinicians have noted an even greater 
percentage among women. Curiously enough, this is not the case when the growth 
affects the biliary passages other than the gallbladder, for in such instances the 
number of men and women affected is practically the same. 

Pathology and Morbid Anatomy. — Carcinoma of the gallbladder is usually of the 
type of cylindrical-cell epithelioma, but in statistics there is much contradiction 
as to this point. This form of cancer is also the type which most commonly affects 
the biliary ducts. When the gallbladder is affected the fundus is the part that 
usually suffers. If the biliary passages are involved, the common duct is the 
part that is usually affected, and that portion of it where it enters the bowel is 
the favorite site of the growth. (See Fig. 110.) 

When cancer attacks the gallbladder, as already pointed out in the article on 
Cancer of the Liver, the liver is affected in a large percentage of cases by secondary 
growths (Musser says 54 per cent.). The pancreas is also very commonly involved. 
When the growth is in the biliary ducts, metastasis to other parts is rare. 

Carcinoma of the gallbladder may also result in the formation of adhesions, 
by which it becomes attached to the abdominal wall, the colon, and even the 



628 



DISEASES OF THE BILIARY TRACT 



stomach and small intestines. In other instances a suppurative cholecystitis may 
develop. 

Symptoms. — The symptoms of cancer of the gallbladder are most varied. If 
the growth is so situated that it interferes with biliary flow, the manifestations of 
hepatic disease may develop while it is still a very small mass ; whereas, if no pressure 
is produced, the tumor may reach a very considerable size before its presence is 
suspected. 

As soon as the tumor reaches any size it can be palpated below the border of the 
last rib in most instances, particularly if it affects the fundus of the gallbladder, 
as it does in the majority of cases. Its position is usually along the outer edge of 
the right rectus muscle and about the neighborhood of the normal gallbladder. 
It may extend downward toward the pelvis, or it may be erect and protrude through 
the abdominal wall, as an aneurysm protrudes from the chest. The tumor feels 
hard and is usually somewhat pear-shaped. It varies in size from that of a child's 
head to that of a small walnut. 

Fig. 110 




Primary carcinoma of the duodenal papilla seen at the upper end of the rod running through 

the duct. (Kast and Rumpler.) 



If the growth is so placed near the neck of the gallbladder that it prevents 
the cystic duct from draining that viscus, the resulting distention of the gall- 
bladder may cause the formation of a greatly distended sac, which may extend 
far below the ribs, and by its pressure upon the bowel cause intestinal obstruction. 

Jaundice and pain are very constant symptoms of cancer of the gallbladder. 
Musser found jaundice in 69 per cent, of his cases, and pain in 62 per cent. When 
the growth invades the gallbladder alone, it does not of itself cause icterus, but 
the neighboring glands are often involved very early, and by this means, or by 
secondary growths in the common duct, jaundice is produced. In this connection 
" Courvoisier's law" is to be recalled, namely, that given an enlarged gallbladder 
with jaundice, the cause is carcinoma, not gallstone. 



MALIGNANT GROWTHS OF GALLBLADDER AND BILIARY PASSAGES 629 

Wasting is usually well marked, not only by reason of the malignant growth, 
but because of the jaundice and gastroduodenal catarrh which are usually present. 
Ascites may develop (18 per cent, of cases, Musser). Death is due to exhaustion, 
aud sometimes to cholemia. 

Diagnosis. — A growth in the gallbladder can usually be differentiated from one 
in the bile-ducts by its size, the readiness with which it can be palpated, and the 
absence of jaundice until it is of some size. Given a case in which jaundice develops 
in a woman well along in years, in which the jaundice remains persistent and in 
which no tumor can be felt, and the diagnosis is in favor of growth in the duct. If 
metastatic masses can be found in the liver, the primary growth is probably in 
the gallbladder, for they rarely develop from a growth in the duct. 

An even more important differential point is that between cancer of the gall- 
bladder with cystic enlargement and enlargement due to hydrops of the gallbladder. 
In the latter case the gallbladder is distended with a clear fluid as the result of the 
presence of stone or other cause, completely closing the cystic duct. As Courvoisier 
found this state of hydrops 79 times in 91 cases of impacted gallstone, it is not a 
very rare condition. The differentiation between these two states is made as 
follows: In hydrops of the gallbladder there is usually no jaundice, and the tumor 
presents a smooth, pear-shaped surface, and there may be a history of gallstone 
colic. Bile is present in the stools and the degree of wasting is not marked. 

In some rare cases the gallbladder undergoes thickening and presents a small, 
hard mass, which may be palpated. This has already been described elsewhere 
as calcification of the gallbladder. The absence of metastasis and of other signs 
of cancer aids us in excluding the morbid growth in these cases. 

Other causes of tumor in the region of the gallbladder are aneurysm, cancer 
of the pylorus, cancer of the head of the pancreas, and tumor of the kidney. A 
fecal mass in the bowel may also mislead the physician. 

Prognosis. — Life, in a case of cancer of the gallbladder, usually does not last 
beyond a year, and in many instances death comes earlier than this. 

Death usually comes much earlier in cases of malignant growth in the duct 
than of malignant growth in the gallbladder. 

Treatment. — The treatment of malignant growth of the gallbladder, of necessity, 
does not offer much promise for ultimate and complete recovery, for medicinal 
measures are, of course, entirely useless, except for the purpose of relieving pain. 
Operative procedures, even if they result in the complete removal of the diseased 
gallbladder, are nearly always followed by the development of secondary growths 
in neighboring parts, where they are inoperable and where they straightway proceed 
to destroy the patient. Nevertheless, given a case in which the gallbladder is 
greatly enlarged, and in which evidence of the presence of a growth in nearby 
parts is not marked, it is certainly permissible, and, indeed, advisable, that opera- 
tion shall be performed, with the hope that the growth can be removed, or that the 
operation will reveal the fact that enlargement of the gallbladder is not cancerous 
in origin, but dependent upon the presence of gallstone, or other cause, or obstruc- 
tion of the cystic or common duct. 

In all of these cases in which jaundice is present, the very grave influence of this 
complication upon operative procedure must be taken into consideration, for 
while, on the one hand, we are learning every year that operations upon the gall- 
bladder can be performed with a surprising degree of impunity, we have also learned 
with increasing experience that jaundiced persons withstand operations badly, 
and that the presence of bile in the blood predisposes the patient to obstinate 
and persistent capillary hemorrhage during and after operation. This has not 
infrequently resulted in death, although the mere operative procedure itself was a 
success. 

When the growth involves the bile-duct the outlook is, of course, even more 



630 DISEASES OF THE PANCREAS 

discouraging, for the bile-duct cannot be excised, and the jaundice is usually so 
extreme that the condition of the patient scarcely justifies operative interference. 
The most that can be done for a patient with a malignant growth in the bile-duct 
is to operate with the idea of providing drainage and relieving pressure. 

ICTERUS NEONATORUM. 

Jaundice of the newborn is a very common condition, and usually appears about 
the third or fourth day after birth. It is noticeable in the skin and in the conjunc- 
tiva, but it is never intense, and in many cases may be so slight as to be overlooked. 
Holt states that it occurred 300 times among 900 babies, and Kehrer asserts that 
in his statistics it was present in 75 per cent. The last of these estimates is much 
too high a proportion for private practice. Hpfmeier and others believe that it is 
hematogenous in origin, and results from the destruction, shortly after birth, of a 
large number of red blood cells. On the other hand it not rarely happens that the 
urine is slightly bile-stained, and the stools are lacking in bile, which would indicate 
disordered hepatic action. In some instances the portal vein may have been 
overdistended in birth, and in this way the finer bile-ducts may have been ob- 
structed. Whatever the cause, in its simple form the condition possesses no evil 
import whatever. 

A severe and rare form of icterus of the newborn may, however, develop and 
cause the death of the child. It is due to sepsis following infection of the umbilical 
vein, with phlebitis, to congenital syphilis of the liver, or to congenital atresia 
of the biliary ducts, so that the bile cannot escape into the bowel. (See also 
Congenital Hemolytic Icterus.) 



DISEASES OF THE PANCREAS. 

PANCREATITIS. 

Definition. — Pancreatitis, as its name implies, is an inflammation of the pancreas. 
It occurs in three forms, although it must be understood that no hard-and-fast 
lines separate these conditions one from the other. These three forms are the 
acute, the subacute, and the chronic. 

Acute Pancreatitis. — History . — As long ago as 1672 Tulpius described an 
acute abscess of the pancreas due to pyemia. In 1799 Baillie studied what was 
evidently a case of chronic interstitial pancreatitis. In 1804 Portal recorded 
an instance of acute suppurative pancreatitis, as did Percival in 1818. In 1879 
Balzer reported a case of acute pancreatitis, with fat-necrosis but it was not till 
the epoch-making paper of Fitz appeared in 1889 that the profession recognized 
the frequency and importance of lesions of this gland, although in 1886 another 
American practitioner, Senn, had written a paper upon its surgery. Von Mering 
and Minkowski made valuable contributions in 1889 and 1890. 

Chronic pancreatitis was not recognized till Birch-Hirchfeld described it in 
1895. Since that time the literature on pancreatitis has become quite voluminous, 
and a number of studies have appeared, of which the most notable, from the surgical 
standpoint, have been those of Robson and Moynihan, of Leeds, and, from the 
pathological standpoint, one by Opie, of Baltimore, who has done more than anyone 
else to throw light on diseases of this organ. 

Etiology. — By far the more common cause of pancreatitis is infection of the 
gland by way of its duct. This results usually from the presence of a gallstone in 



PANCREATITIS 



631 



the ampulla of Vater, which prevents the flow of bile into the bowel, but does not 
occlude the opening of the pancreatic duct. Again, the presence of a gallstone 
is prone to result in the development of a septic process in the surrounding mucous 
membrane, and this results in infection of the bile, which fluid passes along the 
duct of Wirsung and so enters the pancreas. This is particularly apt to occur if 
the gallbladder is so shrunken by disease that it cannot readily expand when the 
bile is dammed back into the duct. Further than this, bile alone entering the 
pancreas, even if it be free from micro-organisms, may cause hemorrhagic pancrea- 
titis and fat-necrosis. 

It has been argued that if these causes are active in the production of pancreatitis, 
this state would be met with much more frequently. The explanation of the 
fact that so many cases suffer from gallstones and gallbladder infections without 
pancreatitis lies in the fact that in a certain proportion of individuals the bile-duct 
and pancreatic duct do not enter the bowel by one opening, but through separate 
openings. In a few cases the chief secretion of the pancreas escapes by way of 
the duct of Santorini. (See Fig. 111.) 

Fig. Ill 




Portion of human pancreas and duodenum, showing a condition in which pancreatic juice may 
enter the intestine, although the gall-duct is obstructed: A, duodenum showing the projection formed 
by Brunner's gland; B, B, the large pancreatic duct; C, C, anastomoses between the small pancreatic 
duct and the large pancreatic duct; D, opening of the superior pancreatic duct into the intestine; E, 
opening of the small inferior pancreatic duct into the bile-duct. (Bernard.) 



Acute- pancreatitis may result from several other causes, as one of the acute 
infectious diseases, such as mumps, or, again, in the course of septicemia. Another 
cause is infection from a neighboring lesion, as in direct extension from a gastric 
ulcer or cancer, or a subphrenic abscess. Still another cause is injury by blows 
or by surgical procedure. 

Pathology and Morbid Anatomy. — Acute pancreatitis is characterized not only 
by a primary hyperemia of the gland, but in some cases by the escape of its ferments 
into its own tissues, and adjacent tissues as well. As a result of this accident, 
a condition of " fat-necrosis" develops in the fatty tissues in the immediate region 
of the pancreas, and often in other parts of the body to which the pancreatic ferment 
may escape in the lymph. The fat is split up into glycerin and fatty acids. The 



632 DISEASES OF THE PANCREAS 

glycerin is absorbed; the acids, being insoluble, are not eliminated, but combine 
with calcium salts, and with the necrotic fat form yellowish-white patches in the 
retroperitoneal fat, and in the fat of the omentum, mesentery, abdominal wall, 
and it may be in other parts. 

In a certain number of cases of acute pancreatitis, but not in all cases, hemorrhage 
into the body of the gland occurs, forming what is known as acute hemorrhagic 
pancreatitis. (See also Hemorrhage into the Pancreas.) Whether this hemorrhage 
is the result of the action of the ferment of the gland upon its own vessels is not 
known. 

Acute pancreatitis may proceed to suppuration (suppurative pancreatitis) 
or to gangrene (gangrenous pancreatitis). The suppurative form may be circum- 
scribed or diffuse. In some cases the pus may be confined to the pancreas or 
peripancreatic structures, but the lesser peritoneum, or even the general peritoneum, 
may be involved. 

Symptoms. — In acute pancreatitis the patient is suddenly seized by a severe 
pain in the epigastric region, which is associated with faintness, or even collapse, 
and it may be active vomiting. Inquiry reveals the fact that constipation is present, 
and so the physician may be misled into a diagnosis of intestinal obstruction, but 
doubt is thrown upon this belief by the fact that gas can be passed by the anus. 
The pain may be paroxysmal in type, and there is great tenderness in the epigastrium 
upon pressure. This area becomes swollen and tense, and as the case progresses 
the entire abdomen may become distended. The face is pinched and anxious- 
looking, and the upper lip drawn as in acute peritonitis. The vomit may become 
black and tarry from the presence of altered blood. 

If the patient survives more than a few hours, a more or less marked jaundice 
develops, provided that the bile is prevented from escaping into the bowel by 
swelling of the mucous membrane or the presence of a stone. Hiccough may be 
an annoying symptom, and the pulse is rapid and running. The temperature may 
be febrile, normal, or subnormal. The urine may contain casts and albumin. 
Death in collapse with profound asthenia usually occurs by the second to the sixth 
day, but recovery may occur in mild cases, and it sometimes happens that these 
acute symptoms gradually merge into the subacute type of the malady. 

Subacute pancreatitis cannot, of course, be sharply separated from the acute 
form, yet cases occur in which the symptoms are sufficiently modified to indicate 
that another form of pancreatitis is present. The malady is not so sudden in its 
onset, the pain is not so excruciating, and the epigastric swelling is neither so 
great nor so rapid in its development. The pulse is less rapid, and the constipation 
is more prone to give place to diarrhea, the stools containing pus, tarry blood, and 
undigested food. Chills also occur, and after a few days a swelling, due to abscess, 
may be felt. This abscess may burrow in such a way as to form a perirenal abscess, 
a psoas abscess, or a subphrenic abscess, or it may burst into the stomach or bowel. 
The symptoms of sepsis are, of course, present in such a case, and if surgical relief 
is not given death is due to this cause or to profound asthenia. Such a case must 
be separated from perforation of a gastric ulcer, from abscess due to caries of the 
spine, from suppurating cholecystitis, and from perirenal abscess. 

Diagnosis. — Fitz gives the following rule for the diagnosis of this state: "Acute 
pancreatitis is to be suspected when a previously healthy person, or a sufferer 
from occasional attacks of indigestion, is suddenly seized with violent pain in the 
epigastrium, followed by vomiting and collapse, and in the course of twenty-four 
hours by a circumscribed epigastric swelling, tympanitic or resistant, with slight 
rise of temperature." These symptoms are still more indicative if there is a history 
of gallstone colic or cholecystitis. 

Acute pancreatitis must be separated from intestinal obstruction, perforation 
of the duodenum, and the perforation of a gastric ulcer. It must not be confused 



PANCREATITIS 633 

with rupture of the gallbladder, suppurative cholecystitis, and fulminating appen- 
dicitis. The differential diagnosis from intestinal obstruction has already been 
touched upon. If doubt exists an operation will reveal the true cause of the 
symptoms, for in pancreatitis fat-necrosis may be evident as soon as the belly is 
opened. The operation is justified, because it ought to be performed in either 
instance to save life. When perforation of the stomach or duodenum is considered, 
the history of an old gastric ulcer or of hemorrhage from the bowel, in which dark, 
tarry blood is passed, will be of importance, and here, again, an operation to save 
life is necessary, whether the condition be pancreatic disease or perforation. 

When suppurative cholecystitis is suspected, it may be confirmed by the discovery 
that the early swelling is in the neighborhood of the gallbladder, and a history of 
typhoid fever or of gallstones will be presented. However, this latter history may 
be equally suggestive of secondary pancreatic disease. Here, again, an operation 
primarily for diagnosis and secondarily for relief is indicated. 

Perhaps the most important differential diagnosis lies between acute pancreatitis 
and fulminating appendicitis, because appendicitis is a common disease, because 
the pain accompanying it is often referred to the epigastrium, and because an 
incision in the pancreatic region is far removed from that required for appen- 
dectomy. 

Palpation of the appendix will usually elicit pain over its site, and, perhaps, 
localized swelling. Examination by the rectum may reveal marked iliac tenderness 
and a history of repeated attacks of appendicitis may be found. 

A very large number of tests, of the urine, the feces, and the duodenal and the 
stomach contents have been proposed to determine pancreatic disease. No one 
of them is in itself satisfactory. For ordinary clinical purposes the test of Loewi 
is perhaps the most interesting. This depends upon the fact that if a minute 
quantity of adrenalin solution (1 : 1000) be injected under the conjunctiva it causes 
mydriasis in 5 to 20 minutes when there is disturbed equilibrium of the internal 
secretions of the tissues of the chromaffine system. The test is positive in diseases 
of the pancreas, hyperthyroidism, diabetes mellitus, diseases of the peritoneum, 
stomach, intestine, and in certain diseases of the central nervous system and 
meninges. It is about as accurate as any of the other tests, capable of being used 
by those who are not trained physiological chemists. (For valuable articles on 
the chemistry of the urine in disease of the pancreas see Cammidge, British Medical 
Journal, April 2, 1904; and Sladden, in the Quarterly Journal of Medicine, July, 
1914.) 

Prognosis. — Acute pancreatitis is always an exceedingly grave state. Death 
ensues in the majority of cases. Recovery occurs in the very mild cases, as has 
been proved by instances in which a subsequent operation has revealed the evidences 
of the disease. 

Treatment. — The treatment of acute pancreatitis consists in the prompt institution 
of surgical proceedings as soon as the shock of the onset of the disease has been 
overcome. Robson insists that the surgeon should not wait until collapse passes 
off, as the collapse may be due to septic absorption, which only an operation can 
relieve. By the relief of pressure, the providing of drainage, and the removal of 
the cause of the attack, if it exists in the gall-duct, relief may be given the patient 
and the process arrested before it has proceeded too far. Ebner's statistics reveal 
a death rate of 90 per cent, in cases not operated upon and of 52.8 per cent, in 
those operated upon. Moynihan makes the seemingly bold but really guarded 
statement that when there is a timely diagnosis (Italics mine) the recovery of the 
patient can generally be assured. In a certain proportion of cases, however, 
the state of the patient from the onset is too grave to permit of surgical intervention. 
Excessive pain is to be relieved by morphine given hypodermically, and collapse 
is to be treated by the employment of strychnine and atropine. 



634 DISEASES OF THE PANCREAS 

The treatment of the subacute form of the disease consists in supporting the 
nutrition of the patient by the use of predigested foods and stimulants, and by 
surgical intervention for the relief of tension and removal of pus as soon as the 
diagnosis is made and the patient is strong enough to stand operative procedures. 

Chronic Pancreatitis. — This form of pancreatitis has been in the past con- 
sidered quite rare, but it would seem probable that it exists more commonly than 
is generally thought. It is usually developed as a result of chronic catarrh of the 
duct of Wirsiing, which, in turn, is caused by chronic gastroduodenal catarrh or by 
cholelithiasis, pancreatic lithiasis, or by gastric ulcer. 

Of chronic pancreatitis, Opie, of Baltimore, thinks there are two types. One 
is an interlobular pancreatitis, with increase in the connective tissue between the 
lobules; the intralobular tissues being unaffected and the islands of Langerhans 
escaping until very late in the pathological process. This is the type of chronic 
pancreatitis which follows blocking of the pancreatic duct by a morbid growth 
or by pancreatic or biliary calculi. Glycosuria is rarely present, because the islands 
escape. This the common form. In the second form there is an interacinar 
pancreatitis, that is, new connective-tissue formation in the lobules themselves. 
The islands of Langerhans are seriously affected in this type, and hence glycosuria 
is usually present. This form is not due to obstruction of the ducts. 

These pathological facts show why it is that glycosuria does not appear as a 
sign of pancreatic disease in most cases in which, as the result of gallstone disease 
or other sources of infection or obstruction, we suspect the presence of pancreatitis. 
For a recent and exhaustive consideration of the Relation of the Islands of Langer- 
hans to Morbid Conditions of the Pancreas and Diabetes Mellitus see Finney's 
article in the Medical Chronicle for June, 1903. 

The interstitial type, like the more acute forms, may be diffuse or localized. 
When localized a single area may manifest the change. A somewhat subacute 
form is also recognized, and in some of these cases there is a conspicuous enlarge- 
ment of the area involved, so that the head of the pancreas when affected may be 
mistaken for a neoplasm. Presumably this enlargement represents a cellular 
infiltration, which later passes on to a fibrosis. The typical fibroid pancreas is 
small, dense, resists incision, and may creak when under the knife. Fatty infiltra- 
tion is usually also present, and evidences of a primary acute process may be 
manifest. On microscopic examination there is a notable increase in the fibrous 
tissue, which, as already stated, may be perilobular or interlobular, or it may be 
interacinar. In the latter form the islands of Langerhans show hyaline or fibro- 
hyaline transformation, or they may be absent from certain areas, or, perhaps, 
cannot be demonstrated in any part of the organ. The ducts may show dilatation, 
and in some instances be stained with bile. 

Symptoms. — Chronic pancreatitis may be divided into those cases in which the 
symptoms are mild and those in which they are severe. In one case there may be 
little if any pain, but there is present persistent loss of flesh, and in the epigastrium, 
near the gallbladder, may be found a hard mass which may be mistaken for a 
malignant growth in the stomach or gallbladder. The patient complains of 
epigastric distress, such as that which follows taking food which is difficult of diges- 
tion, and attacks of vomiting may occur. Somtimes jaundice appears. Fever 
may be present if the infection of the ducts is marked. 

In the most severe form of chronic pancreatitis, the symptoms are in close 
accord with those of the subacute form, in that the symptoms may begin with 
severe pain in the epigastrium, as if the patient had gallstone colic. There is 
tenderness in the midepigastrium. Chills and fever may be well developed. 

Diagnosis. — Chronic pancreatitis is to be separated from gallstones in the ductus 
communis choledochus, from cancer of the head of the pancreas, from cancer of 
the gallbladder and of the liver, and from subphrenic abscess. From impacted 



PANCREATITIS 635 

gallstones in the common duct the differentiation is practically impossible. Tender- 
ness on deep pressure will usually be found over the gallbladder in the case of 
gallstones and over the epigastrium in pancreatic disease, and etherization may 
permit sufficiently deep palpation to feel the enlarged head of the pancreas if 
chronic pancreatitis is present. The distribution of the pain may be of value in 
the differentiation. In gallstone cases the pain is in the gall-bladder area and 
radiates around to the right scapular region; whereas, in pancreatic disease it is 
central and travels directly backward to a space between the ends of the scapula. 

Cancer of the head of the pancreas is a disease of advanced life; its onset is 
usually painless, and the jaundice that may ensue is gradual in onset and persistent, 
because the growth primarily, or secondarily, presses continually on the gall-ducts. 
The presence of great swelling of the gallbladder in association with jaundice and 
with the other symptoms of pancreatic disease already named indicates cancer. 
Sometimes in these cases secondary cancerous nodules are to be found in the liver 
and in other organs. The liver may be much enlarged from the damming back 
of bile and from secondary growths. Robson and Moynihan lay stress on the 
fact that the absence of pancreatic secretion from the stools causes them to be 
clay-colored, even when bile is present, and this may aid in diagnosis. If on testing 
the stools bile is found, and the feces are, nevertheless, light in hue, it is a fair 
supposition that pancreatic secretion is absent. The test of the urine for leucin 
and tyrosin should also be used. . 

There are two other facts which, if present, will decide the diagnosis positively, 
namely, fatty stools due to the lack of pancreatic juice in the bowel and the presence 
of glycosuria due to the invasion of the islands of Langerhans in the pancreas 
by the pathological process. Both of these signs are often absent, but if they are 
associated they are pathognomonic of pancreatic disease. (See Diabetes Mellitus.) 

Prognosis. — Patients suffering from chronic pancreatitis in moderate degree may 
live for months or even for years. If glycosuria develops the prognosis becomes 
very grave, not only because this symptom is grave in itself, but because the 
glycosuria indicates that the involvement of the gland in the disease process is 
well-nigh universal, for as long as but a few islands of Langerhans exist glycosuria 
does not ensue. Great emaciation, marked jaundice, and the development of a 
tendency to have multiple hemorrhages are evil signs. 

It is in this form of pancreatitis that surgery has given its most valuable results, 
often producing perfect recovery. 

Treatment. — The treatment of the mild form of chronic pancreatitis depending 
upon catarrh of the biliary and pancreatic ducts may be medicinal for a time in the 
hope that the condition may be relieved. The measures instituted are practically 
identical with those advised in cases of chronic cholangitis (which see). It is, 
however, a vital mistake to permit these cases to drift along in a state of chronic 
ill health, because the condition is one which will eventually lead to pancreatic 
cirrhosis, and this in turn results in great emaciation and the development of 
glycosuria, which causes death. In other words, if the patient does not improve 
surgical measures should be adopted to give relief. 

The treatment of chronic pancreatitis of the severe type is wholly surgical, 
for it is cured in the majority of instances by abdominal section and drainage of 
the pancreatic and gall-ducts. Robson gives the mortality of operations in chronic 
pancreatitis as 12.9 per cent, in 62 cases. Operations in all cases of jaundice are 
of a grave character, because persistent oozing hemorrhage is prone to follow. 
Robson and Moynihan are firmly convinced that the danger from oozing hemorrhage 
after operation in cases of jaundice without pancreatic lesions is less than in those 
cases in which the pancreas is affected. They strongly advise the use of full doses 
of calcium chloride in all these cases prior to operation, to increase coagulability 
of the blood. They advise 20 to 60 grain doses three times a day for one or two 



636 DISEASES OF THE PANCREAS 

days. It is not to be forgotten that the persistent use of this salt finally decreases 
the coagulability of the blood. Horse serum, a coagulose, is probably better than 
calcium chloride. 

To sum up the subject of treatment, it may be said that all forms of pancreatitis 
should be operated upon if the condition is such that an operative procedure can 
be supported. While in acute pancreatitis the operation can do little good directly, 
it permits drainage and it may remove some provoking cause, and so lead to recov- 
ery. In any case it is the patient's only chance. In the hemorrhagic or suppura- 
tive cases, the relief of pressure or of pus is, of course, advantageous. 

PANCREATIC CALCULUS. 

Pancreatic calculus is an exceedingly rare condition. The stones are composed 
of phosphates and carbonates. They vary in size from two and a half inches in 
length to fine sand, and they may be single or multiple. As many as 300 have been 
reported in one case. 

Symptoms. — There are no pathognomonic signs of the presence of pancreatic 
calculus. Pain in the upper zone of the abdomen near the middle line or, as in 
Minnich's case, near the left costal border may be present. It is often colicky in 
character, and with the pain there may be vomiting, sweating, and collapse, 
as in gallstone colic. Fatty stools from the absence of pancreatic juice may be 
present, and glycosuria may occur. Occasionally pieces of the stone or small 
stones can be found in the stools. 

Treatment. — The treatment consists in removal of the stones from the duct by 
operation. Hypodermic injections of pilocarpine have been advised to increase 
the flow of the pancreatic fluid, but this, of course, cannot remove the stone if it is 
embedded. I would expect it to do more harm than good. 

PANCREATIC CYSTS. 

These occur in four forms, namely, as retention cysts, proliferation cysts, hydatid 
cysts, and pseudocysts. Such cysts are, however, exceedingly rare. Hale White 
states that in 6000 autopsies at Guy's Hospital cysts of the pancreas were found 
only four times. As Jordan Eloyd has shown, cysts in the epigastric area are usually 
collections of fluid in the lesser sac of the peritoneum closed at the foramen of 
Winslow. 

Retention cysts arise from blocking of the flow of secretion by calculi or by a 
single calculus, by the formation of cicatricial tissue, which narrows the duct, and 
by pressure from neighboring morbid growths. If no infection accompanies the 
retention of the fluid a cyst results instead of pancreatitis. 

Proliferation cysts occur as cystadenoma, or multilocular tumors, with a lining 
of cylindrical epithelium, and as cystic epithelioma. Hydatid cysts of the pancreas 
are very rare indeed, particularly in the United States and England; Hale White 
has reported one in England. 

Hemorrhagic cyst results from the occurrence of a hemorrhage into the gland 
tissue. Its existence is doubted by many pathologists. 

Pseudocysts are not real cysts of the pancreas, but small cystic accumulations 
of fluid in adjacent tissues. Sometimes a pancreatic pseudocyst is due to effusion 
into the lesser peritoneal cavity. They are thought to follow some injury to the 
epigastrium. 

Pancreatic cysts occur at all ages from infancy to old age, and are met with 
more frequently in men than in women, but the difference in the two sexes is very 
slight. The fluid varies very greatly in appearance. It may be as clear as water, 
or it may be opaque, or yellow, or coffee-colored, and even green or black. Its 



HEMORRHAGES INTO THE PANCREAS 637 

specific gravity is from 1.010 to 1.020, and it contains albumin. Sometimes it 
contains all the digestive ferments of the pancreas. The presence of any of them 
is of value in diagnosis, but their absence does not negative the pancreatic origin 
of the fluid. Nor does their presence prove that the cysts arose from the pancreas. 
Pressure upon the pancreas and secondary changes in a cyst wall may cause com- 
munication with the pancreas and admit its secretion to the cyst cavity. 

Symptoms. — The symptoms of pancreatic cyst are dependent upon the pressure 
which is produced, and, therefore, more or less discomfort may be the only sign 
of its existence. If the pressure is great pain is present. If the cyst be large 
enough to palpate it will be found to fluctuate, to be flat on percussion, and to 
transmit an impulse as in ordinary ballotment. Puncture with a fine aspirating 
needle may reveal the character of the fluid. 

Diagnosis. — Pancreatic cysts must be separated from cystic kidney, horseshoe 
kidney, ovarian cysts, cysts of the liver, hydrops of the gallbladder, and cysts of 
the suprarenal capsules. It must also be separated from mesenteric cysts, omental 
cysts, and retroperitoneal cysts. 

Prognosis. — Pancreatic cyst may last for years without causing discomfort 
or death. On the other hand, cases occur in which the cyst ruptures into the 
peritoneal cavity or into the bowel or stomach, and when this happens death 
ensues, preceded by vomiting and diarrhea. Rarely hemorrhage takes place into 
the cyst, and this is accompanied by sudden increase in its size, and by faintness 
and collapse. 

Treatment. — The treatment consists in aspiration, evacuation and drainage 
or complete extirpation of the cyst wall. The second procedure is usually that of 
election. 

PANCREATIC TUMORS. 

These growths are exceedingly rare. Park states that in 53,000 autopsies only 
226 showed primary malignant disease of this gland. Tumors of the. pancreas 
consists in carcinoma, sarcoma, adenoma, and gumma. The infrequency of car- 
cinoma is shown by the fact that in 23,581 autopsies made in various parts of the 
world, in only 29 instances was pancreatic carcinoma present. The relative fre- 
quency of these growths is scirrhus, encephaloid and colloid. 

Carcinoma is the most frequent primary growth, according to Osier, and sarcoma 
is a more common secondary tumor because of involvement of the retroperitoneal 
glands by this disease. 

As nearly all cases of pancreatic malignant growth are secondary to disease of 
the gallbladder, a tumor in the region of that viscus will usually be found to confirm 
the diagnosis. 

The prognosis in the case of malignant tumors is, of course, hopeless. In benign 
tumors the outlook depends upon the pressure symptoms. If a gumma is present, 
antisyphilitic treatment is, of course, indicated. 

HEMORRHAGES INTO THE PANCREAS. 

This condition is to be distinctly separated in the physician's mind from " acute 
hemorrhagic pancreatitis." Local hemorrhages may take place into the pancreas 
without any injury being received and without the patient being a sufferer from 
hemorrhages elsewhere. The hemorrhage may occur in a person who has seemingly 
been in excellent health without any other symptoms than collapse, with a feeble 
pulse and evidences of shock. Sometimes hemorrhage into the pancreas occurs as 
the result of aneurysm of nearby vessels, or of cancer of the head of the gland. 
When hemorrhage into the pancreas occurs, it may be a limited extravasation of 
blood into the gland, from which the patient may recover, or it may be so profuse 



638 DISEASES OF THE KIDNEYS 

as to flood the retroperitoneal space, extending back to the kidneys and up to the 
posterior insertion of the diaphragm. 

The differentiation between the symptoms produced by hemorrhage into the 
pancreas and acute pancreatitis is practically impossible if there is no previous 
history of hepatic and duodenal disorder. If the condition is due to hemorrhage, 
an operation to relieve local tension is indicated, as death is due rather to this 
cause than to the loss of blood. 



DISEASES OF THE KIDNEYS. 

MALFORMATIONS OF THE KIDNEY. 

It happens not very rarely- that one kidney is absent, its place being occupied 
by a little fibrous tissue or by atrophied renal tissue and fat. In order that the 
blood may be relieved of effete materials the other kidney is often very large, and, 
as it is usually lower down in the loin for this reason, it may be mistaken for a 
dislocated or cystic kidney, and removed, which means death to the patient. 
Not uncommonly one kidney is larger than the other, even if both are functionally 
active. In other cases one kidney has two pelves and two ureters. Perhaps the 
most common of these malformations is the so-called "horseshoe kidney/' in 
which the two kidneys are joined across the vertebral column by a mass of renal 
or connective tissue. Sometimes this horseshoe kidney is displaced into the pelvis, 
or it may be altogether on one side of the vertebral column. 

Again, the kidneys may be fused into a single mass, usually occupying a median 
position much below the normal level, or even in the pelvis. 

MOVABLE KIDNEY. 

Definition. — Aside from the renal malpositions incident to malformation, and, 
therefore, essentially of congenital origin, the kidney may wander from its normal 
position. Several forms of such displacement are recognized. 

The movable kidney lies behind the peritoneum, and usually can be made to 
assume its normal position, but descends during the erect posture; its malposition 
may be parallel to the axis of the body, or it may show a lateral movement, or 
the two may be combined — the "cinder-sifting" kidney. The organ may be 
pushed from its place and anchored in its new position — the "incarcerated kidney." 

When the kidney falls forward and develops a pedicle, consisting of the ureter, 
vessels, and peritoneum, the last also covering the organ, it then becomes a "floating 
kidney," the pedicle forming the so-called mesonephron. 

Kidneys enlarged from any cause are prone to displacement, and displaced 
kidneys, on account of obstruction of the ureters and veins, are frequently subject 
to enlargement. 

Movable kidney is far more frequent in women than in men, in the proportion 
of about 7 to 1. Again, the right kidney is the one at fault in the majority of 
cases, or in the proportion of about 7 to 1. Sometimes both kidneys are movable. 

Etiology. — The most important etiological factor is undoubtedly bodily configura- 
tion. Women of the lean, lank type with floating ribs that slope markedly down- 
ward and who are hollow in the flank, like a hunting dog in training, are the most 
frequent subjects. Their muscles are usually poorly developed, and, if they have 
been pregnant, as a rule, the abdominal wall is relaxed. If to the natural configura- 
tion and these other causes is added the effect of a tight corset and a sudden effort 



MOVABLE KIDNEY 639 

or fall, the needful etiological factors are all present, and a sharp pain in the side 
may be the sign that the kidney has made its maiden movement from its natural 
site. In one case the woman says she had a fall and has wrenched her side in 
falling; in another she has reached high above her head, as in playing tennis; and 
in a third case a blow or jar in a railway accident may have been the needed trauma. 

Symptoms. — Many patients have no symptoms of this condition for years. 
If on examining the belly in the region of the gallbladder a floating kidney is 
found in a person ignorant of its existence, and anything is said of it, the patient 
not rarely becomes a hypochondriac on this subject, and goes from physician to 
surgeon, insisting on relief of symptoms which are often not really in existence. 
As the condition is, to a large extent, harmless, it should be ignored, unless it is 
causing symptoms. 

When symptoms are present they vary over a wide degree of severity. In 
some they consist of a sensation of dragging in the back and side, in others they 
amount to keen suffering, and in still others they may consist in attacks of agony 
due to twisting or angulation of the ureter by the kidney becoming rotated on 
its axis or bent by great displacement. These paroxysms of pain have been called 
"Dietl's crises." Nausea, vomiting, chills, and collapse are present, and after 
the attack the urine is found loaded with urates and perhaps pus and blood cells. 
Sometimes even free hematuria may be present. When by postural change or 
manipulation the kidney assumes its normal position, a distinct renal pelvis may 
suddenly be emptied and a gush of urine overdistends the bladder and escapes 
by the urethra. 

Diagnosis. — There are several states that resemble the pain of floating kidney. 
Violent pain in the epigastrium may be due to this cause or to appendicitis, or 
gastric ulcer. I have seen a " DietVs crisis" closely resemble a severe attack of 
acute appendicitis. It also may resemble gallstone or renal colic, or the symptoms 
produced by abdominal aneurysm. The presence of the mass in the abdominal 
cavity may lead to a diagnosis of malignant growth or of impacted feces. 

The dislocated kidney may be felt on careful palpation in thin women just 
below the border of the ribs and back of the area in which the tip of the gallbladder 
can be felt when that viscus is enlarged, but gentle pressure often causes it to dis- 
appear. A floating kidney may, however, be found almost anywhere in the abdomi- 
nal cavity, and has even been discovered in the pelvis. When found in the belly 
it is usually so movable as to be easily pushed about, and it is so free and slippery 
that it is often elusive, being found one moment and lost the next. Not rarely 
some movement of the patient may cause it to slip into its normal position. This 
fact often leads the physician to overlook its presence, and only when the patient 
is repeatedly examined is the kidney found "away from home." In other words, 
inability to find a floating kidney at one examination does not prove that the patient 
is not a sufferer from this state. 

Pressure upon the kidney gives rise to a sickening sensation, which causes the 
patient to wince. 

To examine the patient properly the woman should be placed on her back with 
the knees drawn up so that the belly wall is relaxed. If the right side is being- 
examined the left hand of the physician is so placed that the tissues of the right 
side can be grasped close to the last rib, between the thumb in front and the fingers 
behind. The patient is then told to take a deep breath, when the kidney may be 
felt to slip out between the fingers and thumb, as a watermelon seed slips when 
pressed upon in this way. The left hand remaining in situ to block the pathway 
of return, the fingers of the right hand can now feel the smooth, rounded surface 
of the organ below the area grasped by the left hand. If the pressure by the left 
hand be relaxed and pressure upward is produced by the right hand, the kidney 
may be felt to slip back into its place. While the kidney is wandering deep palpa- 



640 DISEASES OF THE KIDNEYS 

tion in the flank may reveal a lack of resistance due to absence of the kidney. 
When the left kidney is examined the same process is followed, save that the right 
hand takes the place of the left. 

Treatment. — No treatment is needed unless the kidney really causes pain. If 
it does it can usually be kept in place by the avoidance of tight lacing and of severe 
exercise, or by wearing a properly adjusted pad and bandage to support the tissues 
just below the floating ribs. Operative interference, with the object of stitching the 
kidney in place, is needed in bad cases, but the difficulty is that the relief obtained 
by operation is not permanent in all cases, the kidney wandering away from where 
it is sutured. Further than this, the operation is not entirely devoid of danger. 
My colleague, Dr. Keen, has placed the mortality at 2 to 3 per cent. Out of 137 
cases which were operated upon and collected by Watson there were 5 deaths, 
but 4 were not the result of the operation. In neurasthenic patients operation 
should be avoided, at least until a rest cure is instituted, when not rarely all signs 
of renal tenderness may diappear. Even in those cases which have had one attack 
of severe pain (Dietl's crisis) the kidney may give no further trouble if a belt and 
pad are worn. 

CIRCULATORY DISTURBANCES IN THE KIDNEY. 

Changes in the circulation in the kidneys produce very great alterations in the 
urinary flow, both as to its quantity and quality. If the vessels of the kidney, and 
particularly those of the Malpighian tufts, are poorly supplied with blood, the 
urinary secretion is scanty, even though the amount of solids in the urine may be 
fairly large. On the other hand, any cause which sends a large amount of rapidly 
flowing blood to the kidneys results in free diuresis. Thus, chilling the surface 
of the body often causes a profuse urinary flow, and nitroglycerin, by dilating the 
renal vessels, may do likewise. 

Any substance which acts deleteriously upon the delicate cells of the Malpighian 
tufts causes them to permit not only the transudation of fluid, but of albumin as well. 

Acute Hyperemia. — An acute hyperemia of the kidneys may follow exposure 
to cold, or the attempted elimination of irritating substances, such as cantharides, 
turpentine, and a host of other drugs capable of damaging the kidney epithelium. 
It is also generally accepted that a similar state of these organs may exist in the 
course of acute infectious diseases, like scarlet fever, but it is exceedingly doubtful 
if this is true even in a modified form. 

Treatment. — The treatment of this state consists in the use of a few dry cups 
on the back over the kidneys and in the liberal administration of some water, 
like Poland water, to flush these organs. Rest in bed is, of course, essential. An 
old-fashioned and useful remedy is watermelon-seed tea or the infusion of flaxseed. 
Often the use of an alkaline diuretic, such as 2 drachms of liquor potassii citratis, 
with 1 drachm of sweet spirit of nitre, is valuable, if given every three hours. 

Chronic Hyperemia. — Chronic hyperemia is a very much more common con- 
dition, and occurs in nearly every case in which the circulation becomes sluggish 
by reason of cardiac weakness, as in valvular disease with rupture of compensa- 
tion, in cases of ascites with pressure on the kidneys, and when tumors produce a 
mechanical interference with the flow of blood in these organs. 

Symptoms. — Albuminuria is a prominent symptom of this state, and hyaline 
casts and tube casts containing blood cells may be found. The amount of urine 
passed in each twenty-four hours is often very scanty. If such kidneys are seen 
at autopsy, they will be found to be cyanotic in the early stages, somewhat enlarged 
and heavier than normal, but the capsule is not adherent and the surface of the 
kidney is not roughened. When this condition has persisted a long time the con- 
nective tissue increases, and when the kidney is incised it is found to be firm and 



ACUTE NEPHRITIS 641 

tough, due to this overgrowth of interstitial tissue. The pyramids are dark and 
purple in appearance. A more minute examination will reveal the fact that the 
capillaries forming the Malpighian tufts are greatly engorged, their walls thickened, 
and that the vasa recta, the interlobular veins, and the stellate veins of the cortex 
are also in a similar state. 

Diagnosis. — Such kidneys may lead the physician to a diagnosis of nephritis 
complicating cardiac disease, but the renal symptoms often disappear entirely 
under rest and proper cardiac treatment, although developed fibroid changes in 
the organ are, of course, irremediable. 

Treatment. — The treatment consists in giving the patient digitalis in full doses 
if the heart is feeble, and in applying a hot compress over the kidneys; or in the 
use of dry cups over these organs, and in the employment of gin and digitalis as 
stimulants to the heart and kidneys. Rest in bed for the tired heart and for the 
congested kidneys is essential. Another very useful remedy is fluid extract of 
apocynum cannabinum in the dose of 5 to 10 minims twice or thrice a day. (See 
Valvular Disease of the Heart.) 

ACUTE NEPHRITIS. 

Definition. — By acute nephritis is meant a state in which the tissues of the 
kidney are involved in an acute inflammatory process, that is to say, it is an 
acute diffuse nephritis. The condition is not far removed from that of acute 
hyperemia already described. 

Etiology. — The causes of acute diffuse nephritis are the acute infectious diseases, 
particularly scarlet fever, and also diphtheria, croupous pneumonia, and septicemia. 
Sometimes typhoid fever or malaria act as exciting causes. In other cases an 
acute infection gains access to the body through the tonsils, and it is remarkable 
how often evidences of renal irritation follow the onset of tonsillitis. Still another 
cause is exposure to cold, particularly if the circulation is disturbed by violent 
exercise, and if the kidneys are irritated by the process of eliminating alcohol and 
other waste products after a Bacchanalian revel. So, too, the ingestion and 
elimination of irritant poisons may cause it. Severe burns or scalds may also 
produce acute nephritis. 

Acute and subacute nephritis are not rare in children, and are produced by 
one of the acute infections. By this term is included not only the eruptive 
fevers, but infections such as bronchopneumonia and the various forms of severe 
summer diarrhea, in all of which nephritis is by no means unusual. Thus, in 70 
cases of gastro-intestinal disorder Morse found signs of renal inflammation in no 
less than 15 per cent., and Holt states that in every case in which these conditions 
become severe the kidneys suffer. 

Pathology and Morbid Anatomy. — As with all acute inflammatory processes, 
great variations as to the severity of the alterations in the kidney are met with in 
different cases. In mild cases the organ may show no gross changes. The essential 
point to be remembered is that the texture of the kidney is inflamed through and 
through, although not uniformly so. The glomeruli, the tubules, the connective 
tissue, and the bloodvessels all share in the process. In typical cases, for this 
reason, the kidney is more or less congested, enlarged and edematous, pitting on 
pressure, and if it is cut it oozes free blood in excess. The capsule strips readily 
and is often less firmly attached than normal. As a rule, the more edematous 
the organ the less adherent is the capsule. Often the pyramids are red and en- 
gorged, while the broadened cortex is comparatively pallid. 

In some instances (glomerular nephritis) the glomeruli appear to bear the brunt 
of the process. Under the microscope the vessels forming the tuft are seen to be 
distended and contain leukocytes and larger cells having large nuclei, which are 
41 



642 DISEASES OF THE KIDNEYS 

probably endothelial in origin. Degeneration of these cells ensues, and as this 
change progresses they are shed into Bowman's capsule with large mononuclear 
leukocytes, which fill it so completely that the vessels of the tuft are compressed. 
The epithelium lining the capsule may escape, although it usually undergoes 
proliferation, degeneration, and exfoliation. Added to these different sets of 
cells we find an albuminous exudate, due to the acute inflammatory state of the 
surrounding tissues, mixed with both red and white blood cetls. 

In the tubules there is also degeneration and necrosis of the epithelium lining 
their walls, so that the cells become albuminous or fatty, and desquamate. In this 
way the tubules are more or less distended, not only with these cells, but with 
red and white cells and granular detritus. Fusion of these materials results in 
the formation of casts of the tubules, which appear in the urine as blood casts, and 
as casts of desquamated epithelium. 

As with inflammations elsewhere, there is an extravasation of fluid into the 
tissues, and when this occurs the interstitial portions of the kidney become edema- 
tous, filled with outwandering leukocytes, and, in addition, a considerable number 
of small spheroidal cells, many of which, in some cases, as shown by Councilman, 
are of the plasma-cell type. If the inflammation is very severe, there is an actual 
hemorrhage into the tissues — "hemorrhagic nephritis." When the extravasation 
of serum and leukocytes is particularly copious, Delafield calls the condition 
" exudative nephritis." This is the form prone to occur during or after scarlet fever. 

Symptoms. — The symptoms of acute diffuse nephritis are usually rather sudden 
in onset. A child convalescing from scarlet fever, or a man suffering from an acute 
infection, or after exposure, suddenly suffers from scanty urinary flow, and almost 
before the scantiness is noticed the face may be seen to be edematous and the ankles 
swollen. The patient may go to sleep with a normal visage and awaken with a 
puffy one, the puffiness being particularly marked on the pendent side. In children, 
if the nephritic irritation be severe, a convulsion may develop as one of the early 
signs. Fever may or may not be present. 

It is an interesting fact that severe anemia develops with extraordinary speed, 
so that the swollen face becomes pallid and white in appearance as soon as it is 
puffy. Nausea and vomiting are often early symptoms, and are to be regarded 
with some alarm, as they are indicative of toxemia. 

The scanty urine is heavily loaded with solids, and if examined microscopically 
it shows red blood cells, epithelial cells from the uriniferous tubules, and tube 
casts composed of blood cells, epithelial cells, and hyaline material. When the 
heat and nitric acid test is applied to the urine, the amount of albumin present is 
found to be very large, forming a thick and heavy, curd-like mass, which, in the 
heat test, gradually settles to the bottom of the tube. The pulse is usually hard 
and the tension high, but sometimes the high tension is more apparent than real, 
the pulse being full, but gaseous in resistance. 

Auscultation will reveal, in the cases which have a high arterial tension, an 
accentuated aortic second sound, and a comparatively feeble first sound at the 
apex. Sometimes acute cardiac dilatation develops, and secondary pulmonary 
congestion aids in the destruction of the patient. In other cases in which edema is 
particularly marked a rapid effusion of fluid takes place into the pleural spaces 
and into the peritoneal cavity, and pulmonary edema develops with remarkable 
rapidity. The only vessels which do not leak freely are those of the skin, the 
kidneys, and the bowels. The skin is dry and harsh, the urine scanty or suppressed, 
and the bowels are usually constipated. 

These are the symptoms of what may be called a severe attack of the disease, 
but it is important to bear in mind that very often no edema is present, and that 
in others the urinary flow is not greatly diminished. Often anemia and pallor 
may be the first sign during convalescence from an acute infectious malady, to 



CHRONIC NEPHRITIS 643 

show that all is not well with the kidneys. In other cases some giddiness may 
be present, and, if the patient is an adult, uremic symptoms are more prone to 
develop than if he is a child. 

The urine of persons suffering from the infectious diseases should be examined 
repeatedly, in order that the earliest signs of renal involvement may be recognized. 
There is no excuse for letting the condition run on unrecognized until it is forced 
upon the physician by marked objective symptoms. 

Diagnosis. — It is evident that this state does not present signs or symptoms which 
are often presented by other maladies, but, on the other hand, it is important 
for the physician to recall the fact that certain prominent symptoms may be absent 
without casting doubt on the diagnosis. Thus the amount of albumin in the urine 
may be small, the degree of edema slight, and the urinary flow may not be greatly 
decreased. Again, the mere presence of large amounts of albumin is not alone 
indicative, because, as already pointed out in the article on circulatory disorders 
of the kidneys, it often happens that scanty urine and a large amount of albumin 
are present in renal congestion. Casts made up of degenerated cells and blood 
corpuscles are pathognomonic. 

Prognosis. — The outlook in cases of acute diffuse nephritis, if the patient has 
previously had healthy kidneys, is fairly favorable, particularly if his habits of life 
have been satisfactory. This statement holds true of the acute condition following 
exposure in young adults rather than in children and in young adults who have 
nephritis from acute infectious maladies, particularly scarlet fever. The younger 
the child the more grave the danger in scarlet fever. (See Scarlet Fever.) Evil 
symptoms are drowsiness from toxemia, a tendency to pulmonary edema, a feeble 
heart, and a free transudation into the subcutaneous tissues. Suppression of 
urine is, of course, a most serious symptom. 

The renal lesions in those who survive the acute stage of the inflammation vary 
greatly in their persistency. In some cases all signs of renal trouble clear up in a 
fortnight, but in others albuminuria in some degree persists for months and returns 
whenever the patient is chilled or takes excessive exercise. When anemia is 
persistent and resists fresh air and tonics, even if the albuminuria is scanty, sus- 
picion of subacute or chronic lesions following the acute stage is aroused. In 
other cases the acute nephritis is but an exacerbation of a hitherto unrecognized 
chronic parenchymatous nephritis, in which case the outlook is most grave. Some- 
times, just as the most encouraging progress is being made, a terminal pneumonia 
occurs, and death ensues. 

Treatment. — The treatment of acute diffuse nephritis consists in putting the 
patient to bed at once and in the ordering of a liquid diet containing nothing which 
can irritate the kidneys, such as condiments like pepper or mustard. Counter- 
irritation over the kidneys in the shape of frequently renewed hot compresses are 
of value, but, as a rule, it is unwise to add any irritating drug to these compresses, 
for it may be absorbed and cause renal irritation. If the pulse is quick, small doses 
of tincture of aconite (1 minim every one or two hours) may be given, with a tea- 
spoonful of sweet spirit of nitre in cool water. 

During convalescence tincture of the chloride of iron and tincture of nux vomica 
may be used as tonics and to combat anemia. Great care should be taken that the 
patient is not exposed to cold and dampness, and that woollen garments are worn 
next the skin to protect it from being chilled, since chilling of the surface may pro- 
duce secondary renal congestion. 

CHRONIC NEPHRITIS. 

Definition. — The term "chronic Bright's disease" is applied to several types 
of slow, persistent, inflammatory process in the kidney which result in very definite 



644 DISEASES OF THE KIDNEYS 

alterations from the normal in these organs. Each type is also so distinct from the 
other in its rapidity of progress and results that it is difficult to regard them as 
related in any way, yet in each instance we find inflammation and degeneration 
forming the chief pathological change. 

The two chief forms of chronic B right's disease are called "chronic parenchymatous 
nephritis" and "chronic interstitial nephritis" because in the first the pathological 
process is chiefly concerned with the parenchyma of the organ, and in the second 
form the conspicuous changes are in the connective tissue. 

There are also cases in which these two forms of nephritis exist simultaneously, 
that is, the kidneys present the changes found in both types. Indeed, these cases 
are much more numerous than is generally thought, because physicians, having 
been taught in student days that nephritis is capable of being divided into two 
forms, are continually trying to force cases that come to them into one of these 
categories, it being forgotten that while classification and division are artificial 
methods devised for teaching purposes, nature does not adhere to any such bound- 
aries, but presents cases which may partake of more than one type at the same 
time. It is perhaps well, then, to consider that chronic Bright's disease is a chronic 
diffuse nephritis, although sometimes the parenchyma and sometimes the interstitial 
tissues suffer chiefly. 

On the other hand, the clinical pictures afforded by the two classes of cases 
constitute adequate grounds for recognizing chronic parenchymatous nephritis 
as different from the chronic interstitial form. There can be no doubt that we 
have been laying too much stress on the results obtained from an examination of 
the urine in differentiating the two conditions. Sometimes a urinary examination 
at once settles the diagnosis, but Cabot is clearly right in his contention that the 
urine, in many cases, offers no information as to the exact type of change going 
on in the renal cortex. Differentiation, when possible, must rest upon symptoms 
considered with the results of urinary examination. 

Etiology. — Chronic nephritis may follow acute nephritis, but this is very rarely 
the case. Its most common causes are alcoholism and exposure, and in the upper 
classes alcoholism and overfeeding, with lack of exercise. Gout and syphilis, 
chronic lead poisoning, and chronic digestive disorders are also causes, in all prob- 
ability. While the latter are not as yet proved to be definite causes, there is good 
reason to believe that the continued absorption of toxic materials from the bowels 
for long periods of time may cause renal lesions in the effort of these organs to 
eliminate the noxious substances. A very important cause, in all probability 
very closely allied to those just named, is arteriosclerosis, it being considered that 
the changes in the bloodvessels are responsible for renal changes, although, on 
the other hand, the renal lesions are often the cause of the vascular degeneration. 
In many cases it is probable that the same causes produce both the arterial and 
the renal changes simultaneously. In some cases, indeed it may be said in the 
majority, the exciting cause of the renal changes is undiscoverable, and perhaps 
may depend upon some congenital defect, which as yet we do not understand. 
This defect may be localized in the kidneys, or lie in other organs whose imperfectly 
performed labor results indirectly in renal disease. 

Chronic parenchymatous nephritis is a disease of early and middle life, while 
chronic interstitial nephritis is observed in patients of more advanced years, but 
exceptions to this rule, of course, occur. 

Frequency. — Chronic renal disease is one of the most common maladies affecting 
man, a large proportion of the deaths of all persons over thirty years of age being 
due to this cause. Not only do the mortality statistics prove the correctness of 
this statement, but it is now becoming a well-recognized fact that many cases which 
die of acute pneumonia are in reality cases of chronic nephritis, in which the pneu- 
monia acts as a terminal infection and destroys the patient when his powers of 



CHRONIC NEPHRITIS 645 

resistance have diminished as a result of his renal state. The United States census 
shows that disease of the kidneys stands sixth in the list of diseases causing death, 
pneumonia, tuberculosis, heart disease, diarrheal affections, and unknown causes 
only leading it. 

Of 41,924 medical cases treated in five large Philadelphia hospitals, 1395, or 
3.32 per cent., were affected with nephritis, and of 24,624 medical cases treated in 
four large Philadelphia hospitals in which the form of the lesion was stated, 797, 
or 3.23 per cent., were affected with chronic nephritis. On the other hand, of 
228,232 cases treated in the medical dispensaries of four large Philadelphia hospitals, 
only 1902, or 0.9 per cent., were affected with some form of nephritis. This remark- 
able difference in frequency in the wards and in the out-patient departments is 
probably due chiefly to the fact that most of the cases of renal disease presenting 
themselves for treatment were so ill that they became in-patients, and are so 
recorded. 

From this point on it will be best to consider the two chief forms of chronic 
renal disease separately. 

Chronic Parenchymatous Nephritis. — Chronic parenchymatous nephritis is 
sometimes called "chronic desquamative nephritis," because of the desquamation 
of the epithelial cells lining the tubules; " chronic tubular nephritis," because 
the uriniferous tubules are involved, or in certain cases, "chronic glomeruloneph- 
ritis," because the glomeruli of the kidney are chiefly affected in this malady. It 
is also called "chronic diffuse nephritis," because all parts of the secreting epithe- 
lium are affected and the intervening connective tissue usually shows marked 
changes. 

Pathology and Morbid Anatomy. — In typical cases the kidney is found to be 
large, pale, its subcapsular veins conspicuous, and the capsule easily detached. 
The organ offers little resistance to incision, and inspection of the incised surfaces 
shows that the marked enlargement of the organ is due to broadening of the cortex. 
The medullary pyramids, while often lighter in color than normal, never attain 
the pale yellowish hue of the cortex, and may be dark from associated congestion. 
In this form the microscope shows the epithelium, especially that of the convoluted 
tubules, granular or even fatty, desquamating, and coalescing to form casts, which 
may readily be recognized in position, or, having been passed, these casts leave 
tubules which are imperfectly lined by epithelial cells. There is a less conspicuous, 
but fairly constant, change of a similar character involving the glomerular epithe- 
lium, and also the epithelial cells of some of the pyramidal tubes. Hemorrhages 
in the interstitial tissue are sometimes present. This is the form called "large 
white kidney." 

In some cases the interstitial tissue is but slightly involved, but in others it 
is notably increased and irregularly distributed, with unequal contractions, giving 
rise to a more or less bossed or granular surface, not unlike that seen in typical 
interstitial nephritis. In this form (small white kidney) the organ may not be 
enlarged, and may be even smaller than normal. It resists incision, due to the 
increase in fibrous tissue, which, with the unaided eye, may be seen as grayish 
patches in the yellow cortex. Hemorrhages may be present, mottling the incised 
surface with reddish or reddish-brown areas. 

Microscopically, the changes in the epithelium are similar to those seen in the 
large white kidney, but the increase in fibrous tissues constitutes a conspicuous 
difference. It has not been definitely decided whether the small white kidney 
is a later stage of large white kidney, an independent affection, or a form of nephritis 
which having been primarily interstitial has had parenchymatous disease super- 
imposed. 

The cardiovascular changes of chronic parenchymatous nephritis are similar 
in kind, but do not approach in degree those found in chronic intersitial nephritis. 



646 DISEASES OF THE KIDNEYS 

With the small white kidney, cardiac hypertrophy and slight arteriosclerotic changes 
are not of infrequent occurrence. There is usually an excess of fluid in the serous 
cavities, a varying quantity of edema in the subcutaneous fat, and also in the lungs 
and meninges. Retinal hemorrhages are occasionally observed. 

Symptoms. — When chronic diffuse nephritis of the "large white type" is well 
developed there are few clinical pictures which are so typical. The more or less 
swollen visage; the greasy, pallid skin; the stupid fades, and the dyspnea on exertion 
strike the eye at once. Not rarely the partly buttoned wiastcoat and the loosely 
laced shoes show that sufficient anasarca exists to cause the patient some discomfort. 

If the pretibial tissues are pressed upon, they pit on pressure. Percussion may 
show the presence of fluid in the pleural and peritoneal cavities, although large 
effusions are not commonly met with in these cases. 

If the heart is examined, its sounds are found to be altered, so that the first sound 
lacks good quality, and the second sound is usually accentuated. The pulse is rapid, 
and the arterial tension higher than normal. The patient is prone to be sleepy 
during the day and restless at night, and may be dyspneic on lying down. The urine 
is scanty and heavily laden with solids, and under the microscope shows a large 
number of fatty, granular, hyaline, and epithelial casts, leukocytes, and even red 
blood corpuscles. Occasionally the granular casts are particularly opaque to 
light, forming the "big black, granular casts," which are so significant of severe 
parenchymatous nephritis. Tested with heat or nitric acid, the urine is found to 
contain an excessive amount of albumin, so that the coagulum may equal half the 
urine. The specific gravity of the urine is high — about 1.025. With the advent 
of marked interstitial fibrosis, the quantity of urine increases and may equal or 
even exceed the normal amount. At this time the albumin diminishes, the casts 
often lessen in number, and cardiovascular changes occur, the chief sign of which 
is increased arterial tension. 

When the function of the kidneys is seriously disturbed, apathy, stupor, and 
finally coma may ensue from uremia, and in some cases convulsions occur. These 
may vary from a slight twitch followed by stupor to a severe general convulsion, 
in which all the voluntary muscles are involved. Sometimes & fleeting monoplegia, 
aphasia, or hemiplegia comes on as the result of the uremic poisoning and without 
any connection with an actual apoplexy. (See Uremia.) Occasionally very 
definite forms of mental disturbance occur so that the disease may first be discovered 
when the patient is committed to an asylum for the insane. The Folie Brightique 
of the French often possesses great medicolegal importance. 

Patients suffering from chronic parenchymatous nephritis are sometimes seized 
by a severe serous diarrhea, which is an effort at elimination on the part of the 
economy, and should be cautiously checked only when it becomes severe enough 
to be dangerous in itself. 

Comparatively rarely in the course of chronic parenchymatous nephritis an 
albuminuric retinitis develops, but when the nephritis complicates pregnancy 
this ocular symptom is very common. 

The combinations of symptoms just recited are met with in the well-developed 
cases which present characteristic manifestations of the disease. It is to be dis- 
tinctly recollected that in many cases few or none of these signs develop until the 
patient is suddenly overwhelmed by the climax of his malady, and that of all the 
chronic and grave maladies which affect man none other advances and develops as 
insidiously as does chronic parenchymatous nephritis in many cases. In one in- 
stance a persistent indigestion which fails to yield to appropriate digestive remedies is 
found to be due to renal disease; in another anemia fails to yield to ordinary chaly- 
beates and is found to be renal in origin; in still another a persistent failure of 
health without apparent cause has its origin in bad kidneys. In yet another 
group of cases a persistent bronchitis is founded x>n this cause. If consulting 



CHRONIC NEPHRITIS 647 

physicians could be polled, I feel confident that they would universally state that 
the average case of grave ill-health seen by them in consultation, when the diagnosis 
is obscure, is not really difficult of diagnosis if the state of the kidneys is care- 
fully studied. It is not sufficient to examine the urine once. It should be done 
repeatedly before deciding that it throws no light on the case. 

An important clinical fact to bear in mind is that a latent chronic parenchymatous 
nephritis may exist for a long time, and finally be recognized by the sudden develop- 
ment of uremia due to an acute congestive nephritis coming on as a complication. 

Diagnosis. — The diagnosis of chronic parenchymatous nephritis is reached by 
the following symptoms and tests: The face is puffy and pallid; there is often 
dyspnea, even without exertion, and the second sound of the heart is usually 
accentuated. If the case is well developed, general anasarca may be manifest. 
The chief diagnostic factor, however, is the state of the urine. It is less than 
normal in quantity, of high specific gravity, and contains very considerable quan- 
tities of albumin. (See Albuminuria.) A microscopic examination of its sediment 
reveals fatty, granular, and hyaline casts, red blood cells, and large amounts of 
desquamated epithelium from the uriniferous tubules. The gravity of the disease 
is usually in direct proportion to the quantity and quality of the casts, the large, 
dark, granular casts being indicative of grave disease. Quantitative analysis 
reveals marked decrease in the total elimination of urea in each twenty-four hours. 

Rowntree and Geraghty have introduced the phenolsulphonephthalein test to 
determine the functional ability of the kidney. It consists in injecting into a 
muscle, or hypodermically, 0.006 of phenolsulphonephthalein preceding it by a 
draught of water by half an hour. The patient must also have an empty bladder. 
The dye begins to be excreted in from five to ten minutes. If there is any retention, 
or obstruction, a catheter must be used to empty the bladder, and allowed to remain 
in place. Its external end is placed in a test-tube containing a drop of 25 per cent, 
sodium hydroxide and the tube watched for the first sign of a pinkish tinge. In 
other cases the patient may pass water every little while, voluntarily. If the urine 
is acid and not neutralized it appears orange colored when free elimination is 
established and becomes light, purple-red when made alkaline. The urine is 
now diluted with distilled water to make one litre and a small filtered portion 
placed in a small test-tube. The contents of this tube is compared with the 
contents of tubes containing different standard solutions of a colorimeter. By 
this means the percentage of the drug eliminated in a given time is estimated. 
Normal kidneys excrete the greater part of the dose in two hours and trace for 
two hours more, moderately diseased kidneys eliminate only 50 per cent, in the 
first two hours. Any delay in the time of the first appearance of the dye in the 
urine is of little value as a test, as it may be due to slow absorption, but much 
importance is to be attached to the rapidity of elimination after it once begins. 

Prognosis. — The prognosis of chronic parenchymatous nephritis is inevitably 
fatal, and the patient's life is often ended in a few months, when once the disease 
is well developed. In those cases of chronic parenchymatous nephritis char- 
acterized by early dropsy which rapidly develops into general anasarca, Senator 
states that the duration of life varies from a few months to a year. In those cases 
in which the development of dropsy is gradual and irregular, varying in degree 
from time to time, he says that death ensues in from one to two years after the 
beginning of the malady. Strumpell gives the average duration of life in chronic 
parenchymatous nephritis as from one-half to one and one-half years. Every 
clinician of experience will, however, agree with Senator in recognizing another 
class of cases which extend over several years, and which are characterized by 
mildness of symptoms. In these cases there is not much albumin in the urine, 
but slight headache, and little swelling of the lower extremities or of the face. 
Gradually these patients become worse, until they finally fall into one of the well- 



648 DISEASES OF THE KIDNEYS 

defined classes already described. They are probably representative of that form 
of the disease characterized by moderate changes in the parenchyma of the kidney 
with associated interstitial disease. 

Treatment. — It has been generally held that diet is a very important factor 
in the treatment of this form of renal disease. While it is somewhat inconoclastic 
to say that this general belief is untrue, it is, nevertheless, a fact that a generous 
diet which does not strain the digestion and the eliminating organs can usually 
be allowed in most cases. We have before us a patient who is bound to die within 
a few months, and the question arises as to whether we can so regulate the diet 
that we will obtain results which compensate for the discomforts and unhappiness 
of the rigid milk diet, which is usually ordered, or one which causes the patient 
to regard his food with loathing and which is a constant reminder that he is ill. 

Although skimmed milk is theoretically capable of maintaining nutrition, it is 
practically incapable, because such enormous quantities must be consumed, to 
provide an adult with a sufficient amount of nutriment. Again, milk lacks the 
quantity of iron which ordinary food contains. It presents to the patient the same 
quantities of calcium, magnesium, potassium, and phosphorus as is found in the 
ash of newborn animals, but it contains only one sixth iron; this lack of iron being 
made up in the young by the storage of this metal in the liver, and possibly in other 
organs during intra-uterine life. Again, the quantity of proteid which is present 
in milk is excessive. A normal adult requires approximately 3000 calories a day 
to maintain full nutrition. One quart of milk has a caloric value of about 700, and 
therefore it takes about four to four and a half quarts of cows' milk to present 
sufficient nourishment. This large quantity of milk contains nearly 170 grams of 
proteid, whereas the normal average quantity of proteid ingested by a healthy 
adult does not exceed 100 grams a day. A milk diet, if taken in the quantities 
which are necessary for the maintenance of nutrition, forces the kidneys to eliminate 
enormous quantities of liquid, which they are illy prepared to do when suffering 
from disease, and if the patient does not take these quantities his vitality is impaired 
by nephritis and starvation combined. Again, such a diet causes the kidneys to 
eliminate large quantities of urea and much phosphates, and so, again, kidneys 
which are impaired in function because of disease are forced to perform an excessive 
amount of work. 

It is entirely possible to arrange a suitable diet for cases of nephritis without 
in any way throwing undue stress on any of the organs of digestion or elimination, 
and at the same time maintain the nutrition of the body. Unskimmed milk — 
that is, milk containing cream — is useful, since the fats add a very considerable 
number of calories to the milk, and by the use of starchy food an additional number 
of calories can be provided the patient, who, at the same time, does not receive an 
excess of fluid. As Crofton well says, one litre and a half of milk, plus a quarter 
of a litre of cream, for instance, contains approximately 50 grams of proteids (equal 
to 225 calories), 75 grams of carbohydrates (equal to 337 calories), and 150 grams 
of fat (equal to 1350 calories), or a sum total of about 1912 calories. In order 
to make up the difference of 1088 calories, a little meat, eggs, sugar, butter, toast, 
zweiback, rice, fresh vegetables, etc., may be allowed with impunity, care being 
taken that the caloric value of 3000 is not greatly exceeded, and that all articles 
of diet that lead to the formation of irritating urinary end-products, and spices, 
condiments etc., are avoided. These views are in accord with opinions expressed 
by Robin, of Paris, Bradford, and Hale White, of London, and other clinicians 
of experience. 

The fact having been established by several investigators that in many cases of 
parenchymatous nephritis with edema there is a retention of sodium chloride in 
the tissues, it has been suggested that this salt be temporarily removed from the 
diet. The ground for this is that the excess of salt in the tissues requires an excess 



CHRONIC NEPHRITIS 649 

of fluid to keep it in the normal molecular concentration. When the patient is 
deprived of salt increased diuresis takes place and the dropsy often diminishes. 
However plausible this may be as a theory it accomplishes little in its practice in 
most cases. 

Much discussion has occurred among physicians as to the quantity of water 
which should be allowed patients suffering from Bright's disease. Some believe 
that the amount should be as small as possible, on the ground that copious draughts 
of water engorge the vessels and increase the labor of the heart. That this cardiac 
influence is an important one I doubt, but as Edsall and others have shown that 
excessive water-drinking increases nitrogenous metabolism, and as the kidneys 
in Bright's disease are unable to fully deal with the products of normal metabolism, 
it would seem evident that excessive quantities of water must be harmful. On 
the other hand, there can certainly be no good results from depriving the patient 
of water to the extent of making him suffer. 

The remedial measures other than diet consist in the use on each alternate 
day, if the heart is strong enough, of an electric cabinet bath, in order that the 
skin may aid the kidneys in eliminating fluids and solids from the body. Fresh 
air and sunlight are essential, and severe exercise is to be prohibited. 

Drugs are of little value, except to relieve symptoms which may be annoying. 
It has been the custom of physicians for many years to prescribe iron, usually 
in the form of Basham's mixture, for the purpose of combating the anemia of 
chronic parenchymatous nephritis. This method of treatment does not possess 
the advantages with which it has been credited. The anemia depends upon the 
toxemia of the disease, and this, of course, is not removed by the administration 
of iron. Further than this, iron has a tendency to produce constipation, and con- 
stipation is prone to increase anemia, and, again, constipation is a particularly 
undesirable condition in Bright's disease, since it prevents the bowels from aiding 
the kidneys in eliminating impurities. 

The administration of very large doses of Basham's mixture is, therefore, unwise. 
It should be borne in mind that iron has no curative effect upon the renal condition, 
and therefore it is useless to administer more than the system can utilize for the 
relief of the secondary anemia in the blood. Small doses of Basham's mixture are, 
therefore, as useful as large ones, so far as the anemia is concerned. If the effect 
of Basham's mixture as a diuretic is desired, the liquor ammonii acetatis of the 
United States Pharmacopoeia may be added to a teaspoonful of Basham's mixture 
and given three or four times a day, as in this way the diuretic effect is obtained 
without an excess of iron being given. 

Should evidence of cardiac dilatation develop digitalis is indicated, and may be 
given in the dose of 5 or 10 minims of the tincture three times a day until some 
evidence of its physiological effect is obtained, when the dose should be cut down 
one-half. While the infusion of digitalis has the reputation of being more diuretic 
than the tincture, it is so much more prone to disorder the stomach that the tincture 
is usually preferable. 

A useful formula in place of digitalis will be found on page 486. 

If uremic symptoms develop, the patient should be given a hot pack, and if 
there is any reason to believe that pulmonary edema is threatened, or that the heart 
is too feeble to endure the hot pack, a hypodermic injection of strychnine, 2V of a 
grain, should be given before the pack is begun. Sometimes a cup of strong black 
coffee is also useful at this time. Pilocarpine should not be employed, as it is too 
depressant and prone to produce pulmonary edema. 

In regard to the treatment of uremic convulsions, it is commonly held that the 
administration of morphine hypodermically for this purpose is dangerous, although 
there are some active practitioners who believe that it is a useful drug. It is 
probably more dangerous in the parenchymatous than in the interstitial form of the 



650 DISEASES OF THE KIDNEYS 

disease. If the convulsion is severe chloroform or nitrite of amyl should be given 
by inhalation. (See Uremia.) If the veins are turgescent free venesection should 
be practised. 

The question as to whether the bowels should be thoroughly purged by one 
of the hydragogue cathartics is debatable. On the one hand, it is claimed that 
by this means the intestines are unloaded and a large quantity of liquid and toxic 
material is removed from the body, and, on the other, that the purging may cause 
concentration of the blood, and so increase toxemia. Probably the best rule to 
follow is to administer a hydragogue cathartic only when there is reason to believe 
that the bowels are confined and are consequently loaded with fecal matter. Hypo- 
dermoclysis, which is sometimes useful in the uremia of chronic contracted kidney, 
is worse than useless in chronic parenchymatous nephritis, owing to the presence 
of edema. 

A valuable drug for the purpose of diminishing arterial tension and so decreasing 
the work of the heart and also because it diminishes the loss of albumin through 
the kidneys, is nitroglycerin, which should be given in the dose of yj-g- of a grain 
three or four times, a day. This drug often increases the urinary flow when it is 
scanty. 

Comparatively recently it has been suggested that cases of chronic renal disease 
should be treated by decapsulation of the kidney. This plan of treatment is more 
indicative of surgical enthusiasm than of a clear conception of the pathology of the 
disease. A knowledge of the pathology and the results of experiments on animals 
show its futility, if not its danger. These views will be found in detail in the editorial 
columns of the Therapeutic Gazette for January, 1904, and June 15, 1904. 

Chronic Interstitial Nephritis. — To this form of chronic renal disease the terms 
"contracted kidney/' "granular kidney," "cirrhosis of the kidney," and "sclerotic 
kidney" are applied. 

Pathology. — Chronic interstitial nephritis is usually a primary process, although 
the small white kidney is really a combination of the fibroid and the chronic par- 
enchymatous form. In this type the overgrowth of the connective tissue of the 
kidney is the dominant part of the pathological process, and the degeneration of 
the parenchyma, as represented by the glomeruli and the tubules, plays a secondary 
role. 

When kidneys affected by this state are examined, it is found that they contain 
large masses of fibrous tissue extending through the organ, which by contraction 
cause a shrinkage in size and a puckering of the surface. The capsule becomes 
thickened and exceedingly adherent, and the tissues beneath it are torn if it is 
stripped off. The surface of the cortex is roughened by rounded granules of varying 
size and cysts may appear at various points on its surface (Fig. 112). When an 
attempt is made to cut through the kidney, it is found to be tough and difficult 
to incise. After the organs split open it is seen that the cortical portion is very 
much wasted. 

When the renal tissues are placed under the microscope, they show an irregularly 
distributed increase in the connective tissue, involving in particular the cortex 
and the interlobular vessels. There is also an associated atrophy of the epithelium 
lining the uriniferous tubules. Casts are seen in the tubules, but not to the degree 
in which they are met with in the parenchymatous form of nephritis. The glo- 
meruli in advanced cases may be converted into thick, fibrous bulbs; the walls of 
the bloodvessels forming the tuft may be thickened, and the capsule is seen to be 
dense and fibrous. Nor does the fibroid process affect the finer bloodvessels and the 
connective tissue alone. It extends to the large bloodvessels, and even to the 
renal arteries and veins. 

It is also a noteworthy fact that while cardiac hypertrophy and arteriosclerosis 
are often met with to some degree in parenchymatous nephritis, they are constantly 



CHRONIC NEPHRITIS 651 

found in a well-developed degree in the interstitial type of the disease. This 
cardiac hypertrophy is not limited to the left ventricle, as it is in the parenchymatous 
form. It affects the whole heart and it is often very great. The cause for the 
hypertrophy has been the subject of much debate, but the conditions present in 
the bloodvessels seem to offer an adequate explanation of the state. These vessels 
are always fibroid and lacking in normal elasticity, and this, of course, offers greater 
resistance to the flow of blood through them and into the capillary networks. 
As the process is a gradual one, there is a gradual increase in the demands made 
upon the heart, and this is met by an increasing hypertrophy. The difficulty 
in forcing the blood through the renal vessels also aids in producing this effect, 
but such influence has no doubt been overestimated. 

Fig. 112 




2 cm 



Kidney of chronic interstitial nephritis. The surface is granulated and irregular and Contains numerous 
cysts. The contraction is quite marked, the organ being but little more than half the normal size. 

This is not the place to dilate upon the relationship of these vascular changes 
to the renal lesions. Many persons think that the renal changes are the cause 
of the vascular lesions, and others hold that the vascular degeneration causes 
the renal state. A most striking illustration of the relation between arterial disease 
and contracted kidney was shown by Welch at the meeting of the American Medical 
Association in 1904. He presented a specimen which consisted of a kidney supplied 
by two renal arteries, one of which was sclerotic. The area of the kidney supplied 
by this vessel was typically fibroid, while the other pole of the organ nourished 
by the uninvolved trunk was but slightly changed. 

Again, it is held by many that the overgrowth of connective tissue takes place 
to fill gaps made by the atrophy of the parenchyma, and by others the view is 
taken that the overgrowth of the connective tissue destroys the parenchyma by 
pressure. The latter view seems the more probable, but the former opinion is 



652 DISEASES OF THE KIDNEYS 

adhered to by many pathologists, who believe the primary change is in the 
parenchyma. 

Symptoms. — This is the type of renal disease which is found in the iron-master 
or stock broker who boasts that he has never had a sick day in his life, and who 
begins to find himself, at forty or fifty, lacking in initiative, and who suffers from 
vertigo or dizziness, which he thinks due to a club dinner or a strong cigar. 
This is the disease of the hard-working, " high-nervous-tension" individual who 
has lived hurriedly, and perhaps quieted himself between periods of great exertion 
by a drink or two of whiskey, repeated it may be many times. Often it develops 
in those who have not used alcohol, but given a man who takes little exercise, 
some whiskey, and who is managing one or more large business interests, and he is 
the individual who is paving the way for or has already developed chronic contracted 
kidney. Very rarely, indeed, the disease develops in early life, but cases have been 
reported by a number of clinicians in children as young as from two to seven years. 
Most of these cases have occurred about puberty. Sutherland and Walker have 
reported 2 patients, aged eight and sixteen months, respectively, who had con- 
tracted kidney due to congenital syphilis. 

The symptoms of contracted kidney are, in a large proportion of cases, absent 
until the disease progresses so far that grave secondary changes take place. In- 
deed, it not rarely happens that the patient continues in what he considers good 
health until an acute attack of uremia or cardiac failure sends him to the hands of 
the physician, who may be misled into the diagnosis of acute syncope, due to 
overexertion, by the fact that the heart seems to be feeble, and because the urine 
shows little or no albumin. The number of diagnoses that have been wrecked 
upon the shoal of "no albumin" is a multitude, because it is a peculiarity of chronic 
contracted kidney that albumin is often absent for brief periods, or present in 
such minute amounts that it is overlooked. It is only when the heart begins to 
fail so that some congestion of the kidney develops that the albumin becomes 
more copious. The albuminuria of contracted kidney is, as a rule, as scanty as 
it is profuse in the parenchymatous form. Again, the scanty urine of the parenchy- 
matous type is replaced by a profuse flow in the contracted type, and the patient 
in consequence is disturbed in his sleep by having to get up at night to empty 
the bladder. The specific gravity of the urine is low, about 1.005 to 1.012, and 
it is clear and lacks color. If the urea is estimated this ingredient is usually much 
reduced, not only relatively, but actually, so that the patient in many cases does 
not excrete half the normal output per day. Casts may not be found and rarely 
are abundant, and often the centrifuge has to be employed to reveal them. Further, 
these casts are readily overlooked, for they are chiefly hyaline and so transparent 
that if careful focusing and illumination are not resorted to they are not seen. 
In some cases granular casts are only periodically demonstrable. Occasionally 
hematuria of a persistent and fairly free type arises in the course of chronic nephritis 
of this character and it must be separated from that due to renal calculus. 

The circulatory symptoms of contracted kidney are as important in reaching 
a diagnosis as the renal signs. Indeed it may be said that a man in middle life 
who presents a blood pressure above 150 or 160 constantly is probably developing 
contracted kidney even if no casts or albumin are to be found in his urine. 

Occasionally hematuria of a persistent and fairly free type arises in the course 
of chronic nephritis of this character — it must be separated from that due to renal 
calculus. But sudden pulmonary edema is more common. The pulse is hard 
and tense, and so high is the blood pressure that it may be almost impossible to 
occlude the vessel by pressing upon it. A blood pressure of 260 is not uncommonly 
met with. If the radial artery is rolled under the fingers, it feels like a piece of 
thick rubber tubing, and it is easily recognized as being distinctly fibrous when it 
is palpated carefully. In other words, the blood tension is high and the vessel 



CHRONIC NEPHRITIS 653 

is thick. If the heart is examined, there is found, as a very constant symptom, 
a sharply accentuated aortic second sound at the second right costal cartilage, which 
is due to the high arterial tension. On inspection the apex of the heart is found to 
be displaced downward and outward because of the cardiac hypertrophy. At the 
apex a more or less distinct systolic murmur is heard in many cases, due, as a rule, 
to stretching of the mitral orifice under the stress of high pressure in the ventricle, 
resulting from great arterial tension. When compensation fails, either because 
the heart becomes exhausted or because of fibroid or other myocardial degeneration, 
these symptoms may be replaced by weak heart sounds and by a feeble pulse. 
It is only while the heart has vigor that high tension can exist. 

The respiratory system does not offer much that is characteristic, but complicating 
lesions often develop in these parts. One of the most common is pneumonia, 
which finds a fair field for its development in all cases of renal disease. Indeed, 
in every case of acute pneumonia the physician should study the renal condition. 
Often the routine examination of the vessels and of the urine in a case of pneumonia 
is the first evidence that chronic contracted kidney is present. Perhaps the most 
common respiratory manifestation is difficult breathing resembling asthma, which, 
coming on in persons not previously asthmatic, should always raise the suspicion 
of renal disease. Effusions into the pleural spaces may occur with suddenness and 
cause death, but sudden pulmonary edema is more common. When the toxemia 
is well marked, Cheyne-Stokes breathing may develop. 

The cerebral symptoms consist in vertiginous attacks, migraine-like seizures, and 
persistent, dull, or throbbing headache. Apoplexy due to the degenerative arterial 
changes may take place. 

It is a most interesting fact that edema is as rare in contracted kidney as it is 
common in the large white kidney. When it occurs it is not renal in origin, but 
due to the failure of the heart. The skin in this type of renal disease is usually dry. 

Next in importance to the examinations of the urine and the study of the periph- 
eral circulation in these cases is the observation of the state of the retinal vessels. 
They very commonly reveal the renal condition. 

Different observers give varying percentages of occurrence of retinal lesions. 
Out of 935 cases of renal disease, Groenouw found retinal lesions in 209, or 22.4 
per cent. The age at which they most frequently are met with is from fifty to 
sixty years, but they have been seen in adolescents. 

Five types of these lesions are recognized by ophthalmologists: (a) typical 
albuminuric retinitis; (b) degenerative albuminuric retinitis; (c) hemorrhagic albumin- 
uric retinitis; (d) albuminuric neuroretinitis, and (e) albuminuric papillitis. In 
the first form irregularly shaped white dots or spots appear in and around the macula, 
and may take a stellate form. When the condition is well developed a zone of 
whitish-yellow may surround the head of the optic nerve. Flame-like hemorrhages 
may also appear. The condition is at first one of hyperemia, then of degeneration, 
and finally one of atrophy. In the second form the white spots are small, and 
hemorrhages are more limited, and the white zone about the nerve head is not well 
developed. The third form, as its name indicates, is chiefly hemorrhagic in type, 
and the hemorrhages are large or profuse, while the other changes are insignificant. 
Only when the hemorrhages are absorbed do these areas become whitish. The 
fifth form shows that the process has been confined to the optic nerve, so that a 
papillitis or choked disk is present, the retina being but little involved. 

In some cases detachment of the retina or hemorrhagic glaucoma develop as com- 
plications. 

Of even greater importance than the states just described in the early diagnosis 
of renal and cardiovascular disease is the tortuosity of the retinal veins and their 
narrowing by the pressure of the retinal arteries wherever these vessels cross the 
veins — the so-called " Hirschberg's vessels" (Fig. 114). 



654 



DISEASES OF THE KIDNEYS 

Fig. 113 




Albuminuric retinitis. Granular kidney. Note hard-edged "asterisk" exudation and the silver-wire 
condition of the arteries, and the punctate and linear hemorrhages, (de Schweinitz.) 



Fig. 114 





^-.■ir S -' 



■-'"--■-i.- 



Retina showing compressed veins. The high tension in the arteries can be seen to be narrowing 

the veins by pressure, (de Schweinitz.) 



CHRONIC NEPHRITIS 655 

Because of the fact that the symptoms of chronic contracted kidney are so often 
insidious in their development, the ophthalmologist is often the first to recognize 
the existence of the disease, because a man who considers himself in perfect health 
asks for glasses for failing vision or seeks relief for blindness in one eye. Not 
rarely these patients have repeated attacks of rupture of subconjunctival vessels, 
as well as hemorrhages into the retina. 

Flexner states that the terminal dysentery of Bright's disease is often due to 
the Bacillus dysenteries. 

Prognosis. — Here, again, chronic contracted kidney presents a widely different 
aspect from that of the parenchymatous form, for, while in the latter lesion death, 
as a rule, occurs inside of eighteen months at best, these cases often live for many 
years, if the process is not already far advanced when the case is first seen. The 
points governing prognosis are the state of the heart and the vessels, the ability 
of the kidneys to approximate the normal daily task, and the life which the patient 
can or will lead. It is manifest, from what has been said as to its pathology, that 
the affection is incurable, but patients often live as long as ten or fifteen years after 
undoubted signs of the malady are present. The development of signs of uremia, 
of feeble heart, or of pulmonary congestion, edema, or pneumonia is, of course, 
alarming. Nevertheless I have seen patients develop repeated attacks of pulmonary 
edema each of which seemed to indicate imminent death recover from such attacks 
and be free from them for years. 

By far the most important factor in determining the probable duration of life 
is the state of the retinal vessels already named, de Schweinitz has studied this 
matter most carefully from the standpoint of the ophthalmologist, and we have 
followed a number of cases together. 

These facts are well emphasized by the following figures, which illustrate the 
duration of life in chronic interstitial nephritis after the occurrence of retinal 
changes: Belt collected 419 cases, of which 72 per cent, died within one year and 
90 per cent, within two years. The cases reported from Haab's clinic by Possauer 
showed that none of the men applying for treatment lived more than two years; 
of the women, 68 per cent, died within the same period of time. Of private patients 
who could live comfortably, only 59 per cent, of the men and 53 per cent, of the 
women had died at the end of two years. Gruening collected 100 cases, none of 
which survived more than two years after retinal changes began, and Bull found 
that 69 out of 103 cases died within two years. Of the remaining 34, 17 died 
after a longer period, and 17 were alive at the time his paper was published. Harlan 
analyzed 40 cases with the following results: 33 ended fatally at various periods, 
averaging four months; 3 lived a year after the discovery of retinal changes; 3 
recovered, and 1 regained his eyesight, although the urine was albuminous at the 
end of two years. Miley traced 45 cases, and found the average duration of life 
to be less than four months from the time eye changes were first observed. One 
of his patients lived eighteen months and two fourteen months, but all the others 
died within a year. Webster mentions the case of a clergyman suffering from 
chronic interstitial nephritis, in whom retinal changes had been recognized ten 
to fifteen years before, and "who is still living," and Wert had a woman under 
observation in whom retinal changes had been noticed more than four years before 
he reported the case. Her general condition was much the same as when she came 
under his charge. I have had under my care a number of patients who have lived 
from six to eight years, during which retinal hemorrhages have repeatedly occurred, 
and whose arterial tension has been astonishingly high. Most of these cases 
with very high tension and retinal changes die from apoplexy or an acute myo- 
cardial failure soon after retinal changes develop, the patient often dropping 
dead without warning symptoms. 

Treatment. — There are few diseases of an incurable character in which the patient 
can be so greatly benefited by treatment. 



656 DISEASES OF THE KIDNEYS 

The question of diet in cases of chronic contracted kidney is to be decided along 
pretty much the same lines as those which have been drawn in the article upon 
the treatment of chronic parenchymatous nephritis. W. Hale White has expressed 
the belief, in which I coincide, that, as a rule, this disease is treated too zealously, 
and that in the desire to spare the kidneys the patient is starved, with the result 
that the only means by which the degenerative process can be retarded, namely, 
the maintenance of general good health, is impaired. 

As we do not know of any articles of ordinary diet which can be considered 
really harmful in granular kidney, it is best to give the patient ordinary plain 
digestible foods containing the normal proportions of proteids, fats, carbohydrates, 
and salts, just as it is necessary to give a person in health a similar mixed diet. 
It need hardly be stated that highly seasoned foods, or foods which are difficult 
of digestion, should be interdicted. Again, I am glad to note that Hale White 
is in accord with me in believing that the limitation of these patients to a diet of 
chicken and fish without any red meat is entirely unnecessary. Not only does such a 
limitation do no good, but it is often harmful in the sense that it makes the patient 
consider himself seriously ill, and also diminishes his appetite. Patients with 
interstitial nephritis, however, should especially eschew all forms of alcohol, since 
it is imperfectly oxidized in these cases, and tends to increase arterial tension. By 
far the best treatment of these cases is removal from business cares, avoidance 
of alcohol and tobacco in excess and the use of hot electric cabinet baths, care being 
taken that there is no exposure to cold after them for several hours. If the heart 
is failing rest in bed all, or part of the day will often do far more good than drugs. 
Massage, if not given too severely, is valuable. Often several nights of good rest 
induced by morphine or medinal will work wonders. 

High tension is not by any means an absolute evil. Indeed, after fibroid changes 
in the vessels have developed it is essential to the existence of the patient, since 
by this means blood is sent in adequate amount to the tissues through narrowed 
blood paths. In the early stages when vascular spasm is a large factor in producing 
high tension the use of nitrites is wise since the work of the heart is thereby decreased 
and the tissues are well fed with blood by the relaxing of the arterioles. When 
the fibroid process is marked and is the chief or sole cause of high pressure the 
nitrites cannot affect the vessels, and in large doses only depress the heart. 

A valuable drug in chronic contracted kidney, both from the standpoint of 
the early fibroid changes in the arteries and the underlying systemic state, is the 
iodide of potassium. There can be no doubt that if any remedy exercises an influ- 
ence for good in arresting the pathological changes in the kidneys and in the blood- 
vessels, that remedy is certainly one of the iodides. Usually doses of from 10 to 
20 grains, three or four times a day, are quite sufficient. A useful substitute for 
the potassium salt is the sodium or strontium salts or the syrup of hydriodic acid 
given in ascending doses, beginning with 2 drachms three times a day. 

Digitalis is rarely needed in chronic interstitial nephritis, as the cardiac hyper- 
trophy is usually adequate, but in some cases there comes a time when the blood 
pressure falls largely because the advancing myocardial degeneration and cardiac 
fatigue prevent the heart from pumping the blood with normal energy. In such 
cases digitalis and strophanthus may do good, and nitroglycerin may do harm. 
(See Arteriosclerosis.) 

Uremia is to be treated by the use of the hot pack, if the patient's heart is strong; 
by the employment of hypodermoclysis, and if the patient is fairly full-blooded 
by venesection as well. (See Uremia.) Cups may be placed over the kidneys, 
if there is any condition of renal congestion, and three or four cups should be 
placed over the base of each lung, if any signs of pulmonary edema develop. When 
evidences of pulmonary difficulty arise, full hypodermic doses of strychnine and 
atropine are advisable. 



AMYLOID DISEASE OF THE KIDNEYS 657 

Many practitioners have thought it wise to employ full doses of morphine 
hypodermically in the treatment of uremic convulsions. I have made a collec- 
tive investigation in regard to this matter, and have obtained the opinion of 
physicians of experience in both this country and in England. This opinion is 
almost universally adverse to this use of morphine. 

The convulsions should be controlled by nitrite of amyl and by chloroform given 
by inhalation. (See Uremia.) 

The question of renal decapsulation has already been discussed under Chronic 
Parenchymatous Nephritis. 

If the progress of the disease is slow, it is advisable to send the patient to some 
warm climate during the winter months, if his home is in a northern latitude. 
The object is to avoid rapid changes in temperature in the atmosphere and con- 
sequent chilling of the surface, with secondary congestion of the kidneys and 
decrease in the activity of the skin. 

The best climate is to be found in the neighborhood of San Diego, California, or 
in Egypt. 

AMYLOID DISEASE OF TEE KIDNEYS. 

Definition. — Amyloid disease of the kidneys is part of a general process affecting 
many organs. The renal manifestation is characterized by the deposit of lardacein 
in the subintimal stratum of the bloodvessels, in the glomeruli, and, to a lesser 
degree, in the connective tissue of the tubules. 

Etiology. — Amyloid disease of the kidney is usually the result of a prolonged 
suppurative process, such as hip-joint disease, chronic pulmonary tuberculosis 
with cavity, or any cause whereby the system is simultaneously sapped by suppura- 
tion and poisoned by the absorption of toxic substances. It may also be a sequence 
of one of the prolonged fevers or occur as an associated change with chronic diffuse 
nephritis of the parenchymatous type. Syphilis is a common cause, and malaria 
may be the only demonstrable antecedent. 

Pathology. — The kidneys are usually enlarged, and when incised the cut surface 
is shining or polished in appearance. When the condition is combined with inter- 
stitial nephritis these organs may be small. The surface of the organ is paler 
than normal, particularly in the cortex, but the pyramids are deep red in hue, and 
the glomeruli are readily seen. 

If an aqueous solution of iodine is painted over the cut surface of such a kidney, 
the areas most affected by the amyloid change stain a deep mahogany brown, 
and if to these areas is applied a dilute aqueous solution of sulphuric acid, the brown 
hue is changed to blue. 

Microscopically the kidney structure when examined reveals the fact that the 
capillary vessels forming the tufts in the capsules are the parts of the parenchyma 
most affected, the tuft being transformed into a waxy mass. The disease process 
also involves the afferent and efferent bloodvessels of the tuft and the straight or 
direct vessels of the kidney. In marked cases the connective tissue of the tubules 
is infiltrated, the interstitial tissue increased, and the epithelial cells may be granular 
or fatty, as in parenchymatous nephritis. In some instances all these types occur 
together. 

Symptoms. — There are no symptoms which, taken by themselves, may be con- 
sidered indicative of amyloid disease of the kidneys. It is only when certain 
urinary signs develop in a case which is the subject of those maladies which predis- 
pose to amyloid change that we can say that a diagnosis is assured. The patient 
is usually pallid, may be well covered by unhealthy waxy fat, and the heart is not 
rarely somewhat enlarged, although no less an authority than Dickinson contradicts 
this view. The urine is passed more freely than is normal. It is clear and has a 
low specific gravity, about 1.005 to 1.010. The quantity of albumin which it contains 
42 



658 DISEASES OF THE KIDNEYS 

varies, but it is usually present in considerable quantity. There is a distinct increase 
in the quantity of serum globulin in the urine. Under the microscope the tube 
casts are found to be hyaline, fatty, or waxy. Occasionally the amyloid reaction 
already named may be demonstrated in the urine. The degree of edema and 
the state of the bloodvessels and heart depend more upon the presence of associated 
nephritis than upon the amyloid change itself. If nephritis is well developed, 
anasarca and high arterial tension may be present as an associated state. 

Prognosis. — The prognosis depends upon the gravity of the causative process 
and the degree to which the secondary change in the kidneys has progressed. Then, 
too, it must be remembered that amyloid disease is not a condition limited to the 
kidneys, but affects such organs as the liver, spleen, and even the heart, and, 
therefore, the patient is peculiarly handicapped in his struggle for health. If the 
casts are fatty or waxy, and are present in large numbers, if the albuminuria is 
copious, and if anemia is marked, the outlook is bad. Indeed, in every case it is 
anything but good, and the longer the suppurative process continues the worse 
the outlook becomes. 

Treatment. — This consists in the same measures as have been recommended for 
chronic parenchymatous nephritis, such as iron, arsenic, cod-liver oil, and fresh 
air and sunlight to combat the underlying cause. If possible, the suppurative 
process, if such is the cause, should be removed. 

UREMIA. 

Definition. — Uremia is a condition in which as the result of faulty activity of 
the kidneys a patient develops a series of symptoms of which the most notable 
are stupor, coma, convulsions, or paralysis, or in other instances gastro-intestinal 
disorders. 

Etiology and Pathology. — The causes of uremia are not clearly understood. It 
is well known, and universally recognized, that the condition is due to perverted 
renal activity, both as to the elimination of the ordinary products of metabolism 
and the effects of renal disease upon the tissues of the body, but beyond this the 
actual cause is as yet undetermined. 

At one time, under the leadership of Traube, the idea prevailed that the symptoms 
of uremia were dependent upon changes in the circulation in the brain produced 
by the constriction of its arteries by the vascular changes associated with nephritis 
or by cerebral edema. In other words, that cerebral anemia due to arterial con- 
striction was the cause of the symptoms. This view has been cast aside because 
it has been shown that ligature of the carotid arteries does not cause uremic symp- 
toms, because it has been proved that the high arterial tension of renal disease 
results in dilatation of the cerebral vessels, since they are poorly endowed with 
muscular fibres, and finally because it is impossible to cause active contraction of 
the cerebral vessels by any drug or measure used for raising arterial tension. 

The theory, that uremia is due to the retention of the ordinary effete materials 
of the body owing to renal disease, also cannot be accepted as a complete explanation 
of the condition, because it has been found that ligation of the renal arteries in 
animals and ligation of the ureters fail to produce uremia, although the function 
of the kidney is by these means completely arrested. Again, suppression of urinary 
secretion by the presence of stone in both kidneys, and even by necrosis of the 
cortex of both kidneys in man, does not cause typical uremia. Further than this 
the injection of urea and even of healthy urine into the blood does not cause any 
symptoms if true uremia. Again, in certain cases of renal disease, as in chronic 
contracted kidney of the aged, when the renal excretion is seriously impaired, 
uremia is rare. All forms of deficient renal activity do not, therefore, cause uremia. 

A third theory is that as a result of the renal disease peculiar poisons are made 



UREMIA 659 

in the body which when they accumulate cause uremia, or that the condition of the 
system in renal disease permits certain micro-organisms to grow and produce a 
toxic substance. 

A fourth opinion is that the kidney secretes when in health an " internal secretion" 
which governs metabolism and so prevents the formation of certain poisons. The 
last theory falls to the ground because ligation of the renal vessels does not result 
in uremia, as it would do if these symptoms were caused by the lack of some internal 
secretion. 

We are left, therefore, with the fact that uremia is due to the presence in the 
body of peculiar poisons arising in Bright's disease, either as the result of the 
growth of micro-organisms or perverted metabolism, and with the knowledge that 
the kidneys are unable by reason of disease to be active in the elimination of any 
poisons. It would seem probable that this combination of extra poisons and 
deficient renal activity are the two factors necessary to the development of uremia. 
This is further supported by the fact that if the labor of the kidneys is increased 
by gastro-intestinal fermentation or putrefaction, an attack of uremia is very prone 
to occur. Finally, there is additional proof of the development of extra poisons 
in the body in renal disease. This is found in the marked loss of weight in patients 
suffering from nephritis, the wasting showing that nutrition is seriously impaired 
and that tissue breakdown is marked. Manifest loss of weight may not be present 
because of dropsy, but, if this is removed by purging, the wasting is manifest. 
The toxicity of the urine is increased. Golla believes there is sufficient evidence 
of a specific toxemia of the nervous system to make imperative a search for a 
specific uremic poison before becoming resigned to any theory of multiple 
intoxication. 

Symptoms. — Uremia occurs in several forms. The most common manifestation 
of uremia is that in which the patient passes into coma, which may be /preceded 
by delirium and drowsiness. In certain cases there is associated with the develop- 
ment of the comatose state twitchings and contractions of widely separated muscles, 
and particularly the extensors and flexors of the forearms. 

The most startling, but by no means the most frequent, form is the convulsive 
type. In this condition the patient, with or without any preliminary indications 
of nervous disturbance, is seized with a more or less severe epileptoid attack, which 
usually involves the muscles of the face and hands, and then spreads rapidly to 
the whole body. No sooner is one seizure over than another comes on, and with 
the repetition of the attacks, or it may be with the development of the first fit, 
the patient becomes unconscious, or has very distinct mental impairment. The 
body temperature usually falls unless the convulsions are so severe as to temporarily 
cause a slight rise. The knee-jerks are usually markedly exaggerated and the 
pupils are contracted. Because these symptoms are so extraordinary, the idea 
has gained ground that convulsive seizures in uremia are commonly met with. 
This is incorrect, as they are not common except in that peculiar form of eclamptic 
convulsion due to toxemia which is encountered in pregnancy. 

A third form is that in which there is marked respiratory disorder of a dyspneic 
type. The patient finds it exceedingly difficult to breathe, and feels as if suffocated. 
Not only is the respiration wheezing, as it is in asthma, but it is peculiar in that it 
is accompanied by a hissing sound, the patient very frequently ending each expira- 
tion with a puffing hiss. Associated with these symptoms there may be some 
duskiness of the skin, but cyanosis is not marked. The patient's mind is usually 
clear, and he not infrequently complains of his great difficulty in getting sufficient 
air. As this condition proceeds, the respirations may become " Cheyne-Stokes" 
in type. Although it is generally held that the development of Cheyne-Stokes 
respirations under any circumstances is indicative of a fatal result, it not infre- 
quently happens that patients with this symptom arising during the course of 



660 DISEASES OF THE KIDNEYS 

uremia recover from that particular attack. Sometimes the Cheyne-Stokes breath- 
ing occurs only during sleep, and it may be the only manifestation of uremia, the 
mind remaining clear. 

There is still a fourth form in which the patient develops mania or acute insanity. 
He is restless, very excited, and may be extremely violent. As a rule, after 
these symptoms have lasted for a short time, the mental excitation is followed by 
gradually increasing drowsiness which finally passes into coma. 

In the so-called paralytic form of uremia, either hemiplegia or monoplegia may 
come on suddenly, as does hemiplegia in cases of cerebral hemorrhage. But the 
paralysis is not due to rupture of a bloodvessel, to a formation of a thrombus, 
or the plugging of a vessel by an embolus. So far as is known, it depends upon 
intoxication of the nervous centres controlling the parts involved in the paralysis. 
It is of course possible for cerebral apoplexy to complicate uremia, and for this 
reason it may be difficult to immediately make a differential diagnosis between 
the hemiplegia of uremia and the complicating hemiplegia of cerebral rupture. 

There is still another form of uremia which manifests itself in persistent insomnia 
with muscular irritability or cramps and hiccoughs. 

In some cases of uremia violent g astro-intestinal disorders suddenly assert them- 
selves, vomiting may be persistent and severe, and nausea intense. Not rarely 
profuse serous purging comes on, which may be an effort on the part of the body 
at elimination. 

In some cases uremic amaurosis develops. This consists in sudden, bilateral, 
and complete blindness. Rarely one eye suffers before the other, and in some 
cases the perception of light may be preserved, although ordinary vision is destroyed. 
In the greater number of these cases the opthalmoscope reveals no changes in 
the retina, although it may be found to be edematous and there may be an appear- 
ance of the optic nerve like that of choked disk. This condition develops more 
commonly in those cases of acute nephritis associated with the eruptive fevers, 
as scarlet fever, than in ordinary chronic nephritis. The amaurosis lasts for a few 
hours to a day or even longer than this, and vision often returns as suddenly as 
it was lost. The prognosis is favorable as to vision. 

All of these forms of uremia differ very materially from that type which has been 
called "latent uremia" by the last Sir William Roberts, and of which mention may 
be found in connection with the article upon Nephrolithiasis. In these patients 
life is maintained for periods varying from one to two weeks in the presence of 
total urinary suppression. They remain conscious almost to the moment of death, 
and the uremic symptoms just described in their various forms are never present. 
There may be some headache and nausea and weakness and drowsiness. The 
temperature is subnormal and the pupils are contracted. In some instances 
vomiting is a prominent symptom in this type of uremia. It is unfortunate that 
the term "latent uremia" should be applied to this condition, as the condition is 
really not one of latency nor of uremia as that term is generally understood. 

A very important symptom of uremia is the peculiar odor about the patient, 
which is quite characteristic and which may be due in part to urea which is being- 
eliminated by the skin or to the presence of some toxic substance as yet not isolated. 

Diagnosis. — The presence of albuminuria with casts of the uriniferous tubules, 
of somewhat thickened bloodvessels, and of an accentuated aortic second sound 
in association with the development of any of the symptoms which have just been 
described, makes the diagnosis of uremia practically certain. If the patient is 
bled for the purpose of relieving symptoms of venous engorgement, it is wise, if 
opportunity offers, to make a determination of the urea in the blood if the physician 
is sufficiently skilful to perform the necessary manipulations. The most difficult 
differentiation lies between uremic monoplegia and hemiplegia due to rupture of a 
bloodvessel, or to an embolus, or thrombus. In some cases such a differentiation 



UREMIA 661 

is impossible because these vascular lesions may be present as a complication of the 
uremic state. The presence of the urinary changes just described and of the other 
signs and symptoms mentioned in the article upon Bright's Disease will serve 
to aid in the differentiation to some extent. 

At times, if the uremic poisoning is not of such a character as to produce con- 
vulsions, but merely semiconsciousness, the patient may live in a state of stupe- 
faction for several days or weeks, and because of the mental condition, of the feeble 
pulse, of the slight fever, and of the coated tongue, be considered a case of typhoid 
fever or general tuberculosis. Curschman first pointed out, and my experience 
is confirmatory of his statement, that a Babinski reflex is of diagnostic and prog- 
nostic value in uremia. Soper and Granat have shown that when the cerebrospinal 
fluid contains more than 0.2 per cent, of urea, uremia is severe, and a rapidly fatal 
termination is likely. Even a content of between 0.1 and 0.2 per cent, is very 
grave. A content of 0.05 to 0.1 per cent, suggests distinct impairment of proper 
renal activity. This observation I have confirmed in a limited number of cases. 

Opium poisoning is to be separated from uremia by the presence of an odor 
of laudanum on the breath, if laudanum has been used instead of morphine, by the 
fact that the pupils are contracted to a pin-point, and by the examination of the 
urine. From alcoholism uremia is separated by the examination of the urine, 
by the odor of alcohol in the breath, and by the history of the patient. But it 
must not be forgotten that many alcoholics have chronic renal disease and that the 
ingestion of considerable quantities of alcohol may precipitate an attack of uremia, 
and so an alcoholic history may be present which will mislead the physician. 

As a rule, sudden fulminating uremic symptoms develop in patients with chronic 
interstitial nephritis, whereas the types of uremia with headache, vertigo, and other 
warnings of toxemia are seen most frequently in the parenchymatous form. 

In hot weather, when men are exposed to great heat in rolling mills and furnaces, 
the distinction between heatstroke and uremia may be difficult, since in both 
conditions violent convulsions with cyanosis may be present. In heartstroke, 
however, the temperature is usually much higher than in uremia and the cyanosis 
is usually more intense. It is, however, quite possible for heatstroke to complicate 
nephritis and to cause an attack of uremia. 

Prognosis. — The prognosis is always grave, but not necessarily fatal by any 
means. A professor in one of the medical schools of Philadelphia had a moderate 
uremic seizure after nearly every lecture for a whole winter course of lectures 
before a final fatal seizure came on. In uremia due to acute nephritis the prognosis 
is good if the patient can but survive the attacks long enough for the kidneys to 
regain their function. In the cases due to chronic renal disease the outlook depends 
to some extent upon the general state of the patient and particularly the condition 
of the lungs. If any tendency to pulmonary edema or congestion is present, the 
outlook is much more serious. 

Treatment. — The treatment of uremia depends to some extent upon the variety 
of nephritis which has produced it and the peculiarities of the individual who is 
suffering from the attack. When uremia comes on as a complication of acute 
nephritis, such as that complicating scarlet fever, the patient should have hot 
compresses placed across the small of the back, and, if diarrhea is not already 
present, one of the saline purgatives, such as the citrate of magnesium or the 
sulphate of magnesium, should be given in sufficiently concentrated form to produce 
several watery movements. After this 5 to 10 grains of the citrate of potassium 
dissolved in Poland water should be given three or four -times a day. If the 
symptoms of uremia persist, it will be necessary to place the patient in a warm 
pack. This may be given in one of two forms, the choice of the form depending 
upon the condition of the patient's skin and the presence of an eruption resulting 
from the disease. The choice also depends to some extent upon the temperature 



662 DISEASES OF THE KIDNEYS 

of the patient. If the rash has to some extent disappeared, the skin is dry and 
hot, and the temperature high, it is well to wrap the patient in a sheet wrung out 
of water at 70° or 80°, and then to immediately surround him with a dry blanket. 
The primary effect of this cold sheet is to aid in the dissipation of heat over the 
body, but it very rapidly becomes warmed by the heat of the body so that the 
patient at first is under the influence of cold, and very shortly afterward is sur- 
rounded by a warm pack. The primary cold drives the blood from the surface, 
and the secondary heating fills the peripheral capillaries so that the temperature 
is lowered by an improved peripheral circulation, and the skin is thoroughly supplied 
with blood so that it has a better opportunity to eliminate poisons. If no fever 
is present, and the rash has not faded, or if for any reason it is considered inadvisable 
to use cold primarily, the hot pack may be given, the patient being quickly wrapped 
up in a blanket which has been wrung out of water as hot as the skin can bear. 
Outside of this is placed a dry blanket and on the patient's head is placed an ice-bag 
to prevent cerebral congestion. Every few moments the patient is given a few 
sips of cold water to drive the blood from the internal portions of the body to the 
skin, the object being to flush the peripheral circulation, and to cause a sweat 
which will relieve internal congestion and eliminate impurities from the body. 
If the arterial tension is high, nitroglycerin may be given in the dose of -g-J-g- of a 
grain to a child, or t -J-q- to a man, every three or four hours; or, in its place for a 
child | to 1 drachm of the sweet spirit of nitre may be given. 

In the uremia of chronic parenchymatous nephritis a plan of treatment identical 
with that which has just been described for that of acute nephritis may be carried 
out. As a rule, the patient is already too anemic to permit of bleeding, and his 
tissues are so edematous that hypodermoclysis is impossible. 

In the uremia of chronic contracted kidney with high arterial tension, the meas- 
ures already indicated for the uremia of acute nephritis may be instituted, the 
nitroglycerin being particularly useful, and being given hypodermically in order 
that it may act promptly. It also has a beneficial effect in that it relaxes any spasm 
of the renal bloodvessels and so produces diuresis. If there is much engorgement 
of the venous system, venesection is exceedingly useful, particularly if it is accom- 
panied by free hypodermoclysis, or, in urgent cases, by an intravenous injection 
of normal saline solution. Sometimes in these cases if the heart seems strong, 
small doses of pilocarpine, f of a grain, may be given hypodermically to aid in 
producing the sweat which is caused by the hot pack, and, with the object of pre- 
venting cardiac depression, it is usually wise to combine with it -£$ of a grain of 
strychnine. The lungs and the heart should be carefully watched, and if any 
signs of pulmonary edema or cardiac failure develop, strychnine and atropine 
should be given freely, and 1 or 2 drachms of Hoffmann's anodyne should be 
administered as a rapidly acting diffusible stimulant. In some cases in which 
there is a tendency to suppression of urine, not only nitroglycerin but cocaine 
in the dose of J to J of a grain may be given hypodermically twice or thrice a day. 
Should convulsions occur, they should be controlled by chloroform, if they are 
exceedingly severe, and by the use of 1 drachm of bromide of sodium and 20 grains 
of chloral by the rectum. Morphine, which has been largely used to control 
uremic convulsions, is not regarded with favor by most practitioners at the present 
time. If the arterial tension is exceedingly high, full doses (5 to 10 minims) of 
the tincture of veratrum viride, repeated every half-hour until some evidences 
of circulatory depression are produced, may be advantageous. 

PYELONEPHRITIS AND PYELITIS. 

Definition. — Pyelonephritis signifies an inflammatory process involving both the 
pelvis of the kidney and the kidney texture itself. The term is usually applied 



PYELONEPHRITIS AND PYELITIS 



663 



to that form in which the condition is suppurative. Sometimes it is called suppura- 
tive pyelonephritis. Pyelitis is an inflammatory state of the pelvis of the kidney 
without involvement of the kidney proper. As synonyms to pyelonephritis we 
may use the terms pyonephritis, pyonephrosis, and caseative nephritis. 

Etiology. — These conditions are nearly always the result of infection from below; 
that is, they are secondary to infection of the lower urinary tract, viz., the bladder 
or urethra. Very rarely infection of the kidney may take place through the blood, 
but this is only when the vital resistance of all the tissues is greatly impaired, or 
when the infection is very virulent, for the healthy kidney quite readily eliminates 
micro-organisms brought to it by the blood stream. It is possible, too, in cases of 
floating kidney, in which the ureter becomes twisted or obstructed so that the 
vital resistance of the pelvis is impaired, that infection through the blood may 
ensue. Although stones in the kidney are now attributed to bacteria, it is conceiv- 
able that a renal calculus by damaging the pelvic wall may prepare the way for 
infection, so acting as a direct cause of pyelitis. Infected emboli may also produce 

this state. 

Fig. 115 




Brewis' case of pyelonephritic kidney. Girth, forty-eight inches; weight, forty-five pounds. 



The micro-organisms which most frequently cause pyelitis and pyelonephritis 
are the Bacillus coli communis, the Streptococcus pyogenes, the Staphylococcus 
pyogenes aureus, the tubercle bacillus, the typhoid bacillus, the gonococcus, and 
the Bacillus proteus vulgaris. Brown has shown that the Bacillus coli communis 
is the most frequent cause in women, probably because of the near relationship 



664 DISEASES OF THE KIDNEYS 

of the anus and the meatus urinarius. Brown also asserts that, whereas some 
devitalizing cause is usually necessary to permit infection, a constantly ammoniacal 
urine is sufficient cause in many cases and Brewer and others have reported instances 
in which an acute hematogenous infection of one kidney occurred with violent 
pain at onset. When one kidney is involved it is usually the right. 

Pathology and Morbid Anatomy. — Pyelonephritis may be catarrhal, pseudo- 
membranous, gangrenous, or suppurative. The first two forms usually depend 
upon, and are overshadowed by, associated diseases such as typhoid fever, and 
rapidly assume the suppurative type. In pyelonephritis the mucous membrane 
lining the pelvis of the kidney is thickened and coated with pus. A fibrinous 
exudate may also be present. The kidney structure may be involved in two ways: 
either small abscesses are scattered through the parenchyma of the kidney or in long 
white streaks which project themselves along the tubules. The renal tissue in and 
near these areas is, of course, necrotic. If the suppurative process proceeds, the 
calyces of the kidney become enlarged, the renal tissues waste and suppurate, 
and the kidney structure is largely replaced by a large single or multiple abscess. 
Finally, if the patient survives so long, the liquid drains off through the ureter, 
and the pus becomes inspissated so that a cheesy mass remains which may become 
infiltrated with lime-salts. This process may extend to the tissues surrounding 
the kidney causing paranephritis. When one kidney is involved the cause is 
nearly always primary disease in the bladder, and to this type the term " surgical 
kidney" is given. 

Symptoms. — The symptoms of pyelitis and pyelonephritis may be in many 
cases so masked by the conditions which produce this disorder in the renal pelvis 
that they are overlooked. Thus the urinary picture is commonly obscured by an 
associated cystitis, which may either precede or follow the renal lesion. The most 
definite symptoms are pain and tenderness in the back over the kidneys, with or 
without frequent urination. The pain is increased by jarring the body or by cough- 
ing, and it is often felt in the testicle or inside of the thigh on the affected side. 
The quantity of urine passed is usually scanty in acute pyelitis but profuse in the 
chronic form. With the development of suppuration septic fever develops, vomiting 
may come on, and occasionally a profuse septic sweat follows a chill and fever. The 
urine is acid and contains pus, blood cells, and degenerated epithelium. At times 
the urine may appear perfectly normal, but soon returns to its earlier state. This 
variation is due to the ureter becoming blocked by a plug of putty-like pus, so 
that for several hours only one kidney, and that the healthy one, drains into the 
bladder. Such a variation in the urine therefore proves the difficulty to be 
unilateral. This plugging of a ureter may give rise to attacks of pain, somewhat 
like those due to a renal calculus becoming engaged in the ureter, but the pain is 
rarely so severe. 

Diagnosis. — Pyelonephritis is sometimes taken for malarial fever, as are other 
septic processes, because of the chills, fevers, and sweats. An examination of the 
patient and of his blood and urine readily excludes malaria and reveals the renal 
disease. 

In other cases the dry tongue, loss of weight, diarrhea, and abdominal tympany 
may mislead one into a diagnosis of typhoid fever. 

From suppurative cystitis the condition is to be differentiated by the fact that 
the pain is felt chiefly in the renal region, by the greater quantity of pus in the 
latter state, by the greater alkalinity of the urine in vesical disease, and finally 
by the use of the cystoscope and the ureteral catheter. 

Usually there is more albumin in the urine in pyelonephritis than in cystitis, 
and more discomfort in the suprapubic area in the latter condition than in the 
former. 

From perinephric abscess pyelonephritis is separated by the greater tenderness 



HYDRONEPHROSIS 665 

over the kidney in the former condition, by the fact that this area is not bulging 
in the latter state. In some cases, however, of pyelonephritis very distinct bulging 
over the kidney is manifested. A valuable sign in this state is that the swelling 
occasionally diappears or diminishes as the pus and urine escapes through the 
ureter, when an obstruction is removed. A bulging or swelling in the renal area 
may also be due to hydronephrosis, but there is usually no fever in this state. 

The possibility of a painful swelling in the region of the kidney being due to an 
aneurysm must always be excluded before operation is resorted to. Most impor- 
tant of all is the absence of pus in the urine in the first condition and its presence 
in the second. 

Prognosis. — Prognosis depends largely upon the cause of the malady and the 
state of the kidney. If the condition is one of simple pyelitis, occurring during 
the course of one of the infectious diseases, the outlook is not necessarily bad. (See 
Typhoid Fever.) If the suppuration is marked the prognosis is not good, and if 
the kidney structure is involved to the extent of pyonephrosis the prognosis is 
bad, and death may come from the exhaustion of prolonged septic fever, from 
the extension of suppuration to other parts, or because of amyloid degeneration 
in other organs. 

Treatment. — The treatment of pyelitis in its milder phases consists in the use 
of mild diuretics if the urine is concentrated, of counter-irritation by cups or heat 
over the loins, and rest in bed. When bacteriological examination of the urine 
reveals the colon bacillus as the causative factor, excellent results often follow 
the use of colon vaccine. No highly seasoned foods are permissible. The reaction 
of the urine must be determined. If the urine is acid, alkaline diuretics and salol 
are useful. If it is alkaline, then we may give 10 grains of uritone,or urotropin 
three or four times a day in a glass of sparkling water, preceding it by one or two 
hours with full doses of acid sodium phosphate in solution. The diet should be 
hearty and easily digested. Bitter tonics and iron are useful, but quinine is 
contra-indicated because of the state of the bladder, upon which it acts as an 
irritant. When hectic fever is developed and remains persistent the patient 
should be subjected to nephrotomy or nephrectomy before he becomes exhausted 
by sepsis. Opium or morphine may be needed to control the pain. Several 
observers have reported cases in which benefit was derived from lavage of 
the renal pelves, by means of ureteral catheterization. This is not always safe. 

HYDRONEPHROSIS. 

Definition. — Hydronephrosis is a condition in which because of obstruction 
in the ureter there takes place in the pelvis of the kidney an accumulation of fluid 
which is not purulent. This fluid as it increases in quantity stretches and dilates 
the pelvis and the calyces until very large amounts of fluids are retained and a 
good-sized cyst is formed. 

Etiology and Pathology. — Hydronephrosis may be acquired or congenital, constant 
or intermittent. It arises from permanent or intermittent closure of the ureter 
so that the urine cannot escape into the bladder. When congenital the ureter 
may never have been patulous or it may have a stricture or be abnormally inserted 
into the bladder wall. When acquired it arises from stricture of the ureter, or 
from plugging by a clot or a fragment of calculus. It may result from twisting 
of the ureter in floating kidney, but calculus is the most common cause of 
unilateral hydronephrosis. When either of these causes is responsible for the 
retention of fluid, the hydronephrosis may be intermittent, because, when the twist 
is undone, or when the calculus slips, the fluid can escape. The patient may remain 
free from trouble for years until the obstruction forms again. The obstruction 
may be at the bladder, as in tumor of that organ, or consist in a paracystitis. In 



666 DISEASES OF THE KIDNEYS 

the female pelvic adhesions, neoplasms, and cysts may press upon the ureter and 
impede the urinary now. 

The secondary effects of this condition upon the kidney are disastrous if it is 
long continued and severe. The pressure acting upon the renal tissues causes 
atrophy and wasting so that finally the kidney structure largely disappears and 
in its place only a large collection of fluid, surrounded by fibrous tissue and rem- 
nants of renal tissue, remain. So large may the tumor grow that it projects down- 
ward into the abdomen, and it has even been mistaken for ascites. The other 
kidney may be similarly affected, but often it undergoes hypertrophy to compensate 
for the inability of its mate. 

Symptoms. — The presence of symptoms depends largely upon the rapidity of 
the accumulation of fluid and the size of the renal pelvis. If it develops slowly 
and if a previous attack has enlarged the pelvic capacity, much fluid may be present 
without the patient presenting any symptoms. If, on the other hand, the fluid 
rapidly accumulates, pain may be very severe. When stricture is the cause the 
accumulation is usually slow, but when a twist or a calculus closes the ureter it is 
speedy and painful. In the slow cases sharp pain may be replaced by a sense of 
weight and dragging. A very characteristic sign in some cases, when the obstruction 
is suddenly removed, is a profuse flow of urine which fills the bladder rapidly, 
although it may have been emptied but a short time before. The tumor which 
may have been present in such a case disappears with the flow. 

Diagnosis. — Palpation of the abdomen reveals in some cases a mass projecting 
from beneath the floating ribs, in which fluctuation may be detected. When the 
history of the causes and symptoms is as clear as has just been detailed the diagnosis 
is not difficult, but the history is frequently not clear. In children such a mass 
has been mistaken for an enlarged spleen and for a sarcoma of the kidney or of the 
retroperitoneal glands. (See Tumors of the Kidney.) In other cases, if the 
kidney is floating and hydronephrotic, the tumor may be taken for an ovarian 
cyst. In still other instances the tumor may so fill the abdomen as to lead to a 
diagnosis of ascites. Thus, Sutton has recorded a case in which the cyst held no 
less than thirty gallons. Aspiration of the fluid may reveal that it contains some 
urea or that it partakes of a urinous odor. 

Prognosis. — The prognosis depends entirely upon the cause of the difficulty 
and the state of the other kidney. When the closure is congenital and complete, 
death ensues in a few days. When the closure is due to a twist of the ureter or to a 
calculus, much depends upon whether the flow is entirely stopped and how long 
it is arrested. A single attack followed by sudden relief may never be repeated. 
When the disease is bilateral the gradual involvement of the kidneys may result 
in uremia, or if infection of the kidneys ensues suppuration may develop. 

Treatment. — It is evident that no medicinal treatment can be curative in hydro- 
nephrosis. Morphine and atropine hypodermically to allay pain and relieve spasm 
may be useful at a time when the obstruction is complete and the accumulation 
of fluid rapid. If the condition is due to a floating kidney with twisting of the 
ureter, the replacing of the kidney in its normal position may give relief. In 
other instances the temporary assumption of the knee-chest position is curative. 
If the attacks occur very frequently, it may be wise to suture the kidney in place. 

When hydronephrosis occurs in a woman, ureteral catheterization is of value: 
first, because it withdraws the accumulated fluid, and, second, because if a stricture 
is present a catheter may dilate the stricture and so exercise a curative influence. 
But catheterization of the ureter is a much more delicate procedure than catheter- 
ization of the bladder, and there is greater danger of infecting the ureter and 
kidney, so that the greatest possible caution in regard to asepsis must be secured. 
In certain cases where the accumulation of fluid is very rapid, and where the 
symptoms are urgent, aspiration has been practised, but this is not devoid of danger, 



CYSTIC DISEASE OF THE KIDNEY 



667 



and gives relief in only about 50 per cent, of the cases. Morris directs that the 
needle is best inserted at the most bulging point, but that if no such point is manifest 
it should be driven in half-way between the last rib and the crest of the ilium and 
between two and two and a half inches behind the anterior superior spine of the 
ilium, if it is the right kidney which is in trouble. An aspirating needle should be 
used instead of a trocar and cannula. When repeated aspirations are required 
for relief, nephrotomy is necessary. 

CYSTIC DISEASE OF THE KIDNEY. 

Cysts of the kidney occur as congenital malformations and as those acquired in 
later life. There is perhaps no more striking object to be found in a collection of 
pathological specimens than a congenital cystic kidney. This condition not rarely 
affects both kidneys, which is an important point to bear in mind if any operation 
on one kidney is thought of. These cystic kidneys are not composed of one large 
cyst, but of a multitude of cysts massed together regardless of shape and size, 



Fig. 116 




Congenital cystic kidney. (Kast and Rumpler.) 

and separated by fibrous bands or by strands of atrophied renal tissue. The con- 
tents of the cyst is usually a clear yellow fluid with an acid reaction and containing 
urinary salts, but occasionally the fluid is opaque and may contain small amounts 
of blood. The causes and processes by which these cysts are developed are not 
definitely known, but it is thought they are formed by extraordinary dilatation 
of the tubules or of Bowman's capsules. Shattock believes they are due to mal- 



668 DISEASES OF THE KIDNEYS 

development of the mesonephron. Such kidneys often weigh several pounds. 
Although congenital in origin, it is to be remembered that life may be continued 
far into adult years before they give any trouble. 

Congenital cystic kidney (Fig. 116) may project well below the ribs and give 
rise to a diagnosis of sarcoma, hydronephrosis, or of enlarged spleen. 

Cysts of the kidney, single or multiple, may be present in kidneys which otherwise 
show no abnormalities, and these cysts may be smaller than a pea or larger than 
an orange. Their contents may be clear or brown in color, and may be gelatinous 
in character. 

Attention has already been called to the small cysts which are seen on the surface 
of the kidneys in chronic interstitial nephritis. At times it is difficult to determine 
whether the kidney is the site of acquired or congenital cysts when these cysts 
become large and multiple. 

Echinococcus cysts of the kidney also occur. (See article on Parasitism.) 

The symptoms of congenital cystic kidney are in no way peculiar unless the 
kidney be large enough to project in the manner described. Aside from this sign 
the patient presents no signs of renal disease until the cyst, by increase in growth 
and resulting decrease in renal tissue, develops renal failure, and the signs of chronic 
nephritis ensue. In some cases a sudden attack of uremia may be the first symptom 
of renal difficulty. When the condition persists and adult life is reached, there may 
be a high arterial tension and hypertrophy of the heart, as in ordinary chronic nephritis. 
Often they interfere but little with the life of the patient. In the museum of the 
Jefferson Medical College is a cystic kidney weighing seven pounds, diagnosed 
during life by the late Dr. J. M. Da Costa, and carried by a busy practitioner of 
medicine for over two years afterward. The other kidney was but slightly affected. 

Beyond the use of pain-relieving drugs, there is nothing that can be done for 
these cases. Operative procedure is contra-indicated in the sense of nephrectomy, 
because the other kidney is so often diseased that it is unable to carry the burden 
of elimination if left by itself. 



TUMORS OF THE KIDNEY. 

The kidney is not rarely the seat of morbid growths. They may be benign or 
malignant. The benign growths are the fibromata, which chiefly affect the pyramids 
of the kidney, and less commonly the lipomata and angiomata. Occasionally 
papilloma of the mucous membrane of the pelvis of the kidney develops. The 
most common malignant growth in the kidney is sarcoma, which is by no means 
very rare in young children, and often grows to a very great size. Sarcoma of the 
kidney secondary to sarcoma elsewhere is also met with in adults. Endothelioma 
may develop. These are all vascular and often bleed, producing hematuria. Ade- 
noma of the kidney usually springs from the cortical tissues, but it may grow to so 
large a size that it takes the place of most of the renal tissue. They occur frequently 
in children and are walled off from the rest of the kidney by a fibrous sheath. 
Adenoma is found in two forms, the papillary and alveolar. Not rarely considerable 
areas of necrosis develop in these tumors. Cancer of the kidney as a primary 
growth is rare. As a secondary growth it is more common. 

Of all the tumors affecting the kidney those arising from ectopic adrenal tissue 
are probably the most frequent. Such tumors, called "hypernephromata," vary 
in size from almost microscopic masses to growths larger than an adult head. 
In their earlier development such neoplasms are benign, but later tend to involve 
adjacent structures, and by metastasis the lungs. If they occur on the right side, 
the liver is often affected. These tumors are soft, vascular, yellowish, or blood- 
tinged masses developing in the kidney, and often cause hematuria. 



NEPHROLITHIASIS 



669 



Fig. 117 




The symptoms of renal tumor, if the growth is benign, are not marked, unless 
it grows large enough to produce pressure. 

When the tumor is malignant, free hematuria, with clots moulded to the shape 
of the ureter, may be present. Pain develops only when the growth presses on 
neighboring parts or on adjacent nerve 
trunks, or when the weight of the growth 
is such as to cause a sense of weight in the 
loin. Severe attacks of colicky pain may, 
however, be present when a clot is being 
forced through the ureter. In some cases 
marked loss of flesh takes place, but children 
with renal sarcoma often remain remarkedly 
well nourished. The tumor, if large, may 
project well forward in the belly and give 
rise to the belief that it is an enlarged 
spleen or liver (Fig. 117). This error is 
frequently made. The colon may give tym- 
pany on percussion over the growth, showing 
that it springs from behind that part of the 
bowel. Sarcoma of the kidney must be 
separated from sarcoma of the retroperito- 
neal space. Care should be taken that it is 
not confused with cystic kidney, or hydro- 
nephrosis, for the malignant growth may be 
nodular and very elastic, or even give a sense 
of fluctuation on palpation. 

There is, of course, no medical treatment, 
of this state. In some cases nephrectomy of 
the sarcomatous kidney has been performed 
in young children with good results, but 
there is usually a metastasis elsewhere, which 
ultimately takes life. 



NEPHROLITHIASIS. 

Definition. — This condition is often called 
"stone in the kidney/' or "renal calculus." 
It is due to the formation in the tissues of 
the kidney, or in its calyces or pelvis, of con- 
cretions composed of solids derived from the 
urine. 

Etiology and Pathology. — The concretions, when in the pelvis of the kidney, 
may be single or multiple, and very great variations in their size may be met with. 
In some instances they are so small as to be scarcely larger than grains of sand; 
in other cases they may be as large as a pea or bean, and in still other instances a 
large calculus may form which completely fills the renal pelvis and projects itself 
into the ureter and into the calyces and infundibula, forming what is called a 
"coral calculus." The latter form is, of course, never passed from the kidney, but 
the smaller stones often become engaged in the ureter, and in their passage through 
it to the bladder cause intense pain. Not rarely the fine renal sand passes so readily 
that it attracts no attention until it is seen in the urine. 

Not only are concretions found in the calyces and pelvis, but also in the tissues of 
the kidney. Thus, formations of uric acid may take place in the tips of the pyramids 




• Sarcoma of the right kidney. The dark 
line on the abdomen is a blue-pencil outline 
of the tumor. (Le Conte.) 



670 DISEASES OF THE KIDNEYS 

after birth and cause much pain in the first month of life. Again, accumulations 
of sodium and ammonium urate are not rarely found in adults at the tips of the 
pyramids, particularly in gouty invalids, and in very old persons a deposit of 
lime-salts is found in streaks in the pyramids. 

The concretions just spoken of may be formed of a number of urinary solids, 
such as uric acid, calcium oxalate or phosphate, urate or carbonate. Cystin and 
xanthin also are ingredients. The mere existence of these substances in the urine 
is not the cause of the formation of stone, however, for if this were true everyone 
would have calculus. There are at least two additional factors present, one of 
which is the presence of an albuminoid substance, which serves to glue together 
tiny particles of these solids, and a condition in which there is an abnormal tendency 
to crystallization of these bodies. The bacterial origin of gallstones and the 
presence of micro-organisms in the nuclei of renal calculi suggest a similar origin 
for both. 

The most common ingredient of stone is uric acid or the urates. Stones of 
this character are met with in people who, because of small quantities of fluid 
ingested, have a scanty urinary flow, or who, by reason of great activity of the 
sweat glands, have little urine. As a consequence of concentration and high 
activity of the urine, the uric acid and urates are readily separated in solid form 
and held together by the albuminous matrix. Stones of this character are quite 
hard, and their surface is smooth and reddish. 

Phosphatic calculi are of the most common occurrence after those formed from 
uric acid and the urates. They are composed of calcium phosphate, ammonio- 
magnesic phosphate, or both, but they are rarely found in the kidney, being 
generally developed in the bladder. They are usually formed when the urine is 
persistently ammoniacal. 

Next to phosphatic calculi, those formed of calcium oxalate are most commonly 
met with. They are peculiar in respect to their great hardness and their roughened 
surface (mulberry calculi). Sometimes when they are small they are smooth and 
rounded, " hemp-seed calculi." They are dark in hue and not infrequently, on 
being split, they are found to be formed about a nucleus of uric acid. Oxalate 
stones are only met with in those who, because of digestive or metabolic disorders, 
pass considerable amounts of oxalates in the urine. 

The effects of the presence of stone in the renal pelvis are not always marked. 
Indeed, calculi may be present for years without causing any discomfort whatever. 
Sometimes they suddenly cause trouble if the patient suffers from a fall which 
causes the stone to damage the lining membrane of the pelvis, and as a result 
hematuria may ensue, or the stone may be started from its nest, and, proceeding 
to travel down the ureter, cause an attack of colic. In still other cases the stone 
may cause a hydronephrosis by plugging the orifice of the ureter. Again, the 
damage done by the sudden movement of a stone against the tissues may open a 
path for infection and consequent pyelitis or even pyelonephritis. 

Frequency. — In certain parts of the world stone is very prevalent, notably in 
some counties in England. This is probably due to certain mineral ingredients 
of the water which is taken for drinking purposes. Stone is also very commonly 
met with in China and in India. The late Dr. Kerr, a Chinese missionary, removed 
hundreds of vesical calculi during his residence in China. So far as I have been 
able to discover, stone is not much more prevalent in one part of the United States 
than in another. 

Prognosis. — The prognosis of nephrolithiasis depends entirely upon the question 
of the state of the kidney tissues about the stone or stones. In many cases the 
stone produces no trouble for years. If, as the result of an injury or infection, 
the surrounding tissues become diseased, the state of the patient may become 
serious from pain or from sepsis. 



NEPHROLITHIASIS 671 

Symptoms. — As just stated, stones may be in the kidney for years without causing 
any signs. When they escape into the ureter they cause renal colic, which is due 
to three causes: first, blocking of the ureter results in obstruction to urinary flow 
which causes distention; second, the pressure of the urine on the stone forces it 
forward through the narrow canal, often wounding its lining, and, finally, the 
walls of the ureter are spasmodically contracted because of the presence of the 
stone. The pain is often so severe as to be a horrible agony. I have seen a strong 
and brave man grovel on the floor groaning with anguish, and vomiting because 
of its severity. The pain extends into the pelvis and the inner side of the thigh on 
the affected side, and even into the testicle and penis. It also radiates into the 
back of the chest. These symptoms may persist for an hour or for several hours. 
In the latter instances there are often temporary remissions in the pain. Not 
rarely the bladder is exceedingly irritable, and the patient continually passes small 
quantities of urine which contains traces of blood from the affected ureter, but 
most of the urine comes from the normal side. 

In cases of suspected renal calculus the urine should be examined microscopically 
for blood cells, both during and between attacks. They are practically never 
absent when a calculus is lodged in a ureter. 

When both kidneys are affected, total suppression of urine due to obstruction 
of the ureter or to reflex irritation may ensue, and the resulting toxemia produce 
death. It is, however, a noteworthy fact that this state is rarely rapid in onset 
or rapidly fatal. The patient often lives for many days, unless there has been 
renal disease present for some time with some degree of toxemia. I have recently 
seen a case in consultation in which no urine had been passed for a week, and the 
catheter obtained nothing from the bladder, yet the patient was conscious and 
alert when spoken to, appearing drowsy only when left alone. This is a state quite 
separate from ordinary uremia, and has been called " latent uremia." (See Uremia.) 

After an attack of renal colic has passed, pain and soreness are felt for some 
hours or days in the affected loin, and tenderness on pressure may be elicited. 

Diagnosis. — The pain of renal colic must be separated from that of acute appen- 
dicitis, that of gallstone colic, and from neuralgia. It must also be distinguished 
from the pain due to hydronephrosis resulting from a twist in the ureter. Some- 
times a diaphragmatic pleurisy may mislead us. The peculiar radiation of the 
pain into the groin, penis, and inside of the thigh is diagnostic. The pain of gall- 
stone is radiated into the back, and is often associated with jaundice. Neuralgia 
does not cause bloody urine. Twist of the ureter can be predicated by finding a 
floating kidney. Pleurisy is defined by the area of the pain, by fixation of the 
diaphragm, and by a friction sound in some cases. A valuable, but by no means 
absolutely reliable, method of diagnosis is the use of the Roentgen rays, which 
may or may not reveal a stone, and which sometimes has caused the surgeon to 
operate when no stone has been found. 

Treatment. — The treatment of nephrolothiasis may be divided into two parts: 
that devoted to the relief of the patient at the time of the attack of renal colic, 
and that devoted to the prevention of the formation of new stones or an increase 
in the size of those already present. For the relief of the attack of renal colic, 
a hypodermic injection of J grain of morphine, with xir grain of atropine, should 
be given at once; or, if atropine is known to be disagreeable in its effects upon 
the patient, nitroglycerin may be used hypodermically, for the double purpose 
of aiding in relaxing the spasm and because it tends to prevent the after-disagreeable 
effects of the opiate. If the heart is in a satisfactory condition, chloroform may 
be given by inhalation, and if the patient will lie quietly enough to permit it, hot 
applications may be made over the painful kidney. 

In the intervals between the attacks the patient should be instructed to drink 
large quantities of some pure water like Poland water, or one of the Lithia waters, 



672 DISEASES OF THE KIDNEYS 

which depend chiefly for their effects upon their purity rather than upon their 
lithia. If the urine is alkaline, lithia is contra-indicated, and under these circum- 
stances it is well not only to use copious draughts of water, but to direct the 
patient to take uritone, urotropin, or benzoate of ammonium, for the purpose of 
making the urine acid. 

When the urine is excessively acid, it is advisable for the patient not only to 
drink large quantities of water, but also to take 15 or 20 grains of bicarbonate of 
potassium three or four times a day. In other instances the citrate of potassium 
may be given. Sometimes good results follow the use of Celestins Vichy water 
when the urine is acid. If an examination of the urine reveals the presence of 
a large number of urates, it must be borne in mind that these have their origin 
in disordered gastro-intestinal functions, and the diet must be carefully regulated, 
and nitromuriatic acid given in full doses. Sometimes, too, these cases are benefited 
by the administration of such intestinal antiseptics as salol, or aspirin, in the dose 
of 5 or 10 grains three times a day. 

The patient should be forbidden to drink any sweet wines or beer, and the only 
form of alcoholic stimulant permitted should be rye or Scotch whiskey. If the 
patient can do without any alcohol at all, it is much better for him to be content 
with non-alcoholic drinks. 

If the patient is one who is accustomed to leading a sedentary life, he should 
be instructed that an amount of exercise which is sufficient to produce healthy 
fatigue is absolutely essential; but if he exercises he should also drink copiously 
of water. 

When pain in the kidney is continuous or so frequent in its recurrence that the 
enjoyment of life is impaired, or if there is any evidence of the tissues of the pelvis 
of the kidney or of the kidney itself being irritated or infected, the question of 
operative interference must be carefully considered, and the patient advised to 
seek surgical relief. 

PERINEPHRIC ABSCESS. 

An abscess sometimes forms around the kidney by the extension of infection 
from the pelvis of this organ, because of transmitted lymphatic infection from a 
suppurative appendicitis, from injury to the tissues by a blow or fall, by extension 
of infection from spinal disease, from perforation of the stomach or bowel followed 
by subdiaphragmatic abscess, and rarely after acute infectious fevers, as typhoid 
fever. The pus may cause pain and bulging over the kidney; it may burrow upward, 
and escape into the thorax, or downward and resemble a psoas abscess. The pus 
is usually very foul and distinct septic symptoms may be present. On the other 
hand, I have seen at least two cases in which there was little pain and no fever. 
There was nothing more than some discomfort, with swelling, over the kidney. 
Not rarely the spine is fixed, and the leg on the affected side is drawn up when the 
patient lies down. 

Treatment. — The treatment is, of course, operative. The patient's vitality 
should be supported by food and stimulants. 

DISORDERS OF URINARY SECRETION. 

Anuria. — Anuria is a condition in which there is a total suppression of urine. 
It arises as the result of thrombosis of the renal vessels, and an intense acute nephri- 
tis such as that which follows the ingestion and elimination of very irritant poisons 
as cantharides and turpentine. Sometimes complete anuria also follows the 
administration of ether when this anesthetic has been given over a long period 
of time and in too large quantities. It is particularly prone to occur if the kidneys 
are already in a state of irritation. In other instances total suppression of urine 



DISORDERS OF URINARY SECRETION G73 

results, reflexly, from the irritation produced by nephrolithiasis. In most instances 
when this occurs both kidneys are affected. Partial or complete anuria also 
sometimes occurs after operations upon the genito-urinary tract. A careful distinc- 
tion should be made between anuria when no urine is secreted and retention of 
urine in which no urine is passed, but in which the bladder is found to be well filled. 

Treatment. — The treatment of anuria varies somewhat with the cause. When 
the arrest of secretion is due to the presence of stone, an operation is theoretically 
demanded, but usually the diagnosis as to the cause is not completed before the 
patient's condition has become so grave that operative interference is of questionable 
propriety. When the suppression of secretion is not due to stone, but to reflex 
irritation or spasm of the renal vessels, I have known full doses of nitroglycerin 
given every three or four hours, hypodermically, to relax the bloodvessels and 
cause free urinary flow. This is particularly apt to occur if, simultaneously, the 
patient receives a large injection of cool water by the bowel. If saline solution 
is used, care should be taken that it is not of more than 0.6 per cent, strength, since 
strong saline solutions abstract liquids from the tissues instead of being absorbed. 
In these instances our desire is that fluid shall enter the tissues, find its way to the 
bloodvessels and so flush the kidneys. Usually about one quart of liquid should 
be given by gentle hydrostatic pressure. Hot compresses, or poultices, may be 
laid across the loins, and if there is any reason to believe that renal congestion is 
present, three or four dry or wet cups may be applied over each kidney. In some 
instances moderate doses of the bromides and the vegetable salts of potash, like 
the citrate, are advisable. If the heart is strong the patient may be subjected to a 
hot pack or may be given a Turkish bath by elevating the bedclothes and allowing 
hot air to surround his body. Small doses of pilocarpine may be given as a diuretic, 
particularly if the heart is guarded by strychnine. The difficulty in using large 
doses of pilocarpine is that it is prone to produce pulmonary edema. 

Hematuria. — Bloody urine, or hematuria, is a condition in which there is found 
in the urine not only the coloring matter of the blood, but red blood corpuscles 
as well. It sometimes occurs with the stage of onset in acute fevers and in certain 
cases of leukemia. It is also met with in certain forms of malarial infection of the 
estivo-autumnal type, and in cases of infarction of the kidney arising during an 
attack of endocarditis or from other causes. Hematuria is a prominent symptom 
in renal tuberculosis. (See Tuberculosis). When there is stone in the pelvis 
of the kidney or any part of the conducting tract, and the patient is jarred or jolted, 
the stone may cause sufficient local damage to produce bloody urine. Parasites 
such as the Filaria sanguinus hominis and the Bilharzia may produce the same 
condition. Blood also appears in the urine as the result of papilloma, cancer, 
or other neoplasm of the bladder, ureter, renal pelvis, or kidney, ulceration of the 
urethra, and of injuries to the genito-urinary tract by falls or blows. Sometimes, 
too, it develops in the course of scurvy and purpura hemorrhagica. In acute, 
and even in chronic parenchymatous nephritis, the urine sometimes contains 
small amounts of blood, but they are visible only under the microscope. 

The appearance of the urine when it contains blood is quite characteristic. 
It is not only dark red in hue, but it is opaque and contains considerable sediment, 
which is chiefly composed of fibrin and blood corpuscles. In pure renal hematuria 
the voided urine is more of a smoky hue, the red cells are of the shadow or phantom 
type and clots are rarely if ever present. If the urine is very alkaline, the red 
blood corpuscles may be dissolved rapidly or become colorless and difficult to see. 
Clots formed before the urine is passed nearly always arise from hemorrhage in the 
bladder, but occasionally moulds of the ureters may appear. An examination 
by means of the cystoscope or urethroscope may be necessary to determine the 
source of the hemorrhage, and if the blood comes from the kidney it may be neces- 
sary to catheterize the ureters to determine which kidney is damaged. 
43 



674 DISEASES OF THE KIDNEYS 

There are occasional instances of hematuria in which, even at autopsy, no 
sufficient cause can be found. These include the angioneurotic hematuria of 
Klemperer, the renal hemophilia of Senator, and Gull's "renal epistaxis." 

Treatment. — Treatment of hematuria depends largely upon its cause. The 
patient should be put absolutely at rest. If the blood comes from the kidney 
there is no treatment which can be relied upon as being efficacious. .Chloride 
of calcium in the dose of 5 grains three or four times a day may be given well diluted 
with water to increase the coagulability of the blood. Gallic acid, tannic acid, 
and sulphuric acid have been largely used by some practitioners, but it is doubtful 
if they really exercise any definite influence. If any one of them does act as a 
styptic it is probably sulphuric acid. Ten drops of the aromatic acid may be 
given every three or four hours, well diluted, and counter-irritation may be applied 
in the shape of cups or hot compresses over the kidneys. Counter-irritants like 
mustard, turpentine, and cantharides should be avoided, as they may be absorbed 
and increase renal irritation. The patient should be protected from cold. If the 
hemorrhage comes from the bladder, an injection of a pint of normal salt solution 
containing \ to 1 ounce of adrenalin chloride solution 1 : 1000 should be injected. 

When the hemorrhage comes from the urethra a similar plan of treatment can 
be resorted to, simply instilling the adrenalin into the portion of the urethra which 
is bleeding. The objection to the use of substances which cause a coagulation 
of the blood is that they produce clots, which may become septic or give rise to 
obstruction. 

Hemoglobinuria. — In all probability hemoglobinuria occurs most frequently 
as a complication of malarial infection. There is much doubt as to the actual 
cause of this condition. In some instances it is probably due to the destructive 
action of the malarial parasite on the blood, but it would seem probable that in 
other instances it is due to an associated infection or a condition which quinine 
cannot be expected to remedy. Indeed, a large number of cases are now on record 
in which the administration of quinine has been followed by hemoglobinuria or 
hematuria. This condition is to be distinctly separated from hematuria, for in 
this case no blood corpuscles are present, but only the hemoglobin or coloring 
matter of the blood. Its presence does not indicate any lesion in the genito-urinary 
tract. Strictly speaking true hemoglobinuria is not present, but methemoglobin- 
uria. The urine is clear, but may be quite dark in hue, and deposits on standing 
a heavy, reddish-brown sediment. It usually gives the reaction for albumin. 

Hemoglobinuria arises from the ingestion of a large number of poisons, such as 
poisonous mushrooms, chlorate of potash, pyrogallic acid, and some of the coal-tar 
products. Not long since I had under my care a physician who suffered from 
repeated attacks of hemoglobinuria whenever he tinkered with his automobile, 
which was stored in a small, tightly closed shed in which the fumes of gasoline 
were quite concentrated. He never suffered with hemoglobinuria before these 
exposures, and since avoiding them has had no return of his trouble. Hemoglobin- 
uria sometimes follows severe burns. It may also develop in Raynaud's disease. 
The discoloration of the urine produced by carbolic acid is not due to hemoglobin- 
uria, but to a dark, oxidized educt, which is in part hydrochinon. 

Hematinuria. Under the name of proxysmal hematinuria, sometimes called 
hemoglobinurie a frigore, a condition rarely occurs in which the urine varies in color 
from a port-wine to a chocolate-brown, or almost black hue, the alteration in its 
appearance lasting, however, for but a few hours. Its specific gravity usually 
ranges from 1.025 to 1.027. The urea is increased. The quantity of blood which 
is represented has been estimated as equivalent to from seven to twelve parts in 
one hundred of urine. Blood corpuscles are very rarely found in the fluid. The 
urine not only contains hemoglobin, but considerable quantities of albumin and 
globulin. Not infrequently hyaline and granular casts are present. This condition 



DISORDERS OF URINARY SECRETION 675 

is chiefly provoked, apparently, by exposure to cold — that is, by chilling of the 
surface of the body. Aside from exposure to cold and chilling of the surface of 
the body, severe muscular exercise seems to be a causative factor, and not infre- 
quently there is also a tendency to vasomotor disorders. Indeed, it is probable 
that a large part of the disorder lies in an abnormal vasomotor condition. Gilman 
Thompson has reported two typical cases and summarized the literature. It 
appears that during the past forty years only 206 cases have been reported, and 
that most of these have appeared in England, Germany, and France, and that 
very few indeed have been reported as occurring in the United States and Canada. 
The condition affects males very much more frequently than females, there being 
only about 4 per cent, of females in the 206 cases so far reported. The period of 
life at which it commonly occurs is between thirty and forty years, but cases have 
been reported as late as the sixty-fourth year. At the time of the attack there is 
usually a sharp rise of temperature, amounting to 102° or 103°, but this falls to 
normal almost as rapidly as it rises, the febrile period lasting only a few hours. 
Chills are often present, and may be the first symptom of the attack. Jaundice, 
which is hematogenous in origin, develops. Some persons have thought that the 
jaundice is hepatogenous, but this is unlikely in view of the fact that the urine is 
not bile-stained and the stools are not lacking in bile. 

Paroxysmal hemoglobinuria is to be separated from the hemoglobinuria met 
with in some cases of malaria by the fact that the latter is a disease of tropical 
or semitropical regions, whereas paroxysmal hematuria usually occurs in cold 
climates. In one case the malarial organism is present and in the other it is absent. 

Paroxysmal hematuria is also associated with a neurotic condition, with urticaria 
and with localized areas of cyanosis. A number of investigators have advanced 
the theory that hemoglobinuria is due to the presence in the blood of a hemolytic 
substance which acts only when the temperature is lowered below normal, an 
intermediary body activated by a complemental body. 

Treatment. — The treatment of hemoglobinuria consists in avoidance of exposure 
to cold and to causes which produce nervous excitement. Tyson has suggested the 
use of suprarenal gland; Thompson suggests the use of thyroid extract; Saundby 
commends calcium chloride; and Chvostek believes that inhalations of nitrite of 
amyl may be useful to abort an attack. If the circulation is feeble, rapidly 
acting diffusible stimulants like Hoffmann's anodyne, aromatic spirit of ammonia, 
and small doses of spirit of chloroform are advantageous. 

The treatment of hemoglobinuria cannot be direct. Copious draughts of water 
to flush the kidneys, careful attention to the state of the bowels, protection from 
exposure of the surface of the body to cold, and the use of foods which are not 
highly seasoned and irritating to the liver and the kidneys are the only measures 
which the physician can institute. When the cause of the condition is malaria 
the debatable question of administering quinine must be discussed and decided. 
(See Treatment of Malarial Fever.) 

Albuminuria. — Albuminuria is a term applied to a condition of the urine in 
which serum albumin, serum globulin, and, by some writers, other urinary proteids, 
including nucleo-albumin, albumose, peptone, or fibrin is found in it. While it is 
true that delicate chemical tests will frequently reveal traces of albumin in the 
urine, it is also a fact that any quantities which can be appreciated by the use of 
heat and nitric acid or by the potassium ferrocyanide or mercuric iodide tests are 
to be regarded as abnormal. 

As albumin is a colloid substance and therefore does not readily diffuse through 
animal membranes it does not pass through the bloodvessels of the kidneys and 
renal tubules unless these structures have undergone some degenerative change, 
or are subjected to a pressure which they cannot withstand. Sometimes, too, 
albuminuria may be due to changes in the blood itself, whereby its albuminous 



676 DISEASES OF THE KIDNEYS 

ingredients are altered or the renal texture is secondarily affected. The presence 
of albumin in the urine when disease of the conducting apparatus can be excluded 
(accidental albuminuria may occur through contamination of the urine by vaginal 
discharges) is therefore indicative in the vast majority of instances of some renal 
lesion, and as chronic parenchymatous nephritis and chronic interstitial nephritis 
are the most common renal diseases, it is usually indicative of one of these maladies 
or of a subacute nephritis complicating one of the acute infectious diseases. Twenty 
years ago albuminuria was considered as pathognomonic of Bright's disease. We 
now know that albumin often appears in the urine when Bright's disease is not 
present. 

As a general rule it may be stated that the quantity of albumin is in direct ratio 
to the severity of the renal lesion, but there are certain notable exceptions to this, 
as in the case of chronic contracted kidney, in which disease the kidney is seriously 
affected, yet the albumin is always in small quantity and may be absent at times. 

Albuminuria is not rarely met with in cases of congestion of the kidney due to 
cardiac failure. Under these circumstances the quantity of albumin present may 
be very large, almost as great as that which is found in chronic parenchymatous 
nephritis. It is due under these circumstances to a structural and probably 
nutritive alteration brought about by passive renal congestion, and the use of 
cardiac stimulants usually results in its disappearance, at least to some degree. 
So, too, albuminuria may develop in certain persons after severe and prolonged 
exercise, as in soldiers after a long march, or in athletes after a long run. One 
cause of this, at least, is feebleness of the heart from exhaustion. 

In still other cases what is known as "Cyclic Albuminuria" comes on, which 
is sometimes due to exposure to cold, and at other times seems causeless. Cyclic 
albuminuria is sometimes called the "albuminuria of adolescence," and is, as its 
name implies, intermittent and is usually not present when the patient rises in 
the morning, but appears as the day progresses. The upright posture is in some 
cases sufficient to induce the condition — "orthostatic" albuminuria. Usually 
the urine is above the normal specific gravity and contains no casts. As its name 
indicates, it occurs at puberty, in easily fatigued, overgrown, pallid children. It 
usually disappears when puberty is passed and the system is established on an 
adult basis. 

In certain persons the ingestion of excessive quantities of albumin in food also 
produces albuminuria. 

A very high arterial tension due to cardiovascular disease may also cause this 
symptom. While it is true that the cardiovascular disease usually results in 
some impairment of the kidney, it is also a fact that reducing arterial pressure in 
these cases by the use of nitroglycerin often stops the albuminuria. 

Albuminuria may be due, as already stated, to changes in the condition of the 
blood itself, met with in certain cases of anemia, and in diseases like purpura, 
scurvy, and other conditions which cause marked changes in the circulating fluid. 

Tests. — Albumin is best detected in the urine by the general practitioner by 
the use of the so-called heat and nitric acid tests, which may be used separately 
or in conjunction. A test-tube is two-thirds filled with urine, which if cloudy 
should be filtered, and if alkaline acidified, and the upper part of it is held over a 
lighted alcohol lamp so that the fluid in this portion of the tube soon boils. Under 
these circumstances if albumin is present the upper portion of the urine becomes 
clouded from coagulated albumin, but the portion below remains clear until the 
coagulated albumin is precipitated. If earthy phosphates are present some cloudi- 
ness of the fluid develops, but the addition of a few drops of nitric acid disperses 
the cloud if it is due to the phosphates, but does not do so if it is due to albumin. 
Many physicians use a somewhat less accurate test, which consists in placing 
| to 1 drachm of nitric acid in a test-tube, and allowing an equal quantity 



DISORDERS OF URINARY SECRETION 677 

of urine to trickle down the side of the tube so that it overlies the acid. If albumin 
is present a layer of albumin appears at the point of juncture of the two fluids. 
Sometimes, if marked intestinal putrefaction is present, a reddish-brown, but 
transparent zone, appears at this level also. 

For the purpose of making a delicate test the potassium ferrocyanide method 
may be employed. The writer has found it most convenient to use for this purpose 
the so-called urinary test tablets which are now placed upon the market. Into 
30 minims of urine is placed a citric acid tablet for the purpose of acidification. 
To this is then added a tablet of potassium ferrocyanide, and the tube is shaken 
or allowed to stand still until both tablets are completely dissolved, when if albumin 
is present tiny flocculi may be seen floating in the fluid, which settle to the bottom 
of the test-tube when it is placed at rest. This is a delicate test for albumin, and 
has the advantage that it does not precipitate mucin, peptones, phosphates, urates, 
or vegetable alkaloids. If the physician does not wish to use these tablets, he may 
add to a test-tube half-full of urine 5 or 6 c.c. of a freshly prepared solution of 
potassium ferrocyanide of the strength of one in twenty, adding 10 to 15 drops of 
acetic acid. In other instances the physician may, if he chooses, employ potassio- 
mercuric iodide test tablets in the same manner, with equally good results. When 
the potassium mercuric iodide acid test is used, the cloudiness due to albumin 
does not break up into flocculi, as it does when potassium ferrocyanide is employed. 

The following facts in regard to these tests should be remembered. If the 
specimen of urine is very alkaline, more than one citric acid tablet, or an extra 
quantity of acid solution should be added. If cloudiness is produced by the acid, 
it is due to mucin, uric acid, or some oleoresin, as, for example, when copaiba or 
cubebs have been taken internally. If the urine is warmed the urates dissolve, 
but the mucin remains. The precipitate produced by the oleoresins clears up 
by boiling, but returns as soon as the urine cools slightly. When the tablet, or 
solution, of potassium mercuric iodide or potassium ferrocyanide is added to the 
acidulated urine, and cloudiness is produced, the urine must be heated. If the 
reaction is due to albumin the precipitate remains undissolved, but if it clears up 
it may consist of peptones or derivatives of vegetable alkaloids if the mercury test 
has been employed. When the potassium ferrocyanide test is used peptones 
are not precipitated, and may therefore be excluded. 

For the quantitative estimation of albumin Esbach's method is most commonly 
employed. It consists in using a graduated test-tube which is called an albumino- 
meter. This test-tube is marked with the letter "U," and higher up with the 
letter "R"; below the letter "U" are graduate lines from 1 to 7. Urine is placed 
in the tube to the level of the letter "U," and the following solution is then added 
until the fluid in the tube reaches the letter "R." The solution used consists of 
10 grams of picric acid; 20 grams of citric acid; 1000 c.c. of distilled water. The 
tube is now corked and inverted several times until the test solution and the urine 
are completely mixed. It is then allowed to stand on a rack in a perpendicular 
position for twenty-four hours. At the expiration of the twenty-four hours the 
albumin is found to be at the level of one of the numbers cut on the side of the 
tube, and this represents the number of grams of albumin per litre. If it is desired 
to know the percentage of albumin, a decimal point is placed in front of the figure. 
In cases where the quantity of albumin is so great that it cannot be measured 
by the ordinary Esbach tube, the urine should be diluted with water, and the result 
in grams multiplied by the number of times the urine has been diluted. 

There is no excuse for neglecting examination of the urine for albumin. In 
the absence of other apparatus and reagents the urine may be acidified with vinegar, 
boiled in a spoon or cup, and if necessary poured into a glass for inspection. 

From what has been said it must be evident that the significance of albuminuria 
varies. Usually, except in the case of chronic interstitial nephritis, its importance 



678 DISEASES OF THE KIDNEYS 

from a prognostic standpoint is in direct relation to its quantity; its cause is also 
an important factor concerning prognosis. The presence of tube casts with the 
albumin is also of great importance, particularly if these tube casts are granular 
and contain fatty globules. Tube casts should always be sought for in the urine, 
if need be with the aid of the centrifuge, but, on the other hand, it should be remem- 
bered that if the centrifuge is thoroughly employed, there are few specimens of 
urine which will not reveal an occasional cast. 

No one perhaps has studied more carefully than has Leube this question of 
albuminuria. His view is that while in many cases physiological albuminuria 
does occur, particularly after severe exercise, we should nevertheless regard all 
such instances with suspicion. Washburn, in studying the records of life insurance 
cases who were supposed to have physiological albuminuria, found that the death 
rate among them was 17.5 per cent, instead of 9 per cent., as it should have been. 

A careful study must be made of the heart, kidney, lungs, and other organs 
before the patient is given a favorable prognosis. 

Wright and Ross have shown that it is sometimes possible to differentiate the 
albuminuria of renal disease and physiological albuminuria by increasing the coagu- 
lability of the blood through the use of calcium lactate. (For dose see article on 
Purpura.) If the use of this drug arrests the albuminuria it does not depend upon 
actual renal disease. 

While casts may be present in the urine of patients who are thought to be healthy, 
but who have albuminuria, these casts should disappear if the patient rests in bed, 
and they should not be epithelial casts. If they are present, then it is not physio- 
logical albuminuria. It is perhaps best to say that albuminuria ought not be 
present, and that its existence at least excites suspicion of some renal change. 
But it does not necessarily mean Bright's disease, and I have seen more than one 
case in which distinct albuminuria was present without the association of casts 
for more than fifteen years. 

Pyuria. — Pus in the urine may arise from pyelitis, pyelonephritis, cystitis, 
urethritis, vaginitis, or the rupture of an abscess into the urinary passages from 
contiguous parts. When pus is in urine, it gives it a peculiar opacity, and on 
sedimentation the bottom of the vessel contains a somewhat ropy mass, presenting 
a wavy surface. It is to be distinguished from the phosphatic deposits mixed with 
mucus by the fact that it is not so white, and does not so closely resemble white or 
pinkish powdered chalk. Further than this, the phosphates are usually cleared up 
by boiling or by the addition of acid, but urine containing pus is not so altered. 

The treatment of pyuria depends upon the cause of the presence of pus. If 
there is an abscess in the kidney surgical measures are required, but if the pus is 
due to a pyelitis or cystitis the use of substances which exercise a mild antiseptic 
influence is to be resorted to, at least for a time. For this purpose the patient 
may receive 10 grains of uritone or urotropin three times a day in sparkling water, 
or 10 grains of benzoate of ammonium three times a day in capsule. For the 
methods and drugs to be employed for irrigating the bladder the reader is referred 
to works on genito-urinary diseases. 

Chyluria. — Chyluria is a condition in which the urine presents a milky appear- 
ance owing to an admixture of fat. It may occur in some cases of pregnancy and 
during lactation. In other instances it follows injury to the lymphatics of the 
abdominal cavity. The most common form of chyluria is that which comes on as a 
complication or symptom of infection by the parasite Filaria sanguinis hominis. 
This condition, as pointed out elsewhere, is met with most commonly in India, 
China, and in the Straits Settlements, and its cause is the obstruction of the lym- 
phatics produced by the presence of the parasites within them. Not rarely urine, 
when chylous, coagulates in the vessel holding it or becomes gelatinous in 
appearance. 



DISORDERS OF URINARY SECRETIONS 679 

Phosphaturia. — This term is applied to a condition of the urine in which it 
contains an excess of phosphates and is supposed by some to be associated with 
unusual activity of the nervous system, particularly in connection with that degree 
of excessive nervous strain which is often productive of neurasthenia. Whether 
this view is correct is debatable. There can, however, be no doubt of the fact 
that in certain of the diseases characterized by great loss of flesh, such as tubercu- 
losis, an excess of phosphates is present in the urine. Such a condition also arises 
in acute atrophy of the liver and in certain forms of grave anemia. On the other 
hand, acute diseases running a febrile course, and supposed to be characterized 
by a great amount of tissue breakdown, are not accompanied by this manifestation. 
In some instances in which there is an excess of phosphates present in the urine 
the patient is also diabetic, and in still others the patient, while suffering from 
polyuria and phosphaturia, and who has such diabetic symptoms as thirst and loss 
of flesh, nevertheless does not develop a glycosuria, sugar being constantly absent. 
It has been thought by some that these cases of so-called "phosphatic diabetes" 
represent an early stage of true diabetes, for in some of them glycosuria ultimately 
develops. 

The best remedy for the purpose of cleaning the urine of an excess of phosphates 
is benzoate of ammonium in doses of 10 to 20 grains three times a day. 

Oxaluria. — Oxaluria consists in a condition in which urine of high specific grav- 
ity contains on standing, when decomposition is absent, an excess of calcium oxalate 
crystals. The condition is an important one in that it frequently points the way 
to the correct diagnosis and treatment of patients who are suffering from dyspepsia, 
nervous irritability, melancholy, and mental depression with a general condition 
of wretchedness. It is said to be present in those cases in which there is lack of 
free hydrochloric acid in the secretion of the stomach. It also develops in patients 
who eat pears, cabbage, tomatoes, and, occasionally, in those who take coffee to 
excess. In many patients it is an evidence of faulty metabolism due to lack of 
fresh air and exercise. The condition is of interest from a therapeutic standpoint 
because of the fact that these patients often gain great benefit if they receive 
moderate doses of nitrohydrochloric acid and take a fair amount of physical exercise 
and lead an out-door life. 

Indicanuria. — Traces of indican, or, to speak more correctly, indoxyl sulphate 
of potassium, are present in normal urine, being derived from the indol which 
is formed in the intestine by the decomposition of proteids through the action of 
bacteria. If this indol is absorbed from the intestine into the blood, it is oxidized 
and forms the indoxyl sulphate of potassium just named. 

When indicanuria is marked, it is an evidence of an excessive amount of intestinal 
putrefactive change, and the discovery of indicanuria in a patient who is suffering 
from the symptoms of auto-intoxication is, therefore, of value from a diagnostic 
standpoint. An estimation of this substance in the urine is also useful to differ- 
entiate intestinal obstruction from ordinary severe constipation, for in the former 
indicanuria is usually marked, and in the latter the trace of indican which is present 
is usually not above the normal. In rare instances, owing to decomposition of 
the indoxyl sulphate of potassium before it escapes from the body, the urine is 
blue when it is passed, but in the majority of cases in which a blue urine has appeared 
it has been found that the patient has taken methylene blue or some similar aniline 
dye, either as a medicine or in foodstuffs. The presence of indican in the urine is 
determined by heating to the boiling point 5 c.c. of nitric acid in a test-tube and 
adding 5 c.c. of urine. If indican is present in excess, a bluish ring develops at 
the point of contact between the two fluids, and if 2 c.c. of chloroform are added 
and the liquids mixed by shaking, and the test-tube then set aside to stand, it 
will be found that the layer of chloroform which soon separates has a violet 
color. 



G80 DISEASES OF THE KIDNEYS 

Lithuria. — Under this heading is mentioned a condition in which an excess of uric 
acid occurs in the urine, chiefly in association with sodium and ammonium, and 
sometimes with potassium, lithium, and calcium. An examination of the urinary 
sediment under the microscope may reveal small, reddish grains or crystals, looking 
under the microscope like particles of red pepper. There is no condition which is 
so little understood at the present time as is this one. Almost every layman, and 
a multitude of doctors, continually speak of being "full of uric acid," meaning 
by this that they have muscular stiffness, or that the urine shows an excess of 
urates, or even uric acid crystals. In the majority of instances this excessive 
deposit of urates, or uric acid, depends not upon any abnormality in bodily metabol- 
ism, but upon conditions of the urine which cause the precipitation or deposition 
of these solids. There is either a condition of acidity or a minimum quantity of 
mineral salts, and as a result precipitation takes place. For this so-called "uric 
acid diathesis," physicians prescribe large quantities of lithium and copious draughts 
of water. There can be no doubt that the water is advantageous, but the lithium 
only does good until a certain degree of alkalinity is reached, when it is of little 
value, and if the doses are large it acts as a depressant to the general system. It 
is quite true that persons who eat heartily, drink alcohol, and take no exercise are 
not infrequently overloaded with effete materials representing imperfect metab- 
olism, which cause disagreeable symptoms. It is also perfectly true that exercise, 
a proper diet, and the use of plenty of drinking water will overcome these symptoms, 
but this does not prove that the patient has been a sufferer from the so-called " uric 
acid diathesis." 

Melanuria. — Melanuria is a condition in which the urine at the time it is passed 
or shortly after its exposure to the air, becomes intensely dark in hue, owing to 
the presence in it of melanin. It is found in certain conditions in which this sub- 
stance is produced in the body by pathological processes, such as melanotic growths. 
If a solution of ferric chloride is added to the urine, it becomes inky black. If 
caustic potash is added, it becomes at first violet and then claret colored, and if 
acetic acid is added to this mixture it may become blue. The test most commonly 
employed is the solution of ferric chloride mentioned. 

Myelopathic Albumosuria. — The presence in the urine of the so-called Bence- 
Jones albumose or proteid has by a number of observations been shown to be 
most suggestive of the rather rare tumor of bone known as multiple myeloma or 
medullary osteosarcoma, "Kahler's disease." The test is quite simple. The 
urine, if not distinctly acid, should be made so with acetic acid and then heated. 
At 50° C, if it contains this albumose, it becomes milky; at 60° C. it deposits a 
thick precipitate which clings to the sides of the tube or collects on the surface. 
Further heating to 100° C. causes the almost complete disappearance of the pre- 
cipitate, which, however, re-forms as the urine cools. 



DISEASES OF THE DUCTLESS GLANDS AND 
LYMPHATIC SYSTEM. 



DISEASES OF THE THYROID GLANDS. 

GOITRE. 

Definition. — Under the terms goitre, bronchocele, thyreocele, or struma are included 
almost all enlargements of the thyroid gland, but the application of so general 
a term is not to be regarded with favor. It is better, therefore, to consider the 
various diseases of the thyroid as inflammatory (traumatic strumitis), infectious 
(tuberculous or syphilitic strumitis), and parasitic (echinococcic) strumitis. Of 
the remaining so-called hypertrophies of the gland it may be said that some of 
them at least are apparently not of the nature of neoplasms, and to these the 
term "simple" or "benign goitre" is applied; whereas, in the case of those enlarge- 
ments which are due to the development of tumors within the gland, we apply 
the term "neoplastic goitre," as, for example, endotheliomatous, sarcomatous, and 
cancerous growths (malignant goitre). (See Tumors of the Thyroid.) 

With regard to some of the simple or benign goitres, it is still unsettled as to 
whether they are neoplastic, that is, adenomatous, in every instance. In some 
cases they are undoubtedly adenomatous. In still other cases the greatly enlarged 
gland may, under the microscope, have a histological formation like that of the 
normal organ. To this type of goitre the name "hyperplastic goitre" is applied, 
including those varieties characterized by reproduction of the parenchyma of the 
gland and called by some writers "parenchymatous goitre." When the enlarged 
gland contains cysts developing from its acini, the mass is called a "cystic goitre." 
Cystic goitres result from the distention of the gland spaces, with absorption of 
the intervening walls, thereby giving rise to cavities of various sizes. The contents 
of these cysts may be gelatinous or colloid. In some instances the enlargement 
depends upon dilatation of bloodvessels, and apparently upon the overgrowth and 
dilatation of new bloodvessels, forming the so-called vascular goitre, and not rarely 
there is a blending of two or more of the types already mentioned. Such conditions 
are known as "mixed goitres." (See Tumors of the Thyroid.) 

In ordinary goitre there takes place an increase in the size of the alveoli in the 
thyroid gland and a simultaneous formation of new glandular tissue. Side by 
side with this increase there is often colloid degeneration, and when this degenera- 
tive process is marked the state is called colloid struma or colloid goitre. Not 
uncommonly still other degenerative changes take place, in which the walls of the 
alveoli break down, and in this way several cavities are thrown together, forming 
cysts, which may hold colloid matter and blood derived from the vessels in the 
alveolar walls. This is called cystic goitre. In still other cases the bloodvessels 
of the gland become dilated, so that a telangiectatic state develops. Finally, 
it sometimes happens that all of these changes take place in the same gland, and 
upon them may be superimposed acute inflammation and even malignant growth. 
The increase in size may be limited to a single part of the gland or be widely diffused. 

Etiology. — The cause of ordinary enlargement of the thyroid gland of the fibroid 
and cystic type is unknown, but there can be no doubt that it depends, at least 

(681) 



682 DISEASES OF THE THYROID GLANDS 

in part, upon the character of the drinking-water used. My former colleague, 
Professor Keen, has investigated a very remarkable prevalence of the disease in the 
interior of the State of Pennsylvania, in which the relationship of water supply 
and goitre is extraordinary, a very large number of the people on one side of a 
mountain ridge being affected, and those across the divide escaping. The disease 
is also very common in some parts of Michigan and especially so in Switzerland. 
The suggestion of Grasset that goitre is of protozoal origin has not been favorably 
received. In support of his view he calls attention to the fact that, like malaria, 
goitre is endemic in certain areas, and he is inclined to believe that the thyroid 
enlargement is analogous to the splenic tumor of chronic malarial infection. The 
disease is more frequent in women than in men, and in adults than in children, 
in which class it is very rare. 

Symptoms. — The symptoms of goitre are usually of no consequence until the 
growth is large enough to be seen or until, by its pressure on the adjacent tissues, 
it causes difficulty in breathing and interferes with swallowing or with the function 
of the vagus nerves. The goitre may involve all of the gland, its isthmus, or either 
one of the lateral lobes. Rarely aberrant goitres arise in ectopic or misplaced 
thyroid tissues, and they may be intrathoracic or occur at the base of the tongue 
(lingual goitre). In still other instances they have been known to develop along 
the course of the thyroglossal ducts or in adjacent areas. The degree to which 
the cervical tissues are displaced in those cases in which the growth is chiefly in 
one lobe is remarkable. I once sent to Dr. Keen for operation a patient whose 
hyoid bone was pushed to one side so that it rested nearly under his right ear. 

Treatment. — There is no medicinal treatment of much value in goitre. Painting 
the part with iodine and the use of various counter-irritant ointments have been 
resorted to, but they have no real effect upon the growth. If it becomes very 
large, it must be excised if the pressure symptoms are severe. 



SWELLING OF THE THYROID. 

This occurs from two chief causes, namely, from inflammation and from hyper- 
emia or congestion. Some writers have described an angioneurotic form. When 
the swelling is due to inflammation it may arise from infection of the gland, as in 
typhoid fever or other acute infectious diseases, and may follow vaccination or 
sepsis; or, again, it may be due to tuberculosis of the gland, or to syphilis with the 
formation of gummata. Occasionally marked swelling arises from trauma, and 
this may be acute or chronic. 

It is asserted by Fothergill that there are recorded five cases of enlargement 
of the fetal thyroid due to the administration of potassium chlorate to the mother. 

Some years ago I reported the case of a woman who, in stooping in a dark room, 
struck her neck against the edge of a chair and at once felt violent pain in the 
thyroid gland. The gland rapidly became swollen, and the patient presented 
all the symptoms seen in persons to whom large doses of thyroid gland have been 
given, such as headache, a rapid pulse, and a tendency to syncope. In still another 
case, seen by me, an army surgeon on the fighting line received a severe blow on 
the thyroid, and developed a chronic enlargement of the thyroid gland, with some 
tachycardia and nervous and circulatory disorders. 

The thyroid gland is also found enlarged by hyperemia in young girls, particularly 
at the menstrual period, and in young women in their first pregnancy. It also 
occurs in young persons who suffer from cardiac disease. Such an enlargement 
usually passes away when the cause is removed. 

Sometimes thyroiditis occurs in the insane, but its etiology and symptomatology 
need further study. 



EXOPHTHALMIC GOITRE 683 

TUMORS OF THE THYROID GLAND. 

The tumors of this gland are adenoma, in which state the condition is practically 
that of goitre as already described, carcinoma, sarcoma, and endothelioma. The 
sarcomata are usually primary. Morf has been able to collect but 39 instances 
of carcinoma of the thyroid; he himself adds 1 case. Of the 173 cases of cancer 
of the thyroid collected by Orcel, 14 invaded the trachea. 

Carcinomata are also usually primary and undergo metastasis to nearby tissues 
or even to distant structures. The growth may develop in the parenchyma or in 
the connective tissue of the gland. 

An interesting form of tumor of the thyroid is the so-called carcinosarcoma, or 
mixed tumor of this gland. 

Occasionally old, quiescent goitres may become malignant, undergoing either 
sarcomatous or carcinomatous denegeration. 

An anomalous condition in this group of affections is thyroid metastasis, consist- 
ing in the growth of typical thyroid tissue at points distant from the glands. These 
growths are quite commonly in bones and are seldom malignant. The thyroid 
itself may show no change. 

EXOPHTHALMIC GOITRE. 

Definition. — Exophthalmic goitre is often called "Basedow's disease," "Parry's 
disease," or "Graves' disease." Parry described it (1825) ten years before it 
was described by Graves (1835) and fifteen years before it was described by Basedow 
(1840). Exophthalmic goitre is an entirely different disease from ordinary goitre 
or simple enlargement of the thyroid gland. It is a malady in which, as its name 
implies, there is protrusion of the eyeballs, and, in addition, palpitation of the 
heart, with a very rapid pulse. There are fine tremors in the hands, arms, and 
head, and disordered vascular tone. A tendency to abnormal sweating of the 
palms of the hands, and great mental depression is often present. 

Satterthwaite recognizes acute, subacute, and chronic forms of Graves' disease, 
and says we may speak of acute or temporary and essential or chronic forms. A 
secondary form is that in which an old goitre takes on the symptoms of Graves' 
disease. 

Frequency. — In 10,603 cases admitted to the Jefferson Hospital, there were 11 
cases of exophthalmic goitre, or 1 in 964. In the University Hospital, out of 
35,076 cases, there were 48 cases of exophthalmic goitre, or 1 in 730. Of 7270 
cases treated at the Dispensary for Nervous Diseases at the Orthopedic Hospital 
and Infirmary for Nervous Diseases, Eshner found that 30 were exophthalmic 
goitre, or 1 in 242. It is therefore by no means a rare disease. 

Etiology. — The cause of exophthalmic goitre is not known, but, as is the case 
with most diseases of obscure causation, a multitude of factors have been named as 
possible causes for its development, varying all the way from rheumatism and 
tonsillitis to fright and traumatism. The disease is very much more frequent in 
women than in men. Thus, out of 1839 cases collected from various sources, 
1553 were females and 286 males, a proportion of about 6 to 1, and its average 
age incidence is between sixteen and forty years. Cases are on record in which 
it has affected children as young as two and a half years. In some statistics, 
collected by me some years ago, it was shown that there is a very distinct hereditary 
influence present in many cases. There can be little doubt that the symptoms 
which are present in exophthalmic goitre are dependent upon excessive internal 
secretion of the thyroid gland, or, if not upon excessive secretion, to the entrance 
into the general system of more of the active principle of the thyroid gland than 
is normal. 



684 DISEASES OF THE THYROID GLANDS 

Pathology and Morbid Anatomy. — So far as the morbid changes are concerned, 
there is an excess of fat in the orbit as compared to the quantity of fat in other 
portions of the body. 

The heart may be normal or dilated. Not rarely there is some undue relaxation 
of the sphincteric fibres around the mitral orifice of the heart. The thyroid is 
enlarged, the veins covering it are dilated and numerous, and the arteries supplying 
its tissues are enlarged and tortuous. On the other hand, certain observations 
have shown that in many instances there is no remarkable change in the vascularity 
of the organ. 

Regarding the histology of the thyroid there is not at present a unanimity of 
opinion. Some pathologists regard the changes as specific and that therefore it 
is possible to make the diagnosis of exophthalmic goitre by study of microscopic 
sections alone. Others do not believe this possible and the question appears 
unsettled. This can be said, however, that evidence in favor of the former view is 
increasing, especially from those who have the opportunity to study a great deal 
of material. Mistaken clinical diagnoses undoubtedly underlie some of the dis- 
crepancy between reports. 

Observers in the Mayo clinic, from a study of over 1,200 cases of exophthalmic 
goitre and probably twice that many simple cases, have reached some very definite 
conclusions on this subject. Wilson states that during 1911 and 1912 every patient 
diagnosed clinically as true exophthalmic goitre and subjected to thyroidectomy, 
furnished a thyroid that showed primary parenchymatous hypertrophy and hyper- 
plasia, signifying increased functional activity of the gland. Histologically this 
means an increase of working tissue — parenchyma cells — within previously formed 
acini. There is an increased number of lining epithelial cells in a single layer, 
due to infolding of alveolar walls and papilla formation, or a reduplication of layers. 
A large amount of thin secretion is shown by a poorly staining alveolar content — 
colloid. 

Kocher, from a most exhaustive study, reaches a similar conclusion, namely, 
that there are no specific or pathognomonic gland elements but instead there are 
changes in the normal parenchyma in the way of increased size and number of 
epithelial cells and fluidification of colloid. 

Wilson also finds that the stage of the goitre can be estimated with considerable 
accuracy from the pathological study alone in about 80 per cent, of the cases and 
the severity of the toxic symptoms in about 75 per cent. These findings lead him 
to the conclusion that the relationship of primary hypertrophy and hyperplasia 
of the parenchyma of the thyroid to true exophthalmic goitre is as direct and as 
constant as is primary inflammation of the kidney to the symptomatology of true 
Bright's disease. Plummer reaches the conclusion that exophthalmic goitre is a 
definite clinical complex always associated with hyperplasia of the thyroid. Black- 
ford and Sanford have found that fresh extract from exophthalmic thyroids and 
the sera of certain patients contain a powerful depressor substance that materially 
lowers blood pressure. 

The thymus gland is persistent and hypertrophic, and enlarged in a very con- 
siderable proportion of cases, but a microscopic examination of it does not show 
pathological changes in most instances. Thus Capelle found a thymus persistans 
hyperplastica in 95 per cent, of all fatal cases. There is reason to believe that 
the symptoms are due not only to the enlarged thyroid but to the thymus as well. 
The parathyroids may be atrophied. 

Certain alterations have been described in the sympathetic system and in the 
central nervous system, but it has not been proved that these have any close rela- 
tionship with the disease. 

Symptoms. — The protrusion of the eyeballs, even when it is present to a moderate 
degree, is so striking that attention is directed to this symptom almost as soon as 



EXOPHTHALMIC GOITRE 



685 



the patient is seen. It varies greatly in degree. In some cases the eyeballs may 
be so prominent that it is impossible for the lids to completely close, whereas in 
others the exophthalmos may be very slight indeed. While it is true that the 
exophthalmos may not be equally developed on both sides, it is nearly always 
bilateral, although a few instances of unilateral exophthalmos have been reported. 
Under the name of von Graefes sign, a condition is found, in which, if the patient 
is directed to look at the floor, the upper eyelid does not follow the eyeball in its 
downward movement as rapidly as it should. This symptom is not always present. 
Stelwag's sign consists in a widening of the palpebral fissure, with retraction of the 
lids, to such an extent that the sclerotic coat of the eye is seen above and below 
the iris. This very distinctly increases the exophthalmic effect. With this symp- 
tom there is also diminished reflex excitability, so that winking is delayed when a 
sudden movement is made toward the patient. Under the name of Mobius' sign 
is described a condition in which there is a lack of power of convergence, so that 
if a pencil is brought near the patient's face the eyes do not converge, as they do 
in a normal individual. 

Fig. 118 




Exophthalmic goitre. The illustration shows the enlarged thyroid gland. The exophthalmos was so 
great that the lids had to be sewed together to protect the eyes. 

Notwithstanding the exophthalmos, vision, as a rule, is not interfered with, but 
ulceration of the cornea sometimes occurs as the result of the inability of the 
eyelids to protect the eye. (See Fig. 118.) 

The increase in the size of the thyroid gland is usually not very great, and it 
never becomes as large as in many cases of ordinary goitre. 

On inspection the gland may seem to pulsate, and on palpation it often transmits 
a thrill to the finger-tip. If the stethoscope be placed over the gland, a distinct 
humming murmur can be heard. This same murmur is also detected, even more 
clearly, if the stethoscope be lightly placed over the carotid arteries. 

The gland is never very hard, but may be soft and fluctuating, and is apt to 
vary in size considerably from week to week or from day to day. Tachycardia 
is practically always present in these cases. The pulse varies from 90 to 100 or 



686 DISEASES OF THE THYROID GLANDS 

even 200 beats a minute, the ordinary rapid pulse being very much increased on 
exertion or excitement. 

If the finger-tips of the patient are rested upon the finger-tips of the physician, 

there can be felt not infrequently a fine tremor, sometimes called " railroad bridge 

tremor," owing to its resemblance to the sensation produced in one's feet when 

standing upon a railroad bridge during the time a train is passing over it. In 

.other instances the tremor is very marked and coarse in character. 

The patient nearly always complains of feebleness and mental depression, and 
in some cases melancholia may be so profound as to result in suicide, as in a patient 
recently under my observation. An irritating nervous cough and occasional attacks 
of dyspnea may occur, and cases are on record in which the patient has suddenly 
died from urgent dyspnea, which has had its origin in intense swelling of the thyroid 
gland, so that it has pressed upon the trachea in much the same manner as does 
the enlarged thymus in status lymphaticus. Another symptom which, when it 
develops, must always be regarded with alarm, is excessive and obstinate vomiting. 
This condition may speedily pass by, but in some cases it has persisted until death 
has ensued. Sudden attacks of diarrhea are not rare. The digestion is fairly 
good, but the appetite is uncertain, and the patient craves abnormal things as she 
does in hysteria. Oftentimes a constant "rifting up" of wind gives great annoy- 
ance. The nervousness is so intense that in many cases the patient's life is almost 
unbearable because of the irritation produced by noises and other sources of irrita- 
tion which ordinarily would not be noticed. Nervous chills or tremblings are 
often a source of great annoyance to the patient, and the palms of the hands are 
prone to be wet with excessive perspiration. Patches of pigmentation on the skin 
often develop. There is usually distinct loss of weight and strength. In those 
cases in which there is a persistent thymus (about 40 per cent.) the symptoms 
consist in absence of Mobius' sign, slight exophthalmos, profuse sweating, diarrhea, 
no glycosuria and some eosinophilia. Palpation in the episternal notch may 
reveal fulness, and pressure causes oppression. The arrays may reveal an enlarged 
thymus but they sometimes fail to do so even if the thymus be present. 

Prognosis. ^-A certain number of cases of exophthalmic goitre undoubtedly 
recover, but they are always liable to relapse. Rapid loss of flesh and strength, 
marked tachycardia, persistent vomiting, and diarrhea are all of them symptoms 
which would cause us to give a guarded or unfavorable prognosis, whereas, if 
the symptoms are mild, we have a right to feel correspondingly encouraged. Some- 
times exophthalmic goitre may last so short a time as a few days or weeks. In 
other instances it may continue for many years. 

Treatment. — The treatment of exophthalmic goitre is not very satisfactory. 
When the thyroid gland was first used as a therapeutic agent it was given to a 
considerable number of persons suffering from exophthalmic goitre, with the idea 
that it might do good, but from the first it must have been manifest that it could 
not be of value because the patient is suffering from too much thyroid secretion, 
and the addition of more of the thyroid substance must in consequence be disad- 
vantageous. 

Lepine has recommended antithyroid serum in the treatment of Graves' disease. 
This serum is obtained from animals immunized against hyperthyroidism. Under 
the name of thyroid serum Mobius has given us serum derived from sheep from 
which the thyroid gland has been removed six weeks before. The dose is 1 to 5 
c.c. three times a day, given by the mouth. A similar preparation is prepared 
in this country by Parke, Davis & Co., and is called "Thyroidectin." The dose 
is 5 to 10 grains t. i. d., in capsules. 

Recently Pfahler and a number of others have recorded a considerable number 
of cases treated by the use of the Roentgen rays over the gland. They assert that 
at least 75 per cent, of these cases are distinctly benefited by this plan. 



EXOPHTHALMIC GOITRE 687 

Still another physiological-pathological plan of treatment has been introduced 
by Beebe and Rogers, based upon the well-known fact that it is possible to pro- 
duce a condition in the blood of an animal so that its serum will have a selective 
destructive affinity for a given organ when injected into another animal, partic- 
ularly the kidney, the pancreas and liver. It occurred to them that it might be 
possible to utilize this fact for the partial destruction or inhibition of the function 
of the thyroid in cases of exophthalmic goitre in which the activity of this gland 
is too great. This plan has given brilliant results in a few cases but signally 
failed in others. According to Beebe and Rogers the cases characterized by a 
hard, nodular, irregular thyroid, the so-called chronic, toxic cases with a good 
deal of varicosity of the thyroid veins, respond very poorly to the treatment, 
and as might be expected the smaller the thyroid and the less the exophthalmus 
the better is the prognosis. 

In most instances the patient should receive a carefully carried out rest cure, 
extending over a period of from four to six weeks, with regulation of the diet and 
massage and electricity. Sometimes a course of hydrotherapy is advantageous, 
and change of air and scene is particularly valuable if the patient has been subjected 
to nervous stress. All forms of exercise or gayety which tend to exhaust the nervous 
system should be forbidden. 

The drugs which seem to be of most benefit are those which belong to the class 
of sedatives. When the heart's action is very excessive, I have known full doses 
of tincture of veratrum viride to be most advantageous, in that they quiet the 
heart not only by depressing its muscle, but also by stimulating the pneumogastric 
nerve. In other instances the bromides may be employed. In still other cases 
I have seen gelsemium employed to advantage. 

The disadvantage of opium or morphine, for the production of nervous quiet, 
is the danger of establishing the "habit." This is a very real danger in these 
patients, because of their lack of nervous equilibrium. Sometimes belladonna 
may be given with advantage to quiet the circulatory and nervous excitement. 

A very large number of operations have been performed upon patients with 
exophthalmic goitre, with the object of curing the disease. In some instances 
the thyroid arteries have been tied. In others the capsule of the gland has been 
stripped from it and made fast in the wound, so that the tissues will shrivel. In 
still another class of cases the cervical sympathetic has been cut, and Jaboulay 
has strongly advocated this measure. The value of operative procedure is, how- 
ever, well summed up by my colleague, J. Chalmers Da Costa, who says : 

"Treat most cases medically and by rest; if medical treatment fails, consider 
the advisibility of surgical treatment. 

" Do not operate if there is great hysteria; if the gland is very large, thyroidectomy 
will fail; if the gland is very small, it will do no good to remove it. 

"If the symptoms are urgent, if the goitre is distinct, but not excessively large, 
if it has relapsed under medical treatment, or if the patient refuses to submit to 
the necessary restrictions of medical treatment, perform thyroidectomy. 

"Take Kocher's advice, and do not promise cure, but realize that the patient 
may die or there may be a partial cure. 

"When thyroidectomy is performed do not remove the entire gland. Remove 
one lobe only, or one lobe and a half or two-thirds of the remaining lobe. Even 
so-called complete thyroidectomies are not often really complete, as a remnant 
of the processus pyramidalis is usually left behind. In addition to removing a 
part of the gland, take Kocher's advice and tie three of the four thyroid arteries. 

"Do not give a general anesthetic, but produce local anesthesia (Kocher). A 
general anesthetic is very dangerous in goitre operations." 

Halsted and others have shown that not only should the thyroid be operated 
upon but that the thymus must be in part at least resected if a cure is to be induced. 



688 DISEASES OF THE THYROID GLANDS 

MYXEDEMA. 

Definition. — Myxedema is a disease in which extraordinary nutritional changes 
take place in the body as the result of absence, atrophy, removal, or inactivity of 
the thyroid gland. When the condition is due to operative removal of the gland 
it is called cachexia strumipriva. It is characterized by a peculiar swelling of 
the subcutaneous tissues, by falling of the hair, by mental failure, and by feebleness 
of the circulation. Myxedema is closely related to cretinism in children. It is 
sometimes called "Athyrea" and "Gull's disease." 

Etiology. — The cause of myxedema is failure of the body to receive the normal 
quantity of secretion from the thyroid gland. In this sense it may be considered 
the antithesis of exophthalmic goitre. The cause of the atrophy or inactivity of 
the gland is unknown. 

Myxedema occurs more frequently in married than in single women, and it 
appears most commonly after thirty years of age. It affects women and men in 
, the proportion of 6 to 1. 

Pathology and Morbid Anatomy. — When the thyroid gland undergoes atrophy, 
when it is removed by surgical operation, and when, as the result of a specific 
infection, as actinomycosis or morbid growth, its function is destroyed, myxedema 
ensues. In most cases the atrophy of the thyroid gland can be readily recognized, 
but in others the gland may seem larger than normal. This increase in size may 
be due to infiltration, tumors, cysts, subacute or chronic inflammatory processes 
leading to an overgrowth of the connective tissue of the gland, and is not a sign of 
any actual increase in glandular structure. 

The state of the subcutaneous tissues is very remarkable. They are puffy and 
swollen, and if incised are found infiltrated with a mucoid or jelly-like material. 
This material is present in such excessive quantities that the cutaneous glands are 
pressed upon and their nutrition interfered with, so that the skin becomes dry and 
harsh, and the hair falls out. Nor does this process of infiltration cease with the 
involvement of the subcutaneous tissues, for in the liver and in the kidneys the 
cells are pushed apart and compressed. The kidneys are larger than normal, and 
considerably toughened in texture. 

Frequency. — Myxedema is a rare disease, particularly in the United States. 
Physicians connected with large hospitals may see a case only once in many years. 

Symptoms. — The symptoms of myxedema are infiltration of the tissues of the 
entire body, so that they appear at first glance to be dropsical, but they do not 
"pit" on pressure and are quite firm and resistant. The skin is dry, pallid, and 
poorly nourished, the hair falls till only a few strands are left, and the eyebrows 
disappear. The expression is altered by the obliteration of the facial lines, and 
by the stupidity from which the patient suffers, for a form of mental inertia develops. 
As the disease advances muscular feebleness often arises, so that the patient falls, 
and there may be difficulty in holding the head erect. The temperature is slightly 
subnormal, the heart is feeble, and albuminuria is sometimes present. It is important 
to bear in mind that not infrequently the symptoms of myxedema are so slightly 
developed for some years that a diagnosis is not made. A tendency to obesity, 
mental torpor, physical inertia and some associated pallor should arouse the sus- 
picion of the presence of the disease in its larval form. 

Prognosis.— The prognosis depends entirely upon the treatment. If no specific 
treatment is resorted to death invariably ensues as a result of general asthenia 
or from some intercurrent malady. If specific treatment is adequate recovery 
usually takes place, provided the patient is seen before the disease is very far 
advanced. 

Treatment. — Aside from the use of antitoxin in diphtheria, there is no therapeutic 
measure which produces such extraordinary results and acts in so specific a manner 



CRETINISM 689 

as the administration of thyroid gland in myxedema and in cretinism. The dried 
thyroid gland of the sheep should be given the patient in gradually ascending 
doses, beginning with 2 grains in capsule twice or thrice a day, and gradually 
increasing the amount until 10 to 15 grains are taken daily, provided the patient 
does well on these doses and seems to need large quantities. When the extract 
of the thyroid gland is used, the dose is J grain three times a day to start with. 
Meltzer states that the extract and dried gland prepared by Parke, Davis & Co. 
have given him the best results. When overdoses are taken symptoms of cardiac 
weakness develop. These are dangerous and should be controlled by the use of 
strychnine and by insisting that the patient remain in bed for several days. Indeed, 
rest in bed is the safer plan whenever ascending doses are being employed. After 
thyroid gland has been given long enough to cause great improvement, so that the 
patient is practically well, it is essential that about one-half the dose be continued 
indefinitely or at certain periods, in order to prevent a relapse, for the sheep's 
thyroid must take the place of the wasted gland in the neck. 

A full proteid diet is essential. 

As these patients are very susceptible to cold, they should be carefully clothed 
and sent to a warm climate in the winter months, if possible. 



CRETINISM. 

Definition. — Cretinism is sometimes called congenital myxedema, or the myx- 
edema of childhood, and depends upon the same causes as does myxedema, in 
that the curious systemic changes which develop in the patient are the result of an 
absence of the secretion of the thyroid gland. 

Cretinism occurs in two forms, as endemic cretinism and sporadic cretinism. 

The conditions leading to thyroid absence or inadequacy are not known. It 
is true that in some instances the results of the marriage of near relatives or the 
presence of a tuberculous history has seemed to indicate that there might be some 
connection between these factors and the development of the disease, but in most 
cases these causes are absent. 

Symptoms. — The symptoms of cretinism rarely develop before the end of the 
second year, but the symptoms may be noticeable from the time the child is twelve 
months of age, when the parents usually consider that the child is somewhat " back- 
ward." At this time it is found to be stunted and mentally dull. The head and 
the hands and feet may seem unduly large in proportion to the size of the trunk and 
limbs. The face is stupid and heavy, and the eyes dull. The palpebral openings 
are narrow and elongated, and the nose is broad and flat, with heavy nostrils. The 
lips are coarse, are apt to protrude, are usually held apart, and not infrequently 
there is a good deal of dribbling of saliva. The tongue is swollen, and there seems 
to be some weakness of the cervical muscles, so that the head is not well carried 
on the shoulders. An anteroposterior curvature of the spinal column is often present, 
so that the abdomen is very much protruded. The legs are short and bent, as in 
rickets, and the skin is sallow and greasy. The hair is scanty and brittle, and the 
skin is badly nourished. The temperature is subnormal, but there are no important 
changes in either the urine or the blood. The most marked alterations from normal 
in the blood are a diminution in the quantity of hemoglobin. In many instances 
the child has little more intelligence than that which is needed to take its food. 
In other cases it is vicious and dirty. 

An autopsy in a case of cretinism usually reveals an absence of the thyroid 
gland, its place being taken by a few fatty granules, or*by a fibrocystic growth. 
On opening the skull there is found to be an excess of intraventricular and inter- 
arachnoid fluid. 
44 



690 



DISEASES OF THE THYROID GLANDS 



Diagnosis. — There is no difficulty in diagnosticating cretinism if a typical case 
is presented. Given a patient suffering from rickets and idiocy, some resemblance 
to true cretinism may be present, but the state of the skin and hair and the absence 
of the thyroid gland in true cretinism render a separation possible. 



Fig. 119 



Fig. 120 





A case of cretinism, showing the improvement produced by the administration of thyroid gland. 

(Davisson's case.) 



Prognosis. — The prognosis in cretinism is very good, even better than in the 
myxedema of adults, provided the treatment is instituted while the patient is 
yet a child in years. If the patient has survived till adult years are reached, the 
results are not so satisfactory and extraordinary. 

Treatment. — The treatment consists in the administration of thyroid gland or 
thyroid extract, beginning with J of a grain of the extract three times a day and 
gradually increasing it, or using 1 or 2 grains of the dry gland once, twice, or thrice 
a day, according to the size and age of the child. Under the administration of 
these substances the most remarkable change takes place in the patient. The 
first noticeable alteration is a great decrease in body weight, with a similar decrease 
in the bulkiness of the child. The skin becomes more moist and appears better 
nourished, and the expression improves. There is also an improvement in the 
color of the skin and in the quantity of hemoglobin in each blood corpuscle. Still 
later, after this primary decrease in weight, a real improvement in nutrition takes 
place, and the child begins to gain, so that it no longer looks stunted, but appears 
more like a healthy individual. The mental improvement is perhaps the slowest 
part of the cure, and in some instances the mind never fully reaches the development 
of that of a healthy child, although the nutrition of the body may be excellent. 
The effect of the administration of thyroid upon the growth of the teeth is equally 



TETANY 691 

remarkable with that upon the general nutrition. Before thyroid is given the 
milk teeth are usually badly formed and rapidly decay ; but if thyroid is administered 
freely before the permanent teeth appear, they are often developed as they would 
be in the jaws of a healthy child. 



DISEASES OF THE PARATHYROID GLANDS. 



TETANY. 

Tetany is a condition in which intermittent unilateral or bilateral tonic and 
painful spasm affects certain muscle groups, usually of the upper limbs, although 
occasionally it involves the legs as well. It is sometimes called "tetanilla," or 
"idiopathic muscular spasm." The disease is exceedingly rare in America, but 
comparatively common in certain European countries, notably Sweden and Austria. 
It is probable that tetany is merely a symptom of several different conditions. 
One type of it occurs in epidemic form in Austria, particularly during the months 
of March and April, affecting chiefly youths between fifteen and twenty-five years 
of age. These persons usually belong to the lower walks of life. Occasionally 
it develops in women, particularly at the time of pregnancy or during nursing, 
a very few cases have been reported in children below puberty and in persons of 
advanced years. 

Etiology. — Tetany is sometimes due to atrophy of the parathyroid bodies. It 
has been frequently reported as occurring in persons who are suffering from chronic 
gastro-intestinal disorders, particularly cases of gastric dilatation, and it has occurred 
in such cases after the gastric contents have been removed by lavage. It seems 
to be more frequent in persons who follow certain occupations than in others. 
Thus, out of 314 male patients mentioned by Frankl-Hochwart no less than 141 
were shoemakers and 41 were tailors. This has caused certain persons to believe 
that certain types of tetany were of the nature of an occupation neurosis. Tetany 
sometimes develops in those who have suffered partial or total extirpation of the 
parathyroid gland. It is also met with in children who are suffering from rickets. 
It is also a complication of chronic gastric dilatation arising from any cause. In 
some cases tetany is a manifestation of hysteria. 

Pathology and Morbid Anatomy. — As few of these cases come to autopsy, we know 
little concerning their morbid anatomy. In a few instances autopsy has revealed 
hyperemia and minute hemorrhages in the anterior cornua of the spinal cord, but 
it is very doubtful if these are characteristic of the malady. 

Symptoms. — The prodromal symptoms of tetany are usually those indicative 
of a toxemia. The patient first suffers from some aching or pain in the extremities, 
and may have headache and dizziness, and feel heavy and stupid. As already 
stated, the disorder usually affects one or both arms and involves in particular 
the muscles of the forearms and hand, causing the palm of the hand to be flexed 
upon the wrist while the fingers are extended. Sometimes the forearm is flexed 
at the elbow. In other instances the phalanges are flexed and the distal phalanges 
extended. When the lower extremities are affected, the feet and toes show some- 
what similar contractures. The toes may overlap one another and be forcibly flexed, 
and the foot may be bent at the ankle in the position of club-foot. Occasionally 
in very severe cases, some of the muscles of the trunk and those of the neck and 
throat may be involved, and even the ocular muscles may contract, so that a form 
of nystagmus is present. It is a noteworthy fact, first enunciated by Trousseau, 



692 DISEASES OF THE PARATHYROID GLANDS 

that pressure exercised upon the affected limb will generate an attack, provided 
that the nerve trunks or the bloodvessels are affected by the pressure. This is 
known as "Trousseau's symptom." The pressure must be continued from thirty 
seconds to five minutes to produce an effect. While the presence of Trousseau's 
symptom is pathognomonic of tetany, its absence does not disprove the presence 
of the disease. 

Under the name of "Trousseau's sign" tapping of the nerves of the arms, or 
legs, when surrounded by an elastic band, may induce the spasm. Spasm may 
also be induced if the facial nerve is irritated in this manner (Chvostek's sign). 
Under the name of "Erb's sign" lies the fact that the motor nerves manifest a 
marked increase in electrical irritability, particularly with the galvanic current. 
Hoffmann has pointed out that the superficial sensory nerves are also exceedingly 
sensitive, and that moderate pressure upon them, which ordinarily would not be 
felt, may cause a severe pain similar to that produced by striking the ulnar nerve 
at the elbow (" Hoffmann's sign") . If the irritation of the motor nerve is repeatedly 
produced, a marked increase in the excitability of the tributary muscles follows. 
Occasionally, nervous lesions appear in the skin such as urticaria or herpes, pigmen- 
tation, and loss of the hair and nails. An attack of tetany may last from a few 
minutes to several days. It may be so moderate that it can be overcome by the 
will of the patient, or so severe that the limb is entirely beyond control. If an 
attempt is made to reduce the spasm by force it causes great pain, and if the con- 
tractions of the muscles are marked and cramp-like the pain is also severe. The 
attack passes off gradually and is often followed by impaired sensation and loss 
of power in the affected parts. There is no loss of consciousness in the great 
majority of cases but in severe cases the movements may be as severe as in true 
epilepsy. 

Diagnosis. — The development of comparatively localized tonic spasms in associa- 
tion with the other symptoms already described renders the diagnosis of tetany 
quite easy. The disease must be separated from Jacksonian epilepsy and hysteria. 
This can be done by the development of Trousseau's, Chvostek's, and the other 
signs just named, by the absence in tetany of the various stigmata, including the 
reversal of the color fields, found in hysteria. It is differentiated from Jacksonian 
epilepsy by the prolonged character of the attack and the fact that it can be pro- 
duced at the will of the physician. Hysterical contractures sometimes assume 
the form of tetany, and cases of apparently true tetany may have hysterical features. 

Prognosis. — The prognosis as to life is good unless the provoking cause is in 
itself serious, as, for example, when the parathyroid glands have been removed. In 
other words, in no instance does tetany itself threaten vitality, although the under- 
lying cause of the tetany may. Most cases recover. Some suffer from only one 
attack. In others the symptoms disappear after many attacks as soon as the cause 
is removed. 

Treatment. — This deals largely with the removal of the exciting cause. If 
gastric dilatation is present and if its nature is such that it can be benefited by 
lavage or operation, these measures must be instituted. In some instances where 
there is reason to believe that the condition results from auto-intoxication, mild 
saline purgatives, diuretics, and moderate doses of calomel or blue mass are advis- 
able, and, in addition, hot packs may be given to aid in the elimination of poisons 
by the skin and to act as nervous sedatives. Recent investigations have shown 
that tetany in animals developing after the removal of the parathyroid glands can 
be at once arrested by the injection of an extract of parathyroids. Calcium chloride 
or lactate often exercise a remarkable effect for good. If there is present a general 
condition of debility, anemia, iron, arsenic, and similar tonics combined with an 
out-door life and avoidance of nerve irritation are essential. 



DISEASES OF THE THYMUS GLANDS 



693 



DISEASES OF THE THYMUS GLAND. 

The thymus gland is found well developed in infants up to the second year of 
life, after which time it gradually decreases in size till it reaches a degree of degenera- 
tion and atrophy in which it may be said to no longer exist. This occurs about 
the time of puberty. In fully developed adults it is represented by a small aggrega- 
tion of lymphoid and fatty cells. Very rarely the thymus persists without any 
change in its tissues, even in adult life. When it remains large, or increases in 



Fig. 121 




Hyperextension of the head, showing how compression of the trachea by a hyperplastic thymus can 
take place. The cervical vertebrae are displaced forward; the larynx and mediastinal organs are 
raised upward; the thymus is caught like a wedge between the sternum and spinal column. Hence 
compression of windpipe. (Klose and Crotti.) 

size as the result of disease, as in the status lymphaticus, it may cause symptoms 
by pressing on the trachea and the great vessels of the neck and chest. Persistent 
large thymus is commonly met with in exophthalmic goitre and probably plays 
an important part in its symptomatology. (See Exophthalmic Goitre.) 

Actual disease of the thymus gland is very rare. In some cases a state of so- 
called hypertrophy is present, but this is rarely a true hypertrophy, the gland being 
swollen and filled with lymphoid cells. Occasionally minute hemorrhages may 



694 DISEASES OF THE THYMUS GLAND 

take place into its tissues or beneath its capsule. Abscess has been recorded as 
having occurred, and growths, benign and malignant, have been found in its tissues. 
It has been found affected by tuberculosis. 

Many years ago enlarged thymus was supposed to be the cause of spasmodic 
croup. That an enlarged gland may cause some interference with respiration 
is conceivable, but we now know that spasmodic croup is usually due to rickets 
or postnasal adenoids. For an excellent summary of the subject see J. P. C. 
Griffith, New York Medical Journal, September 4, 1909; and Andre Crotti, Jour, 
of A.M. A., February 22, 1913. 

Enlarged Thymus. — There is a close relationship between enlarged thymus and 
status lymphaticus discussed below. Indeed some have considered that it is the 
real cause of death in the latter disease. Death from enlarged thymus without 
general lymphatic tissue does occur without doubt. As. early as 1614 Plater 
noted the frequent presence of enlarged thymus in cases of sudden death. Since 
then a large number of reporters have recorded such cases. Numerous theories 
have been advanced varying from hyperthymusism, that is, oversecretion of the 
gland, or a toxicosis. Others have thought that the gland pressed on the trachea 
or caused disorder of the cardiac nerves. The important point is that life has been 
saved in at least 10 cases by excision, partial or complete, of the gland. There 
have been chronic cases however in which tracheal pressure has been recognized 
for months. Griffith believes that the condition causing death may be pressure 
on the trachea or a "neurosis." 

STATUS THYMO-LYMPHATICUS. 

Definition. — The term status thymo-lymphaticus or "lymphatic constitution," 
sometimes called " constitutio lymiphatica" is applied to a state which occurs chiefly 
in children or infants, and which is characterized by hyperplasia of the lymph nodes, 
the thymus gland, and the spleen, and by a %poplasia of the heart and arteries. 
The lymphoid bone-marrow is also affected. The fact of particular interest is that 
patients with this condition sometimes suffer sudden death, which, coming on 
in children who, on superficial examination, appear unusually robust and plump, 
is all the more startling. 

History. — As long ago as 1614 Plater made note of the fact that the thymus 
gland was found enlarged in certain cases of sudden death, and in 1830 Kopp 
described a form of difficult breathing which he called "thymic asthma," and which 
he considered was due to pressure upon the trachea by an enlarged thymus gland. 
This view, which was apparently disproved by Friedleben in 1858, received no 
further support until in 1888 it was revived by Grawitz, only to be controverted 
again by Paltauf in 1889. 

Etiology. — The etiology of this state is not known, but it is apparently a congenital 
fault, and is associated with a low degree of vital resistance to infection. Hedniga 
has reported an instance in which out of a family of nine children, five died of this 
malady. 

Blumer has put forward certain facts which seem to show that this condition 
is the result of the development in the body of a toxic substance, a cytotoxin. 
To this state the term lymphotoxismus has been applied. According to this view, 
the overgrowth of the lymphatic tissues in the different parts of the body is a 
sequence of the action of this poison and not the cause of its development. 

Pathology and Morbid Anatomy. — An autopsy in a case of this character reveals 
an overgrowth and swelling of the lymph nodes in the thorax, abdomen, and 
cervical and inguinal chains, and enlargement of the tonsils. The lymph nodes 
of the intestinal tract are very markedly swollen and sharply defined. The spleen 
appears larger than normal, and the lymphoid tissue of the Malpighian bodies 



ADDISON'S DISEASE 695 

is in a state of overgrowth. The changes in the thymus gland are, however, the 
most important, because it is supposed that the sudden congestion, hyperplasia, 
and swelling of the gland which occurs causes death by pressure upon the great 
vessels of the neck and upon the trachea. The thyroid gland may also be enlarged. 
If the shafts of the long bones are opened, yellow marrow is found to be substituted 
for red marrow. The heart and aorta are poorly developed. 

Congestion and edema of the lungs have been found in some cases at autopsy, 
and in others atelectatic patches have been discovered. In all of these cases the 
pressure upon the air passages was responsible for these changes. 

Symptoms. — There are no pathognomonic symptoms, but the following symptoms 
or signs are very suggestive. An enlargement of the thymus gland and overgrowth 
or excessive prominence of the circum vallate papillae of the tongue. Back of 
these papillae are enlarged lymph nodes seen by the aid of a pharyngoscope. The 
thyroid gland is unduly full or enlarged and the heart sounds distant and feeble. 
There may be a soft systolic murmur at the base or apex. Lastly there is manifest 
a tendency to general hyperplasia of all the lymphatic structures. The child is 
often overgrown and unduly heavy. The x-rays may reveal an enlarged thymus. 
The recollection of the possible presence of this state should make the physician 
particularly careful when administering an anesthetic to a child of the lymphatic 
type, especially if the condition to be relieved is overgrowth of the lymph tissues, 
such as postnasal adenoids and spongy tonsils, as sudden death may ensue. 
Hand has reported a case in which tetany was present. Miloslavich has called 
attention to the frequency of the status thymolymphaticus in suicides. In 88 
of 110 autopsied cases in soldiers of the Austrian army he found evidence of the 
lymphatic constitution as follows : Status thymolymphaticus in 52 ; status lympha- 
ticus in 23; status thymicus, 9; combined lesions, 4. He believes that this condition 
induces mental changes leading to suicide. 

Treatment. — We know so little of the cause of this state, and so few cases have 
been subjected to treatment, that no definite plan of treatment can be outlined, 
save that fresh air and sunshine and iron iodide, and arsenic are useful. 

If the thymic enlargement be demonstrable, operation might be resorted to. 
Rehn opened the mediastinum, drew the gland forward and stitched it in position; 
recovery followed. Carter operated on a case for tracheal obstruction, recognized 
the thymic enlargement, and introduced a tube which gave temporary relief, but 
the child died. More recently a number of surgeons have advocated extirpation 
in whole or in part. 



DISEASES OF THE SUPRARENAL GLANDS. 

ADDISON'S DISEASE. 

Definition. — The name Addison's disease is applied to a condition in which the 
patient suffers from a characteristic pigmentation of the skin, pallor, and loss of 
strength, and in which the chief microscopic changes are alterations in the supra- 
renal bodies. 

History. — Addison's disease gets its name from Thomas Addison, the physician 
who first clearly described the malady in 1849 at Guy's Hospital, London. The 
condition did not receive attention from the profession in general until 1854, when 
Addison wrote a special monograph on the subject. 

Etiology and Pathology. — The cause of Addison's disease is not known in the 
sense that we recognize a cause which is responsible for all cases. In about 50 
per cent, of the cases so far reported which have come to autopsy, tuberculosis of 



696 DISEASES OF THE SUPRARENAL GLANDS 

the suprarenal glands has been found. That this lesion is not sufficient in all 
cases to cause the general systemic manifestations of the disease is proved by the 
fact that identical changes have been found in the suprarenal bodies when none of 
these symptoms have been present. In certain cases hemorrhages into the supra- 
renal bodies as the result of injuries have caused the symptoms to develop. 

As a matter of fact, the view, as to the relationship of these causes to the disease, 
expressed by Addison fifty years ago is probably correct, namely, that any lesion 
of these bodies which interferes with their function may cause the malady. 

In some instances the disease seems to be primarily the result of pathological 
changes in the semilunar ganglia of the abdominal sympathetic nervous system. 
Rolleston has expressed the plausible view that in these cases the disease arises 
in all probability by reason of the fact that the glands are cut off in circulation and 
nerve supply by growths or inflammatory exudates. 

Morbid Anatomy. — The common lesion in cases of Addison's disease is, as already 
stated, tuberculosis, and next to this in frequency is atrophy. The tuberculous 
change is of the fibrocaseous type, except in rare instances, and usually begins in 
the medulla of the gland. The stage of infiltration is followed by caseation and 
commonly more or less fibrosis; in other words, there is an attempt at healing. 
The fibrocaseous area may be restricted to the adrenal or extend beyond it. Calci- 
fication is not uncommon, and pyogenic infection may cause abscess. The tuber- 
culous process may be primary and confined to the adrenal body, as in the two 
cases reported by Symes and Fisher. 

In the form of the disease in which atrophic changes occur in the glands, the 
wasting may be so complete that only a small fibrous mass remains to indicate 
their former existence. In still others an overgrowth of fibrous tissue resembling 
the sclerosis found in the other organs of the body may take place, with secondary 
atrophy of the parenchyma. Peterson has collected 26 such cases. In still other 
cases the glands have been found to be the seat of hemorrhage (adrenal apoplexy), 
thrombosis of the vessels, or malignant disease. The changes found in the semi- 
lunar ganglia and in the plexuses composing the abdominal sympathetic system 
are, as already stated, in all probability, indirect causes of the disease, although 
Hale White has shown that changes take place in these tissues in ordinary individ- 
uals as the result of advancing age. It is difficult to determine, therefore, whether 
the reports of changes in these tissues made by some observers have been really 
etiological factors in the disease. Further, a very large proportion of cases in 
which Addison's disease has been present have failed to show alterations in the 
semilunar ganglia or in the abdominal sympathetic. In some cases a hyperplasia 
of the lymphoid structures in the alimentary canal has been noted. 

That there have been, and are in existence at present, several theories as to 
the lesions which result in Addison's disease must have been evident from what has 
already been said. The only ones that have received general recognition have 
been the "nervous theory," that the disease was due to changes in the abdominal 
nervous apparatus; or the original theory of Addison, that it is due to failure of 
the suprarenal glands to carry out their normal function. The nervous theory 
has now been generally cast aside, and we have left Addison's own proposition 
modified by our extended knowledge of internal glandular secretion. Space does 
not permit a discussion of the views for and against this opinion. These can be 
found exhaustively, and most capably, discussed by Rolleston in Allbutt's System 
of Medicine, vol. iv. Suffice it to say, that the opinion generally held today is 
that these symptoms come on because the suprarenal secretion fails to find its 
way into the general economy. Changes in the sympathetic nervous system may 
also be a factor. 

Finally, it is not to be forgotten that Addison's disease may be present without 
noticeable lesions in the suprarenal bodies, and it is also a fact that these bodies 



ADDISON'S DISEASE 697 

may be almost completely destroyed by a growth or by tuberculosis without any 
symptoms of this malady developing. 

The pigmentation of the skin is. due to the deposition of pigment in the cells of 
the Malpighian stratum, and according to Earkshevitch, who studied the skin 
removed from a living subject, in the subjacent tissues. The pigmented cells are 
supposed to obtain their pigment from the hemoglobin of the blood, but they 
contain no iron. The discoloration of the mucous membranes is due also to the 
deposit of pigment. The pigmentation of the mucous membranes is in patches, 
and Mann asserts that it is deposited only where the parts are rubbed or subjected 
to causes that produce hyperemia. 

Symptoms. — The symptoms of Addison's disease are chiefly those which are 
represented by the term general asthenia. The patient gives the history of being 
easily tired and, indeed, of a constant sense of fatigue. Even after a night's rest 
he feels as weary in the morning as when the went to bed. The sensation of feeble- 
ness is associated with profound muscular weakness as the disease progresses, but 
there is little or no true emaciation. The term "invincible languor^ used by 
Rolleston well describes the patient's state. An examination of the heart shows 
its muscle is greatly enfeebled, so that the cardiac sounds are lacking in normal 
tone. The pulse is soft, and easily extinguishable by the pressure of the finger. 
The extremities are cold and the general body temperature may be subnormal. 
Anemia is well marked, but usually not excessive, the blood cells being decreased 
to 3,000,000 or a little lower. 

No mention as yet has been made among this list of symptoms of the one char- 
acteristic manifestation of the malady which is practically pathognomonic, namely, 
the pigmentation of the skin. While its peculiarities would naturally lead one to 
speak of it first, mention of it has been delayed because its appearance is often 
delayed until the other symptoms are quite well developed. In other words, 
it usually follows and does not precede the constitutional manifestations of the 
disease. There are, however, rare exceptions to this, and cases have been recorded 
in which the pigmentation has been present for long periods before any other signs 
of Addison's disease developed. The pigmentation may be over the entire body, 
but as a rule it is in patches, and chiefly affects the skin of the face, of the neck, 
and the extensor surfaces of the hands and forearms. If the mucous membrane of 
the mouth is examined the lips at the point of contact are noticeably darkened and 
the edges of the tongue, particularly on its under surface, may show discoloration 
as if ink had been taken into the mouth. 

Diagnosis. — Except in well-defined cases it may require weeks or months of 
watching to determine that a patient has this malady. Pregnancy not rarely is 
associated with the presence of pigmented spots on the skin, but the condition 
of the uterus and its contents prevent a mistake being made as to the cause. In 
some cases of hypertrophic cirrhosis of the liver there may be in addition to jaundice 
very marked pigmentation. I have under my care at the time this is written a 
man who has hypertrophic cirrhosis, jaundice, and such deep pigmentation of the 
skin that he looks as if coated with coal-dust. In such a case the state of the liver 
reveals the cause. 

In the rare malady called diabetes bronze, in which there is hypertrophic cirrhosis, 
jaundice, diabetes, and pigmentation of the skin, the state of the liver and urine 
will aid in the differentiation. In certain cases of advanced pulmonary tuberculosis 
the skin is pigmented a dirty brown, and in patches may be considerably discolored, 
but here the pulmonary state prevents confusion as to its cause. 

The prolonged use 'of arsenic may have a similar effect, not only on the extremities, 
but on the skin of the chest and abdomen, which may become much darker than 
normal without any neuritis being present. In syphilitics the site of old eruptions 
may be stained, and in vagabonds who are infested with lice, and have been much 



098 DISEASES OF THE SUPRARENAL GLANDS 

exposed to the weather, areas of discoloration of the skin may be present. It is 
said that the discoloration of the skin called chronic argyria, due to the prolonged 
use of silver internally, has been confused with the state of the skin in Addison's 
disease. This would be scarcely possible if the observer had ever seen a case of 
chronic silver poisoning, for the discoloration of argyria is a peculiar lividity rather 
than the appearances of a pigmentation, and it is uniform on exposed parts of the 
body. 

As Addison's disease is due in a large proportion of cases to tuberculosis of the 
adrenal bodies, the tuberculin test may be employed to give additional information 
in the case; but even if this test is positive the possibility of tuberculous foci else- 
where giving the reaction, and the fact that syphilitics sometimes react, should 
make us hesitate before resting too heavily upon this means of diagnosis. (See 
Tuberculin, in section on Tuberculosis.) 

Prognosis. — It may be stated that given a patient with Addison's disease 
developed so far that a diagnosis is certain, then death from the malady is certain 
also. Lewin in a collection of 500 cases found that 5 were cured and 28 improved. 
In the 2 cases I have seen, 1 of which is now under observation, the disease had, 
at times, certainly been arrested in its progress under the use of full doses of supra- 
renal gland. Because of the gradual development of the malady, its average 
duration is difficult to determine, but its course is not very rapid. Wilks believes 
it to be about eighteen months, but in some cases it lasts for years. Very rapidly 
fatal cases are also on record. 

Treatment. — The question of the proper plan of treatment of Addison's disease 
cannot be answered positively until the pathologist is able to give us a clear con- 
ception of the morbid processes which produce the chain of symptoms already 
described. The very fact that different pathological changes, or diseases, affect 
the suprarenal bodies, and so produce the symptoms of this malady, indicates 
that the therapy must vary with the cause. Theoretically the use of suprarenal 
gland of the sheep is indicated in every case, but practical experience has shown that 
only in a small proportion of those cases in which it has been used has it done good. 
It is not, therefore, to be compared to the value of thyroid gland in myxedema or 
cretinism. It has been proved that suprarenal gland has little effect on blood 
pressure if it is taken by the stomach, and that its active principle when in concen- 
trated form often causes abscess when it is given hypodermically. Probably the 
best plan is to give the patient adrenalin chloride in normal salt solution by hypo- 
dermoclysis every day or every other day, using 1 to 2 drachms of the adrenalin 
chloride (1: 1000 solution), as put upon the market, to a half -pint or pint of saline 
fluid. When the desiccated gland is used by the mouth, from 2 to 10 grains may 
be given three times a day in capsule. It is unfortunately true that even when 
the adrenalin gland is freely used, the disease is, at the best, only delayed in its 
progress in most cases. 

Adams has collected 97 cases treated with suprarenal gland. Of these 7 were 
made worse, 43 experienced no real benefit, 31 showed marked improvement, and 
16 were said to be cured. In the successful cases the gland was given solely by 
the mouth. If the patient is at all feeble he should be kept in bed, not only because 
in this manner we conserve his flagging energies, but also because a number of 
cases of syncope and sudden death from this disease have occurred in patients 
who have made a sudden effort. An easily digested diet, the avoidance of purga- 
tives which may induce dangerous purging, and the use of iron and arsenic as 
tonics form the rest of the treatment. 



ACROMEGALY 699 



DISEASES OF THE PITUITARY BODY. 

DYSPITUITARISM. 

A number of remarkable disturbances of nutrition and growth are now known 
to be due to perverted function, or loss of function, of the anterior and posterior 
lobes of the pituitary body. They vary according to whether the secretion of the 
lobes is increased or decreased. In many instances a lesion in the cella turcica 
is revealed by the x-rays or the surgeon. Those in which the secretion of the anterior 
lobe is increased are chiefly acromegaly and gigantism. 

ACROMEGALY. 

Definition. — Acromegaly is a slowly developing chronic disease of nutrition 
characterized by an overgrowth of the extremities and head, and, to a less degree, 
of the trunk, with associated curvature of the dorsal and cervical spine. It is 
sometimes called "Marie's disease," because Marie first described it in 1886. 

Etiology. — The condition arises from disease of the anterior lobe of the pituitary 
body caused by hypersecretion of this lobe. Acromegaly rarely appears before 
the thirtieth year, but several cases have been recorded at an earlier age. 

Symptoms. — The appearance of a patient suffering from this disease is so peculiar 
and striking that there is no difficulty in diagnosis, if the malady is well developed. 
The massive and gigantic appearance of the head, of the features of the face, and, 
on closer inspection, the enlargement of the hands, and the increase in the length 
of the long bones, combined with the kyphosis of the spine, make the clinical picture 
complete. The upper part of the forehead appears low because of the abnormally 
prominent superciliary ridges, and this effect is exaggerated by the projection of 
the lower jaw. As a consequence, the shape of the face is elliptical. The skin of 
the face is thick and sallow and greasy in appearance, and lies upon the forehead 
in heavy transverse creases. The cheeks appear sunken, chiefly because of the 
great overgrowth of the malar bones. The nose is not only greatly enlarged, but 
often increases in size more rapidly than the other features, so that it seems out of 
proportion with the rest of the head. The nostrils are heavy, thick, and immovable. 
Not rarely the superior maxillary bone fails to develop as rapidly as nearby tissues, 
and as a consequence the upper jaw may seem sunken, an effect increased by the 
enormous nose above and the overgrown lower jaw below it. This effect is also 
increased by the great enlargement and thickening of the lower lip. An examina- 
tion of the mouth will reveal the fact that the tongue and uvula are broader and thicker 
than normal. The thorax on inspection will be seen to be greatly increased in its 
anteroposterior diameter, which is in excess, as compared to its lateral diameter. 
The ribs are enlarged and the clavicles thickened, but the abdomen often appears 
sunken because of the projection forward of the lower part of the thorax. The 
muscles may, in the early stages, seem increased in size and in power, but the 
dominant tendency is to muscular atrophy. No changes of importance take place 
in the internal viscera. Blindness, partial or complete, may develop, due to optic 
neuritis. Rarely nystagmus and squint have appeared. (See Figs. 122 and 123.) 

The subjective symptoms — that is, those complained of by the patient — consist 
in headache, dimness of vision, and pains in the joints. There is usually slowness 
of thought and perhaps actual drowsiness. 

Diagnosis. — Acromegaly must be differentiated from gigantism, leontiasis ossea, 
myxedema, arthritis deformans, osteitis deformans, and pulmonary hypertrophic 
osteo-arthropathy. Perhaps the most frequent error in diagnosis is that of confusing 
myxedema with acromegaly, but in myxedema there is never any actual increase 



700 



DISEASES OF THE PITUITARY BODY 



in the size of the bones. The face in myxedema is round and full instead of ellip- 
tical, and the ends of the fingers are swollen and thickened instead of the whole 



Fig. 122 




Fig. 123 




Acromegaly, showing the large hands, nose, and superciliary ridges. 



ACROMEGALY 701 

hand being manifestly enlarged, as in the disease under consideration. Again, 
in myxedema the skin is pale, puffy, and waxen in appearance, devoid of hair and 
also of wrinkles, whereas in acromegaly the skin upon the face is wrinkled and there 
is no marked falling of the hair. 

Gigantism is separated from acromegaly by the fact that there is a symmetrical 
overgrowth all over the body, whereas, as has already been pointed out, the enlarge- 
ment in acromegaly affects chiefly the extremities and the tissues of the face. 
Further than this, in gigantism the ends of the bones are not enlarged to such an 
extent as to be out of proportion to the shaft, and in acromegaly this disproportion 
is quite constant. (See below.) 

Leontiasis ossea is characterized by the development of bony tumors or osteo- 
phytes on the face and cranium which produce great deformity, but there is no 
marked enlargement of any one feature nor of the extremities. 

Osteitis deformans is differentiated from acromegaly by the fact that the long 
bones are chiefly affected, are apt to be curved, and so produce great deformity. 
But there is no marked enlargement and the deformity is very apt to be asymmetri- 
cal. In osteitis deformans the facial bones are rarely affected, but the cranial 
bones are involved in the pathological process; whereas, in acromegaly it is the 
facial bones which are affected, the other cranial bones being but slightly diseased. 
Finally, and perhaps most important, the face of a case of osteitis deformans is 
broadened in its upper portion and narrowed in its lower portion, giving it a triangu- 
lar appearance; whereas, in acromegaly the lower part of the face is broad, and 
therefore the general effect is elliptical. 

In pulmonary hypertrophic osteo-arthropathy there is enlargement of the hands 
and feet, but no enlargement of the face, and there is always found marked chronic 
pulmonary lesion, such as bronchiectasis, empyema, or other serious thoracic 
disease. A close examination of the hands and feet will show that the enlargement 
is confined chiefly to the joints, and that the whole hand is not thickened and 
increased in size as in acromegaly. 

Gigantism occurs instead of acromegaly from hypersecretion of the anterior 
lobe of the pituitary, in cases in which the epiphyseal centres have not undergone 
ossification. 

The cases in which there is hypersecretion of the posterior lobe are divisable as 
follows : 

The Type Frohlich are characterized not by overgrowth of bone but by excessive 
adiposity and the peculiarity that in males the fat is deposited in the regions char- 
acteristic of its distribution in females. There is arrested development of the 
genitals, a lack of growth of hair, a small stature, a subnormal temperature and an 
extraordinary tolerance of an excess of carbohydrate food. Thus, such cases can 
ingest over 150 grams of glucose or 100 grams of levulose without developing 
glycosuria. There are present also various psychoses. Such patients are usually 
children. 

The Type Burnie is due apparently to hypersecretion of both the anterior and 
posterior lobes and is characterized by dwarfism, atrophy of the genitals, internal 
and external, adiposity and optic nerve atrophy and is due probably to the growth 
of a tumor in the gland. 

The Type Cushing apparently depends upon an alternating hyposecretion and 
hypersecretion of one or the other lobe. These cases may present the chief symp- 
toms already described as to overgrowth of the bones and adiposity with lack of 
development of the sexual apparatus but do not develop acromegaly. 

Treatment. — The treatment is chiefly surgical and is designed rather to relieve 
symptoms caused by pressure induced by the growth in the gland than to effect 
a cure. Decompression may be performed or part or all of the growth removed. 



702 DISEASES OF THE SPLEEN 

Medically the administration of the anterior or posterior lobe from an animal may 
be resorted to by the mouth, or an extract may be given hypodermically. The 
transplantation of the pituitary gland of an animal to the subcutaneous tissues of 
the patient may be tried. Where the condition arises from hypersecretion these 
latter measures are of course useless. 



INFANTILISM. 

Infantilism is an anomaly of development characterized by the persistence of 
the morphological characters of childhood in an individual who has reached or 
passed the age of puberty (Meige) . This delay of physical development is accom- 
panied by a delay in psychical development (Hutinel) . There are two chief types 
of infantilism: the Brissaud type is associated with thyroid deficiency; whereas 
the Lorain type is associated with other conditions, and presents a picture of quite 
a different character. The first type is often overgrown; the second type has 
been well compared to the figure of an adult seen through the wrong end of a pair 
of opera-glasses, thereby emphasizing their diminutive stature. As a matter of 
fact, aside from the appearance of being a miniature of a man, there are other abnor- 
malities which show in the expression of the face and in the movements. Predis- 
posing causes or direct etiological factors are tuberculosis, congenital syphilis and 
disease of the glands which carry on internal secretion, namely, the pituitary, 
the suprarenal, the thyroid, thymus and testicles. Sometimes the direct etiological 
factor seems to be heart disease, especially mitral stenosis, or hypertrophic hepatic 
cirrhosis. In a few instances gastro-intestinal infections characterized by recurrent 
attacks of diarrhea seem to be provocative. In so-called "celiac disease," in which 
a child suffers from a chronic condition characterized by the passage of bulky stools, 
infantilism sometimes occurs and is thought to be due to pancreatic insufficiency. 
Diabetes and syphilis occurring in infancy also seem to be causes, and various 
poisons, such as lead, mercury, tobacco and carbon bisulphide may induce it. 
The prognosis is unfavorable unless the underlying cause can be removed or the 
secretion of an internal gland substituted, as thyroid extract. If the pituitary 
gland is deficient, an extract of the entire gland rather than of one lobe should be 
used. Hutinel warns against the use of thyroid extract in those patients who are 
tuberculous and recommends that if it is given arsenic should also be administered. 



DISEASES OF THE SPLEEN. 

Diseases of the spleen occurring independently of other diseases may be said 
not to exist. In myelogenous leukemia, in splenic anemia, in malarial fever, and 
in cases of hepatic cirrhosis or heart disease, the spleen is often greatly enlarged, 
but in no case is this condition primary. So, too, in the prolonged infectious 
fevers, such as typhoid fever, the spleen is usually swollen. 

In some cases the surface of the spleen may be traversed by a crevice or indenta- 
tion which almost divides its body into different parts, and in others there may be 
found an accessory spleen or accessory spleens in nearby parts of the abdominal 
cavity. In very old people the spleen is often greatly atrophied. 

An infarct of the spleen is due to an embolus which usually has its origin in the 
heart, or which arises from some area of septic infection, or in other cases a thrombus 
forms in the splenic vein and produces a similar effect. The latter condition is the 
cause of the infarct met with in typhoid fever and in leukemia. 



DISEASES OF THE SPLEEN 703 

Abscess of the spleen as the result of septic infection is by no means rare, and 
such abscesses always depend upon infected emboli. 

Hydatid cyst of the spleen is rare not only because hydatid cyst is rare in this 
country, but also it seldom develops in this gland even in those parts of the 
world in which hydatid disease is common. 

Malignant growths in the spleen are among the rarest pathological lesions. Pri- 
mary growths are practically unknown and secondary growths are also very rare. 
From statistics at St. George's Hospital, London, collected by Walker, it is found 
that in 161 cases of carcinoma involving all parts of the body secondary growths 
appeared in the spleen seven times, and in 50 cases of sarcoma the spleen was 
affected once. Taylor in 677 cases of carcinoma, epithelioma, and sarcoma found 
secondary growths in the spleen in twenty-three instances. Sometimes in cases 
of cancer of the gallbladder or of the pylorus the growth extends to the spleen 
by direct invasion. 

Movable spleen, like movable kidney, is a condition in which this organ wanders 
away from its normal position so that it may be found far removed from its ordinary 
area, and even so low as the pelvis. Its displacement is usually associated with a 
sense of dragging in the left hypochondrium or loin, and if the pedicle becomes 
twisted great pain may be suffered, with fever, collapse, and finally necrosis of the 
splenic tissues. Osier records a case in which this occurred and in which abdominal 
section resulted in recovery, although a considerable part of the spleen was lost by 
sloughing. 

It is necessary to separate wandering spleen from floating kidney. This can 
be done by the discovery of the splenic notch, by the greater sense of resistance in 
the otherwise normal kidney, and by the presence of resonance on percussion in 
the splenic area where splenic dulness is usually demonstrable. 

Rupture of the spleen is a rare accident, but occurs occasionally in those who, 
while suffering from great congestion or enlargement of this organ, meet with an 
accident in which the splenic area is subjected to a severe blow. Cases are also 
on record in which the spleen has ruptured as the result of great distention. Rup- 
ture of the spleen will be found discussed under Malaria. The symptoms are those 
of internal hemorrhage and demand an immediate abdominal section. 

The treatment of wandering spleen consists in the wearing of a bandage and 
pad to retain the organ in its place, and, if need be, we may resort to an operation 
to fix it by causing adhesions to form around it. Extirpation of the spleen has 
been advised in cases in which the symptoms are very distressing, but this should 
be done only when the condition is very urgent. 

In considering disease of the spleen several facts must be borne in mind. During 
embryonal existence it is an important factor in the formation of red blood cells 
but after birth this function ceases, the bone marrow taking its place. It is con- 
cerned in the production of leukocytes, chiefly lymphocytes. On the other hand 
the spleen seems to control the activity of the bone-marrow and there is evidence 
that it may be actively engaged in hemolysis and for this reason extirpation may 
cure certain cases of excessive hemolysis. When the cause of hemolysis is not in 
the spleen this operation is useless. Among the diseases in which the spleen is 
responsible may be mentioned congenital hemolytic icturus, in which during the 
whole of a long life there is moderate icturus with sharp exacerbations and more 
or less anemia with excessive urobilinuria; acquired hemolytic icturus which 
may last for years or cause death in two or three years and is characterized in 
its severe forms by jaundice, stupor or delirium, sometimes fever, and as severe 
anemia, as in true pernicious anemia. There is marked urobilinuria and the icterus 
is not hepatic but hemic. The dividing line between this type and the splenome- 
galie hemolytique of Banti is difficult to draw. (See Banti's Disease.) 

There is still another class of cases in which splenomegaly is associated with 



704 DISEASES OF THE SPLEEN 

anemia and true hepatic jaundice with or without hepatic cirrhosis, the hepatic 
lesions being induced by thrombosis and rupture of the bile capillaries, possibly 
due to excessive hemolysis. When the urine is loaded with urobilin this type may 
be benefited by splenectomy. The dividing line between Hanot's cirrhosis of the 
liver, Banti's disease, and this condition, is often impossible to define. 

SPLENIC ANEMIA. 

Definition. — Among the types of splenomegaly the condition known as splenic 
anemia is one about which great difference of opinion has existed. Its existence 
has been denied by some physicians and asserted by others. At present it is 
generally considered that a distinct morbid state really exists to which this name 
may be applied. It is essentially a condition of anemia with enlargement of the 
spleen, and lacks all of the additional conditions which are associated with this 
state in other maladies, as, for example, leukemia, lymphadenoma, or lymphatic 
leukemia. 

Etiology. — This is unknown, but some suppose it to be due to intestinal infection. 

Pathology and Morbid Anatomy. — An examination of the spleen in this disease 
shows that it is not only greatly enlarged, but that it shows signs of the existence 
of a perisplenitis with localized areas of capsular thickening. In some portions 
of the organ old infarcts may be found which in turn have caused puckering of its 
surface or depressed scars. When the spleen is cut it is found to be more resistant 
to the knife than normal, and it is somewhat fibroid. If a section is placed under 
the microscope it is found that the connective tissue is increased and the lymphoid 
elements wasted. The Malpighian bodies are fibroid. There is also in some 
cases a marked proliferation of the endothelial cells which line the blood sinuses. 
These cells are very large and may be so numerous as to fill these spaces till they 
resemble an endotheliomatous growth. 

Dock and Warthin have called particular attention to hyperplasia of the hemo- 
lymph nodes and thrombosis of the splenic vein. The association of splenic fibrosis 
with enlargement and cirrhosis of the liver constitute the type studied by Banti 
(Banti's disease), and this is thought to be a later stage of the process characterized 
in its early manifestations by splenic enlargement. (See Banti's Disease.) 

Symptoms. — The symptoms of splenic anemia are pallor, dyspnea on exertion, 
and feebleness, associated with enlargement of the spleen. An examination of the 
blood does not throw any great light on the character of the case. Indeed, the 
blood changes are often in no way different from those of lymphadenoma or gumma 
of the spleen. The red cells number about 3,500,000, and the hemoglobin equals 
about 50 per cent. When the disease is advanced poikilocytes and nucleated red 
cells are present. The white cells are not increased as in leukemia, but usually 
are below the normal number, amounting to about 4500 per c.mm. 

Diagnosis. — The diagnosis of splenic anemia is very difficult and should not 
be reached until a careful study of the patient's past and present condition has 
been made and his blood repeatedly examined. A considerable number of cases 
of so-called splenic anemia have proved to be other diseases when studied longer 
or examined postmortem. All possible causes for enlargement of the spleen should 
be excluded before a decision is reached. 

Splenic anemia must be separated from the "anemia infantum" of von Jaksch, 
in which the spleen is enlarged, but in which the changes in the blood consist in 
a great increase in the white cells and marked oligocythemia. This condition 
must also not be confused with enlargement of the spleen due to syphilis with the 
formation of gummata; nor with sarcoma of the spleen; nor with the anemia of 
chronic malarial poisoning, with secondary splenic enlargement, nor with amyloid 
disease. It must also be separated from the anemia associated with enlargement 



GAUCHER 'S DISEASE 705 

of the spleen secondary to cirrhosis of the liver, and from a condition described by 
Gaucher of chronic inflammation of the spleen (epitheliome primitive) . Sometimes, 
too, in children suffering from rickets and marasmus with gastro-intestinal intoxica- 
tion, there is a considerable degree of anemia and some enlargement of the spleen. 
Such cases have been thought to represent an infantile form of splenic anemia, 
but the subsequent history of the patient seems to contradict this view. 

Rolleston gives the following as the clinical characteristics of splenic anemia: 

1. Splenic enlargement which cannot be correlated with any known cause. 

2. Absence of enlargement of the lymphatic glands. 

3. Anemia of a type midway between secondary anemia and chlorosis. 

4. Leukopenia, or at most no increase in the number of white blood corpuscles. 

5. An extremely prolonged course lasting years. 

6. A tendency to periodic hemorrhages, especially from the gastro-intestinal tract. 
Prognosis. — The prognosis under medical treatment is always unfavorable. 
Treatment. — The treatment consists in the administration of full doses of arsenic, 

but, so far as we know, no method of medical treatment has yet been devised which 
materially alters the general progress of the disease. 

According to Harris and Herzog, of 19 cases subjected to splenectomy, 14 recov- 
ered. To these series Scott has added 6 cases with 4 recoveries. Queen and 
Duval collected 6 cases and added 1 original case in which removal of the spleen 
was followed by a cure. They state in addition that a beginning hepatic cirrhosis 
may be arrested by splenectomy, although it is difficult to understand how this 
operation can exercise this effect. 

BANTI'S DISEASE. 

Under the name of Banti's disease a condition characterized by enlargement of 
the spleen, anemia, cirrhosis of the liver, jaundice, and ascites is met with. It is 
thought by some that Banti's disease is a terminal stage of splenic anemia; but, 
on the other hand, it is certain that this is not always the case. The disease is very 
rare. 

Banti's disease is characterized by gradual enlargement of the spleen which may 
be present for several years without any signs of illness. Sooner or later a secondary 
less. When the disease reaches its terminal stage it is characterized not only by 
as low as 1,000,000 to the cubic millimeter and the white cells as low as 2000 or 
anemia develops associated with leukopenia. The number of red cells may be 
splenomegaly but cirrhosis of the liver with jaundice and ascites. 

Several clinicians have recently brought forward evidence that certain cases of 
splenomegaly and Banti's disease are due to an infectious agent, and A. G. Gibson 
has reported no less than- 6 cases, 3 of Banti's disease and 3 of splenomegaly, in 
which the spleen contained a streptothrix which he believed to be responsible 
for the disease process present. So far as is known there is no cure by the use 
of drugs, although arsenic may at times seem to induce temporary arrest. The 
only curative procedure is splenectomy and this must be done in the early stages 
if a cure is to be effected. 

Banti's disease is separated from splenomedullary leukemia by the leukopenia 
instead of the characteristic high white cell count of the latter malady. From 
hepatic cirrhosis, with or without jaundice, by the leukopenia and the history of 
alcoholic abuse or syphilis in cirrhosis. 

GAUCHER'S DISEASE. 

Synonyms. — (Large-cell Splenomegaly; Primary Splenomegaly; Primary Epithe- 
lioma of Spleen.) This is an affection about which so many conflicting opinions 
45 






706 DISEASES OF THE SPLEEN 

have been given that it is impossible to formulate a description that will apply to 
all reported cases. Brill and Mandlebaum furnish the most recent discussion of 
the subject and conclude that only 14 reported cases really belong to this group. 
They have studied material from 5 subjects. Their definition comprises one of the 
best descriptions of the disease that has yet been offered : 

"The characteristic features of Gaucher's disease are its incidence in childhood, 
its frequent presence in other members of the family of the same generation, a 
progressive increase in the size of the spleen which often reaches colossal dimensions, 
followed by a similar huge enlargement of the liver, a characteristic brownish- 
yellow discoloration of the skin, usually restricted to the face, neck, and hands, 
a peculiar yellowish, wedge-shaped thickening of the conjunctivae commonly 
seen on both sides of the cornea, and the prolonged and chronic course of the 
disease, which does not materially disturb the health of the individual. After 
the disease has been present for a considerable time there is a definite tendency 
to hemorrhages, especially appearing as epistaxis, bleeding from the gums, and 
ecchymoses in the skin following the slightest trauma. The positive finding in 
the blood, even in the early stage of the disease, is a definite leukopenia. The 
erythrocytes, however, show no definite change either in number, form, size, or 
hemoglobin content until the disease has existed for a long time, when an anemia 
of the chlorotic type makes its appearance. The anemia is rarely pronounced at 
any stage. The disease is not accompanied by palpable enlargements of the super- 
ficial lymph nodes. There is no jaundice and ascites is exceptional. The disease 
has none of the characteristics of malignancy, and usually is terminated by some 
intercurrent affection. 

The pathological feature of the disease is the presence in the spleen, liver, lymph 
nodes, and bone-marrow of distinctive large cells, with characteristic cytoplasm 
and small nuclei. The enlargement of the spleen and liver is due to the presence 
of these cells in enormous number. In well-established cases all of these organs 
contain pigment giving the reaction for iron. Whereas the nature and origin 
of these cells are still moot questions, the histological picture is uniformly character- 
istic and pertains to no other form of disease." 

Etiology. — This is entirely unknown. 

Treatment. — Arsenic, the x-rays, and other agents have been used with but 
little effect. Splenectomy has been performed in 8 out of the 14 cases with 3 imme- 
diate deaths, continued enlargement of the liver in 1, signs of improvement in 
another case, and the other 3 unreported as to result. 

HEMOLYTIC SPLENOMEGALY. 

Under this term Banti has reported 5 cases of a condition which he regards 
as differing from other types of splenomegaly, even those called hemolytic jaundice. 
The disease begins early in life, and is chronic, lasting six to twelve years or 
more with periods of improvement. The chief features are splenomegaly, anemia 
reaching a severe grade, and jaundice. The spleen, though weighing 800 to 1,580 
grams, presents no marked microscopic change. It is congested and in it are 
found numerous macrophages containing red cells and much blood pigment. The 
liver also contains pigment. 

No cause is known but the anemia appears due to a pathological increase of 
hemolysis in the spleen. This assumption is borne out by the fact that removal 
of the spleen leads to a rapid and apparently complete cure, one patient now having 
been well for nine years. Of the 5 cases, splenectomy in 4 was followed by recovery. 
The spleen was not removed in the fifth and death occurred. This necessity for 
operative treatment is the special point about the disease as distinguishing it 
from several other types of splenomegaly. 



DISEASES OF THE BLOOD. 



ANEMIA. 

Definition. — The word anemia signifies a state of the blood in which there is 
lacking the normal quantity of red cells or of hemoglobin in these cells. When the 
cause of this state is due to some disorder of the blood-making or blood-destroying 
tissues, it is called essential or primary anemia. When due to some other cause, 
such as hemorrhage or one of the acute infectious diseases, it is called secondary 
anemia. Fortunately, most cases of anemia belong to this latter class, and they 
will, therefore, be considered first. 

Secondary Anemia. 

Secondary anemia arises from a host of causes and is characterized in most 
cases by a diminution in the number of the red cells, and an even greater reduction 
in the hemoglobin content of each cell. In some cases it comes on as a result of 
breathing vitiated air, as in factory girls and stenographers. In other cases it 
is due to overwork and insufficient or improper food, and in still other cases to 
protracted digestive disturbance or to chronic constipation, which, by causing 
auto-intoxication, is the active factor in producing the condition. The late Sir 
Andrew Clark was an earnest exponent of this view. 

Hemorrhage is, of course, a very potent cause. When it is profuse the change 
appears so promptly that the cause is evident, but in many cases anemia arises 
as the result of repeated small losses of blood, as from hemorrhoids when the patient 
is at stool. Under conditions of persistent hemorrhage, nucleated cells and a few 
poikilocytes may be found. After a single large hemorrhage the rapidity of recovery 
is often extraordinary, being more rapid than when the loss of blood has been pro- 
longed. Cases are occasionally met with in which, by reason of lack of regenera- 
tive power in the blood-making organs, a sharp hemorrhage is followed by death in 
a short time. 

Toxic states due to renal disease or to the various infectious maladies, particularly 
malaria, acute rheumatism, and syphilis, often cause anemia, and prolonged lac- 
tation, frequent child-bearing, and the growth of tumors of large size also produce 
it. When the tumors are malignant, the anemia is also partly toxic. Not infre- 
quently we meet with cases in which the anemia is due to chronic metallic 
poisoning, as from arsenic, lead, and mercury. In other instances the anemia is 
due to intestinal parasites, such as the Ankylostomum duodenale or the tapeworm. 

In all cases of marked and apparently causeless anemia, the possibility of the 
condition being due to intestinal parasites should be borne in mind, and the stools 
examined, not only for the ordinary tapeworm, but for uncinaria as well. Further 
than this, the marked increase in the eosinophiles in the blood in nearly all cases 
of parasitic infection should be recalled. Walker has collated the following interest- 
ing table in this connection : 

Eosinophiles. Polymorphonuclears. Large mononuclears. 

Normal 1 to 4 per cent. 60 to 60 per cent. 5 to 8 per cent. 

Tenia 6 to 13 

Ankylostoma duodenale . 12.43 " 

Filaria medinensis ... 6 to 36 " 

Filarialoa . . . . . 53 " 23 

Oxyuris vermicularis . 0.4 to 13.7 " 

Bilharzia hematobia . . 16 to 48 " 44 to 58 " 12.5 

(707) 



708 DISEASES OF THE BLOOD 

He makes the interesting statement that a practical application of this has been 
already made. In the feces obtained from one of the closets in a large college the 
eggs of the Ankylostomum duodenale were found. The pupils who had used the 
receptacle on the specified day were asked to submit themselves to examination, 
but their feces yielded negative results. An examination of the blood of each 
pupil was made, eosinophilia was observed in 2 cases, and ova subsequently detected 
in their feces. 

Symptoms. — The symptoms of secondary anemia vary greatly in different individ- 
uals, some patients with marked pallor presenting no other noteworthy symptoms, 
while others whose cheeks have color, nevertheless suffer from palpitation and 
dyspnea on exertion. It is important to bear in mind that there are fat anemics 
and red-cheeked anemics, and that many persons who look pallid really have a 
normal number of red cells and a normal percentage of hemoglobin. Headache, 
neuralgia, loss of appetite, constipation, and attacks of syncope are sometimes due to 
anemia, and in women amenorrhea is often due to this cause. 

Diagnosis. — The diagnosis between secondary and primary anemia is to be made 
by the history of the patient, and chiefly by the fact that the abnormalities, as to 
the shape and character of the red cells found in the primary anemias (which see), 
are far more marked than in the secondary forms. 

Treatment. — In the treatment of secondary anemia three things are absolutely 
essential: the removal of the cause, if possible, the institution of a proper diet, 
a hygienic mode of life, the administration of iron and arsenic, and often of 
the bitter tonics, in order that the condition of the blood may be directly im- 
proved. If the method of life of the patient is unhealthy, it must be corrected, 
and, above all, plenty of fresh air and sunshine must be obtained. The sleeping- 
rooms should be well ventilated, and the patient must be dieted in such a way that 
the bowels are moved regularly and adequately every day, at least once, for con- 
stipation, as already stated, is usually present, and is often the cause. Under 
these circumstances aloes and cascara sagrada are probably the best laxatives to 
administer, particularly if iron is given. When persistent diarrhea is the cause 
of the anemia, it is advisable to give one of the astringent preparations of iron like 
the dried sulphate in the dose of J to J grain three times a day. If the anemia is 
due to a loss of blood by hemorrhoids, this loss must be arrested by local treatment, 
and if to intestinal parasites, these must be expelled. The appetite should be 
stimulated by the use of drugs like mix vomica, quinine, or other bitter tonics 
like cardamom or gentian. A good prescription for many of these cases is a pill 
composed as follows : 

1$ — Ferri redacti gr. v. 

Arseni trioxidi gr. i. 

Ext. nucis vomicae gr. v. — M. 

Ft. in pil. No. xx. 

Sig. — One t. i. d. after meals. 

The nux vomica may, in some cases, be replaced by 2 grains of quinine. If the 
digestion is impaired, hydrochloric acid and pepsin, or pancreatin and bicarbonate 
of soda, or taka-diastase in 2 to 5 grain doses with meals is advisable. 

Primary or Essential Anemias. 

Chlorosis. — Definition. — Chlorosis is a condition of the blood usually met 
with in young girls, characterized by a marked diminution in the quantity of 
hemoglobin, and by a less marked decrease in the red cells. Until recently it 
was considered a secondary anemia but hematologists now class it in the primary 
anemias chiefly because it is believed to be due, at least in part, to defective 
hemogenesis, 



ANEMIA 



709 



Fig. 124 


47 » 




46 A 




45 '\ 




44 , 




43 




42 / 




41 r 




40 | 




39 V 




38 \ 




37 \ 




36 




35 I 




34 \ 




33 f 




32 




3! i 




rn 30 




UJ 29 I I 




CO 26 I 




O " 




° 26 




"- 25 




o M , 




CE 23 | 


T_ 


UJ 22 | 


t 




I 


^■ 20 


I 


3 19 f 


1 


Z 18 f * 


1 


17 ! 




16 I 




15 




14 




13 




12 




1 1 


t 


10 


t>^ 


9 


5 s ? 


8 


* A 


7 


1 


6 r i 


H 


5 1 


^A 


4 ' 


t" 


3 J 


U \r 


2 / 


' **cr 


1 »■* 




AGE 2™|J^^^22gSS 


j^cjcjct »ao mmm m 



Age incidence of chlorosis. 
(Bramwell.) 



Etiology.— There are still many who believe that chlorosis is a secondary anemia. 
It is certainly associated with many causes of secondary anemia, such as constipa- 
tion, inanition, and bad air. Whatever influence these causes may have, there 
can be no doubt that the processes which take place about the age of puberty 
in the female sex are closely concerned in its production, 
for the disease is scarcely ever met with except at a period 
of life near these changes. Occasionally, however, it 
develops in later life, and it is then called "chlorosis tarda" 
Bramwell and others have shown that there is also an 
hereditary influence. 

The two chief causes are a natural predisposition to 
anemia and an inability to utilize iron from the food. 
Some believe that the intestinal mucosa is at fault, others 
that the spleen is functionally perverted, but, as Ewing 
well says, there can be no doubt that chlorosis results from 
a functional insufficiency of the bone-marrow, which is 
prone to occur at puberty. 

Pathology. — The following are the chief changes in the 
blood: The chief alteration is the decrease of the hemo- 
globin in each corpuscle, so that a low color index is one 
of the points necessary to a diagnosis of the disease. So 
low a percentage of hemoglobin as 10 has been recorded 
by Bramwell, but the average low limit is from 30 
to 40 per cent., and the color index about 0.5 The 
second change is a diminution in the number of the red 

cells, but usually this is not so marked. Taking the normal for a woman as 
approximately 4,800,000 to the cubic millimetre, the fall is usually not more than 
from 500,000 to 1,000,000. When a very great fall in the number of red cells is 
present, they may amount to only 2,000,000, but in such a case a suspicion of 
pernicious anemia comes forward. 

If the chlorosis is severe, the red cells vary as to size and shape, and a number 
of large red cells, with a full complement of hemoglobin, may be present. As a 
rule, the size of the red cells is reduced. Imperfectly formed cells (poikilocytes) 
are found, but they are present in very small numbers. Basophilic granulation of 
the red cells has been particularly well studied by the former chief of my medical 
clinic, Dr. J. C. Da Costa, Jr., and by Stengel, White, and the younger Pepper. 

The leukocytes in cases of chlorosis do not suffer much change, as a rule, but 
some patients show an increase of the lymphocytes. Dr. Da Costa has shown that 
most of these are large lymphocytes, and that the lymphocytes may amount to 40 
per cent, of all the white cells. The specific gravity of the blood is reduced pari 
passu with the hemoglobin. Although extravascular coagulation is retarded, in 
some cases there is a tendency to thrombosis. The blood picture in chlorosis is 
not characteristic, that is, the diagnosis of the disease is not to be made from the 
blood findings alone. 

Aside from the blood changes, a state of hypoplasia of the tissues of the heart 
and larger arteries is often present, but this condition is not peculiar to chlorosis, 
but to the lymphatic constitution. When recovery begins to take place the number 
of undersized red cells decreases and the cells of normal size increase their hemo- 
globin content. 

Symptoms. — -The symptoms of chlorosis are a peculiar pallor of the skin, which 
often has a greenish hue, whence the name "green sickness." The patient is 
nearly if not always plump and possessed of a good quantity of subcutaneous fat. 
Occasionally the superficial vessels are well supplied with blood, so that the patient 
is ruddy, thereby misleading the physician who fails to study the blood. This 



710 DISEASES OF THE BLOOD 

type is called chlorosis florida. The subjective symptoms are dyspnea on exertion, 
palpitation of the heart, vertigo, and perhaps attacks of partial syncope. Constipa- 
tion is nearly always marked. Headache is quite constant, and there is usually 
a most persistent absence of appetite. There is also mental depression and apathy. 
Physical examination may reveal a diastolic hemic murmur at the third left costal 
cartilage, and over the right carotid artery a bruit is often heard. 

The complications of chlorosis which are serious are the development of thrombi 
in the veins of the legs and in the cerebral sinuses. From such thrombi fragments 
may arise, which may result in pulmonary embolism. Slight fever may occur, 
but the hands and feet are usually cold. Amenorrhea is a very constant symptom. 

The blood changes, as discovered by the hemoglobinometer and hematocytometer 
have already been described. 

Diagnosis. — The well-nourished state of the chlorotic patient is also present in 
pernicious anemia, but the differentiation is found in the blood picture (see Per- 
nicious Anemia), for in that disease the blood findings are quite different. The 
irritability of the heart must not be taken for a sign of cardiac disease because a 
murmur is present, nor, in the absence of urinary changes, should the puffy face 
and ankles be thought to be due to renal disease, unless the urine reveals albumin 
and casts. 

Prognosis. — The ultimate prognosis in cases of chlorosis is usually very good, but 
a long period often passes without much improvement. When the number of 
the red cells is not greatly reduced and they are normal in shape and size, recovery 
under proper treatment is usually rapid. This holds true even if the color-index 
is very low. When the red cells are as low as 3,000,000, are badly shaped, and 
many of them undersized, the prognosis as to rapid recovery is bad. So, too, when 
the lymphocytes are very numerous, a speedy cure is rarely seen. Relapses are 
very frequent. 

Treatment. — The treatment of chlorosis does not differ materially from that 
which was given for the treatment of ordinary secondary anemia, except that 
chlorotic patients are usually more obstinately constipated, and, therefore, particu- 
lar attention must be given to the state of the bowels. Fresh air and sunshine 
are also very essential in these cases. More important than all, it must be remem- 
bered that chlorotic patients usually need very much larger quantities of iron than 
do ordinary anemic cases. Whether this is due to an inability to absorb iron or 
whether there is an excess of sulphides in the bowels, which change a goodly portion 
of the iron into a sulphide of iron, is not known. Citrate of iron may be given hypo- 
dermically. During the winter months chlorotic patients usually do best at seaside 
resorts or at places like Lakewood, N. J., which are low in altitude. In the sum- 
mer months they should be sent to high altitudes, varying from 3000 to 5000 feet, 
unless these high altitudes tend to increase palpitation of the heart and dyspnea. 

Pernicious Anemia. — Definition. — Pernicious anemia is a disease of the blood 
arising from faulty hemogenesis and excessive hemolysis or blood disintegra- 
tion. It is a fatal malady characterized by three chief changes, viz., an extraordi- 
nary decrease in the number and alterations in the morphology of the red cells and 
by certain changes in the bone-marrow. It is sometimes called "x\ddison's 
anemia." 

History. — -Andral in France, in 1821, reported cases of what was probably this 
disease, and Channing in Boston recognized them in 1832. Pepper and Tyson 
showed the bone-marrow changes in 1875. Sorenson, in 1874, made the first 
observations as to the number of the red cells, reporting cases with only 470,000 
corpuscles. 

Etiology. — The etiology is still unknown, but it is probable that certain of the 
causes of ordinary secondary anemia may antedate pernicious anemia. Age 
has no great influence. Most cases appear between twenty and forty years of 



ANEMIA 711 

age, but even young children of less than five years have been seen with the malady. 
In some of the reported cases the Ankylostomum duodenale, the Bothriocephalus 
latus, or tapeworm, and the Oxyuris vermicularis have been found. The first-named 
parasites can cause grave anemia, but it is doubtful if any of them alone can cause 
pernicious anemia. So, too, severe hemorrhage, syphilis, and pregnancy have 
been found associated with the development of the disease. They are not the 
actual cause, but rather predisposing causes. The various fevers, as malaria and 
typhoid fever, exert only an indirect effect, and the condition of the gastro-intestinal 
tract, at one time thought to be responsible, has been proved to be only a predis- 
posing or secondary condition. Hunter thinks the disease is due to bacterial 
infection of the alimentary canal from a foul mouth. Some cause, or causes, which 
induce hemolysis is responsible for the condition, so while pernicious anemia is 
classed as a primary anemia it may be justly called secondary. 

Morbid Anatomy. — The most noteworthy pathological changes are the alterations 
in the blood and in the bone-marrow. Unlike cases of chlorosis, the blood may 
be difficult to obtain. In marked cases it does not form a rounded drop, but flows 
from the puncture made by the needle or scalpel sometime after the wound is 
inflicted. Coagulation is usually delayed, and even at an autopsy made many 
hours after death the blood may still be fluid. The red cells are decreased to 
2,000,000, then to 1,000,000, and sometimes to less than 500,000 to the cubic 
millimeter. A great proportion of the remaining cells are larger than normal 
(megalocytes), and some are smaller (microcy tes) . Many of the red cells are 
misshapen (poikilocytes), and the amount of hemoglobin in most of the red cells 
is considerably increased, although some of them may be poor in hemoglobin. 
Red cells possessing nuclei (erythroblasts) are also present in considerable number. 
Some of these are large (megaloblasts) and others of normal size (normoblasts). 
Small nucleated red cells called microblasts are also present. The presence of 
the megaloblast is an important aid in reaching a positive diagnosis. These 
nucleated cells, both large and small, contain a great amount of hemoglobin, and 
some of them differ from ordinary red cells in one very important particular — 
namely, they possess ameboid movement — and, further, when the blood is examined, 
they are seen to form rouleaux as do ordinary red cells. Basophilic granulation 
also occurs in the red cells. 

In mild cases the leukocytes may not be altered in number, although usually 
they are slightly reduced. Rarely they are greatly reduced in number if the case 
is severe. As a rule, but few myelocytes occur and the lymphocytes may be 
increased. 

The hemoglobin is reduced, the average being 25 to 30 per cent., but not in 
proportion to the red cells, hence a high color-index, often above 1, is the rule. 

When the bone-marrow is examined very marked changes are manifest. There 
is an excess of large nucleated red cells, many of which are gigantoblasts. The bone- 
marrow is pale, shows lack of erythrocyte formation, and may undergo lymphoid 
hyperplasia. The liver, spleen, lymph glands, and particularly the liver, are 
loaded with iron derived from the destroyed red blood cells, and even the urine con- 
tains pigment from this source; Hunter denies an excess of iron in the spleen. Fatty 
degeneration of the liver, kidneys, and of the heart muscle are often present, and 
because of similar changes in the walls of the arteries and of the altered character of 
the blood, hemorrhages into the retina and into other parts may occur. In some 
cases marked atrophy of the gastric tubules is found. A diffuse degenerative change 
occurs in the posterior and lateral columns of the spinal cord. When regenerative 
changes in the bone marrow are slight or lacking, the disease assumes the form 
known as "aplastic anemia." The blood picture differs from that of the ordinary 
type in that the color-index is lower and megaloblasts are absent. (See Aplastic 
Anemia.) Leukopenia is present and accompanied by a decided lymphocytosis. 



712 DISEASES OF THE BLOOD 

Symptoms. — A patient with pernicious anemia usually first seeks medical advice 
because he is feeling weak and lacks initiative. Often he suffers from some dyspnea 
on exertion and has a throbbing headache or attacks of vertigo. His tissues are 
well filled with fat and his appearance is plump, but he is pallid and cheesy looking. 
The sclerotic part of the eyes is peculiarly pearly and the lips, gums, and tongue 
are prone to be very pale and bloodless. There may be slight puffiness of the face 
on the dependent side if the patient lies on his side in bed. A purring hemic murmur 
is often heard over the pulmonary artery at the third left costal cartilage, and 
the arteries of the neck pulsate and throb with a peculiar jerking, expansile move- 
ment. An irregular fever is very constantly present. When the disease is far 
advanced a state of mental torpor with muttering delirium may occur. 

Diagnosis. — The fact that the patient is in middle life, or even older, serves to 
separate this state from chlorosis, which has its greatest frequency at the eighteenth 
or nineteenth year. Again, pernicious anemia is more common in men, chlorosis 
in women. The skin in pernicious anemia is prone to show a cheesy-yellow hue 
in distinction from the greenish-yellow of chlorosis. From the blood of the chlorotic 
that of pernicious anemia differs so radically that a diagnosis is readily made in 
typical cases, for in the former we have cells poor in hemoglobin and here we have 
cells rich in hemoglobin. In the former the red cells are not greatly decreased 
in number, here they are markedly diminished. In chlorosis the size of the red 
cells is below the normal, in pernicious anemia the average is above the normal. 
Again, in chlorosis we do not find, to the same degree, nucleated red cells or cells 
with mitotic nuclei, nor red cells with ameboid movement. The color-index in 
chlorosis is low and in pernicious anemia high. In cases of gastric cancer there 
is present ordinary secondary anemia and the presence of gastric symptoms to 
aid the diagnosis. Unless the blood picture is typical the possibility of small 
repeated hemorrhages as a cause of profound anemia, such, for example, as bleeding 
from hemorrhoids, should be borne in mind. In other words, the stools should 
be tested for occult blood. Finally, Ewing states that unless at least 33 per cent, 
of the red cells are oversized, the diagnosis of pernicious anemia must be made 
with reserve. 

Prognosis and Treatment. — The prognosis of true pernicious anemia is almost 
invariably fatal, athough there have been a considerable number of cases in which 
recovery has been said to have occurred. Many cases have periods of extraordinary 
improvement in all the symptoms as well as in the blood, and then a disheartening 
relapse takes place. This may be repeated several times. Most cases die within 
a year after they are first seen. A great decrease in the number of red cells and a 
large number of megaloblasts are bad signs. 

The prognosis in pernicious anemia depends not a little upon the quantities 
of arsenic which the patient can take without developing disagreeable symptoms 
from its use, for many of these cases are markedly benefited if they can take what 
might be called massive doses of this drug. By a process of training with ascending 
doses I have known patients to take as much as 30 minims of Fowler's solution 
three times a day with no bad results except some exfoliation of the skin of the 
hands after several weeks' treatment. Arsenic administered in this manner up 
to the point of tolerance sometimes produces periods of remarkable improvement 
in this disease, the patient's symptoms becoming modified and the number of 
red blood cells becoming markedly increased. 

Of course, all measures which tend to increase the general health of the patient 
are advantageous, such as plenty of sunshine, fresh air, and good food. Small 
quantities of iron may be given from time to time with advantage. Diarrhea is 
to be controlled by the use of sulphuric acid or one of the vegetable astringents, 
such as fluidextract of hematoxylon, kino, or catechu. Constipation, if present, 
is to be relieved by the use of cascara sagrada and aloes. In some instances hypo- 



CHRONIC SPLENOMEGALIC POLYCYTHEMIA 713 

dermic injections of cacodylate of sodium in 2 grain doses every few days have 
been resorted to with asserted advantage. If the patient is very anxious to carry 
out a plan of treatment which may possibly be advantageous, inhalations of oxygen 
may be suggested. 

In the treatment of pernicious anemia it is the universal experience of clinicians 
that iron is by no means as beneficial as is arsenic. Indeed, the general proposition 
may be stated that if anemia is associated with diminution in the number of red 
blood cells, arsenic is more advantageous than iron; whereas, in those anemias 
which are characterized by a low color-index or a diminution in hemoglobin, iron 
is more useful than arsenic. 

In certain cases the direct transfusion of blood from a healthy person greatly 
improves the state of the patient, provided it is found beforehand that the blood 
of the donor does not hemolyze that of the recipient. The improvement is however 
only temporary. 

Aplastic Anemia is a term applied to a form of anemia characterized by retro- 
gressive changes in the bone-marrow, the ordinary red marrow becoming fatty, 
the spleen presenting at autopsy a hyperplastic appearance such as is seen in 
pernicious anemia. It is possibly of the class of secondary anemias, as it may 
follow profuse hemorrhage, but the primary lesion is in the marrow and not in 
the blood. The blood picture is typical and pathognomonic. There is a profound 
anemia as to red cells and hemoglobin, but the color-index may be high or low, 
usually high. There is no poikilocytosis or change in the size of the red cells and 
no polychromatophilia. Leukopenia is marked, as low as from 200 to 800 per cubic 
millimetre. There is, however, no change in the relative number of the white 
cells, unless it be a slight relative lymphocytosis. Some clinicians have regarded 
it as a severe form of pernicious anemia, but it differs in several important respects 
from that disease, namely, there is no excess of the iron pigment in the liver or 
spleen and the bone-marrow is very light in color and fatty instead of red as is 
seen in pernicious anemia. The disease is very rare, only 59 authenticated cases 
having been recorded (Musser). It was first described by Ehrlich in 1888. The 
disease is progressive and rapid in its course, the patient rarely living after two 
months, and is characterized by increasing exhaustion, subcutaneous hemorrhages, 
and bleedings from mucous membranes. 

CHRONIC SPLENOMEGALIC POLYCYTHEMIA (ERYTHREMIA). 

Definition. — A chronic condition characterized, as its name indicates, by a great 
increase in the number of the red cells with enlargement of the spleen and great 
fulness of the entire vacular system, arterial and venous. Because of the poly- 
cythemia and vascular turgescence there is usually cyanosis. The condition is 
to be clearly separated from the polycythemia occurring after hemorrhage and 
that found in cases of congenital cardiac disease. 

Etiology. — This is unknown. The disease occurs in middle life, the youngest 
patient so far reported being twenty years of age, and it is about equally frequent 
in both sexes. A large proportion of the cases have occurred in Jews. 

Morbid Anatomy and Pathology. — The spleen is always enlarged and sometimes 
has contained tubercles. Its blood spaces are engorged with blood cells. The 
liver is also engorged, but presents no definite lesions neither do the kidneys present 
any peculiar lesions. Occasionally the intestines, which share in the congestion 
of the spleen and liver, are ulcerated. The increase in the total quantity of the 
blood is actual. Haldane estimated the total amount in a patient of Parkes Weber 
and found it to be nearly double the normal quantity. The red cells are propor- 
tionately increased by the abnormal activity of the red bone-marrow. There is 
also a great but not commensurate destruction of red cells, for the spleen contains a 






714 DISEASES OF THE BLOOD 

great excess of broken-down erythrocytes and the urine shows an excess of urobilin. 
Polychromatophilia is present. The leukocytes are materially increased. It is 
noteworthy that the enlargement of the spleen usually antedates the polycythemia 
by some months or years. There is no poikilocytosis, a somewhat diminished 
color-index, and very rarely nucleated red cells. 

Symptoms. — The symptoms presented by the patient are persistent cyanosis, 
engorgement of the bloodvessels, large and small, dyspnea on exertion, progressive 
asthenia, pigmentation of the skin, and albuminuria. The red blood cells when 
counted may amount to 15,500,000 per cubic millimetre. The white cells may or 
may not be increased. The hemoglobin may be increased to 200 per cent, although 
such an excess is rare. The ophthalmoscope reveals very great engorgement of the 
retinal veins but retinal hemorrhages have not been recorded although hemorrhages 
from mucous membranes may occur. 

Treatment. — No treatment has been of value. Bleeding has been resorted to 
with temporary benefit, and stimulants like digitalis may be used for the laboring 
heart. A very exhaustive study of erythremia has been contributed to the Archives 
of Internal Medicine for December, 1912, by one of my clinical assistants, Dr. 
Walter Lucas, who reports 2 cases from my wards. 

LEUKEMIA. 

Definition. — Leukemia is a disease in which the blood suffers an extraordinary 
increase of leukocytes with associated alterations in the bone-marrow, the spleen, 
and in the lymphatic glands. It is divided into two types, that form in which the 
spleen and bone-marrow are chiefly affected, and that in which the lymphatic 
glands are chiefly involved, the first being called splenomedullary leukemia and the 
second lymphatic leukemia. Because of the important role played by the bone- 
marrow in splenomedullary type it is sometimes called myelogenous leukemia. 
Leukemia is also sometimes called leukocythemia. 

Although a division of the disease into two types is to some extent justified 
because it renders the study of leukemia less difficult, and because changes in 
certain tissues preponderate in one instance and in other tissues in other instances, 
it is not to be forgotten that intermediate cases occur in which both types of the 
malady are represented, or at least in which no definite dividing line can be drawn. 
Thus cases are recorded in which the blood cells presented the picture of lymphatic 
leukemia, the lymphatic glands were not involved but the bone-marrow was 
altered. Again, it has been thought, in times past, that acute and rapidly pro- 
gressive leukemia was usually of the lymphatic type, and that the subacute or 
chronic form of the disease was commonly of the splenomedullary variety. While 
this view still holds true, we have been forced to recognize the fact that acute 
cases may be of splenomedullary type and that some of the chronic cases may be 
lymphatic. 

History. — As long ago as 1801 Bichat, in France, noted a condition of the blood 
which was probably identical with leukemia as we know it today. Thirty years 
later because of the peculiar appearance of the blood it was called "suppurative 
hematitis," and in 1839 Donne described the blood in these cases as consisting 
largely of " white or mucous globules." Virchow, about the middle of the last 
century, described it as " Weisses Blut," and showed that there was no suppurative 
process present. Bennett made the first complete study of the disease in 1851. 
Since then a host of investigators have thrown light upon its characteristics. 

Etiology. — The cause of leukemia is unknown. It may occur at any time of 
life, but is most frequently met with about the fourth decade. It is about twice 
as common in males as in females. A very large number of conditions have been 
brought forward as causes, but none of them have been proved to exercise a deter- 



LEUKEMIA 715 

mining influence. Among these may be named syphilis, malaria, and intestinal 
intoxication. The view has been advanced that leukemia and tuberculosis are 
nearly related in the sense that the latter may act as a cause of the former. This 
view is incorrect. Gowers tells us that the appearances of the lungs in one or 
two cases have been those of tubercle, that extravasations of blood into the lungs 
are common, and that these organs may undergo caseation and a tuberculous 
process may be simulated. Cavities may result from lymphoid infiltration. This, 
however, is not phthisis. Susmann has been able to collect only 25 cases from 
literature in which tuberculosis and leukemia were even associated. Further, 
when the diseases are combined there is a tendency to a decrease in the number 
of leukocytes. A number of observers are strongly inclined to the belief that 
the condition is due to an infection by a parasite, but careful observation and 
experimental studies have afforded no conclusive result. Lowit and others have 
sought to establish a protozoal origin, but their observations are inconclusive, 
and bacteriology, so far, has yielded no promising results. 

Pathology and Morbid Anatomy. — When defining the disease leukemia it was stated 
that it is a malady which appears in two forms, and that these forms may be quite 
dissimilar in their chief features, or overlap one another, according to the degree 
to which the lymphatic system and the bone-marrow are chiefly affected. It is 
probable that in nearly every instance the bone-marrow is involved in the disease 
process, and almost never are the lesions situated only in the lymph nodes and 
other lymphatic tissues. Further, although the lymphocytes of a person in good 
health are usually derived from the lymphatic system, in the patient suffering 
from lymphatic leukemia they are derived, to a large extent, from the bone-marrow 
as well. 

Having made these preliminary remarks, we can best proceed to the study of 
two forms of leukemia by considering them separately. 

Splenomedullary Leukemia. — The color of the blood may be normal in some 
cases, but if the disease is well developed it is much paler in hue because of the 
anemia and the excess of white cells. The coagulability of the blood is greatly 
decreased or lost. The red corpuscles are not very greatly diminished in number 
until the disease is far advanced, and sometimes not then. They rarely fall below 
3,000,000 to the cubic millimetre, but they may drop to 1,000,000. Nucleated 
red cells, especially normoblasts, are present in varying numbers, but megaloblasts 
are rarely present in any great degree. There is a decrease of hemoglobin so that 
the color-index is about 0.6 to 0.8. 

The white cells show remarkable changes as to number, shape, size, and variety. 
Even in cases which may be called moderate they usually amount to 200,000 or 
more, to the cubic millimetre, and as high as 1,000,000 have been reported, as 
against a normal of about 6000 to 8000. Of the varieties of white blood cells 
we find a form which never appears in normal blood, and which, if present in con- 
siderable numbers, is pathognomonic of the disease, namely, large mononuclear 
leukocytes containing neutrophile granules. These cells are called neutrophile 
myelocytes and appear in two forms, viz., the smaller myelocytes, about the size 
of the polymorphonuclear leukocyte, possessing a central nucleus which stains 
quite deeply, and a larger cell, which has a pale staining nucleus placed at one side 
of the corpuscle. Eosinophilic and basophilic myelocytes also may be found. The 
relative percentage of polymorphonuclear cells is decreased, although the total 
number of these corpuscles far exceeds the normal. The presence of the myelocytes 
is at the expense of the polymorphonuclear cells. 

The eosinophile cells, leukocytes the granules of which stain intensely with eosin, 
are generally increased in myelemia, although they are never as numerous as are 
the other forms already named. 

The number of lymphocytes, both large and small, varies within wide limits 



716 DISEASES OF THE BLOOD 

in cases of splenomedullary leukemia, and at different times in the same case. 
Relatively they are reduced (as low as 2 per cent.), but even in this percentage the 
blood may contain more mononuclears to the cubic millimetre than in health. 
Very large mononuclear leukocytes with faintly staining nuclei are rarely conspicu- 
ous by their number. " Mast-cells'" are usually present, not infrequently reaching 
5 or 10 per cent. When present in large numbers they are second to myelocytes 
only in diagnostic significance. These mast-cells are polynuclear cells with coarse 
basophile granules. 

The onset of any one of the acute infections may completely change the appear- 
ance of the blood so that it is no longer characteristic and there may be a great 
increase in polymorphonuclear cells. 

The normal red bone-marrow shows marked hyperplasia and the fatty marrow 
of the long bones undergoes a similar transformation. It contains nucleated red 
cells in unusual numbers, and is crowded with leukocytes which are ancestral to 
those found in the blood, including all forms, but particularly, myelocytes. In 
some cases, however, these changes appear in patches rather than all through the 
bone cavity. At certain points the compact portion of the bone may atrophy 
before the hyperplastic marrow, and new subperiosteal nodes may develop. 

The spleen is very much enlarged, sometimes to fifteen times its normal size. 
It is frequently attached to adjacent tissues. Its capsule is usually thickened and 
roughened, and the consistency of the organ increased. On section it is seen to be 
mottled red and gray, or it may be a homogeneous red. The trabecular may be 
thickened and hemorrhagic infarctions may be present. The venous system is 
engorged and purulent-looking clots may be found in the heart and vessels. The 
liver is often enlarged and leukemic nodules may be found in it and in the kidneys 
and thymus gland. 

Lymphatic Leukemia. — The conspicuous blood changes in this disease are con- 
fined to the lymphocytes, which are greatly increased in number so that they may 
exceed 80 per cent, of the total number of white cells. For this reason the condition 
is sometimes called lymphemia. Usually most of the cells are small lymphocytes, 
but the large form may predominate, especially in the acute type of the disease. 
The total increase in leukocytes rarely approaches that seen in the splenomedullary 
form. Nucleated red cells are rarely encountered. 

The lymphatic glands, particularly those which are deeply situated, are enlarged, 
but the spleen and the medulla of the long bones are not greatly altered. Cases 
are on record in which chronic lymphatic leukemia has occurred without any 
enlargement of the lymph nodes, and in some instances there is an actual increase 
in the number of white cells, but only a relative lymphocytosis. 

Symptoms. — The symptoms of splenomedullary leukemia are at first those of 
anemia, the patient presenting himself because of dyspnea on exertion, or because 
of lack of energy and poor digestion. Sometimes the swollen spleen first calls his 
attention to his condition. In other cases nosebleed or gastric hemorrhage or renal 
hemorrhage comes on very early in the disease. In other cases there is purpura 
hemorrhagica. If the hand is placed over the splenic area and the abdominal 
wall moved over the enlarged spleen a creaking sensation may sometimes be felt. 
Not rarely the liver is greatly enlarged, and ascites may be present. There is 
dizziness and vertigo. Occasionally a violent diarrhea develops. The urine is 
normal, save that it contains uric acid in excess. The heart sounds are normal, 
although the first sound may be feeble, and anemic murmurs can occasionally be 
heard. Retinal hemorrhages may cause blindness. Hemiplegia with coma, the 
result of cerebral hemorrhage, may occur. A moderate but varying febrile move- 
ment is nearly always present. Occasionally persistent priapism, probably due to 
irritation of the spinal cells by anemia, is present. Sudden death may take place. 

In cases of lymphatic leukemia the symptoms complained of by the patient are 



LEUKEMIA 717 

not different from those just described, but the spleen is not so much enlarged. 
The lymph nodes are, however, increased in size, and so the appearance of the 
patient may not be unlike that of Hodgkin's disease. 

It is important to recall the fact that in both of these states an irregular febrile 
movement may be present and give rise to the belief that some one of the acute 
or chronic infections characterized by fever are present. This is particularly 
true in certain cases of acute lymphatic leukemia, in which the condition of the 
patient may be so like that of typhoid fever that an examination of the blood is 
required to determine the exact nature of the illness. The condition often runs 
its course in three or four weeks; fever of moderate degree is present, and the general 
state is asthenic. Even an autopsy may not reveal the real cause of the illness, 
because the lymph nodes in the solitary and agminated glands of the intestine 
are infiltrated as in typhoid fever. 

Diagnosis. — The pallor, the enlarged spleen, and the state of the blood are all 
part of a picture which cannot be mistaken for any other disease, but in doubtful 
early cases repeated blood examinations may be necessary to determine the diagno- 
sis positively. 

Prognosis. — The prognosis of leukemia, like that of pernicious anemia, is, in the 
great majority of cases, fatal, but rare instances have been recorded in which 
recovery has taken place. Life may be preserved from a year to three years. 
Unfavorable prognostic signs are marked dyspnea, an excessive number of leuko- 
cytes, a tendency to exhausting diarrhea or to hemorrhages, and high fever. The 
lymphatic type usually runs a more rapidly fatal course than the splenomedullary 
form. When death occurs, the cause is usually pulmonary edema, pneumonia, or 
exhaustion. 

Treatment. — The treatment of leukemia in both its forms is identical, but, unfor- 
tunately, it is by no means successful, for the disease in all instances proceeds by a 
more or less rapid course to a fatal ending. There can, however, be no doubt that 
the administration of arsenic in ascending doses until the point of intolerance is 
reached seems to exercise a favorable influence upon the malady, at least in so far 
that it delays its advance. Cases of leukemia not subjected to treatment not 
infrequently have periods of remission, in which temporary improvement may take 
place. It is, therefore, difficult to determine how much credit should be given to 
arsenic when the remissions occur under its use. Those members of the profession 
who have had the most experience in the treatment of leukemia, however, regard 
arsenic as being practically the only remedy of any value, and it should always 
be tried, preferably in the form of Fowler's solution. The beginning doses should 
be 3 drops three times a day, rapidly increased until the patient has some puffiness 
of the face or some griping of the bowels. Recently several clinicians have reported 
"cures" of this disease by exposing the long bones of the patient to the Roentgen 
rays. This results after several applications in a diminution in the size of the 
spleen which continues as the treatment is continued. After this organ has been 
materially reduced in size and the patient generally improved the spleen itself 
is exposed. Not rarely such exposure is followed at first by a great increase in 
the leukocytes. The main effect, a notable decrease in leukocytes follows. The 
treatment requires several months with about twenty or thirty applications a 
month. The plan also relieves the pain in the long bones. As well shown by 
Warthin in his exhaustive discussion of this subject the final outcome of most if 
not all of the cases thus treated is relapse and death from the disease. Warthin's 
experimental studies indicate a possible danger from the absorption of substances 
liberated by the destruction of cells brought about by the Roentgen-ray exposures. 
Further investigations will be necessary to place this procedure upon a sound 
therapeutic basis, as it deals with a disease that is notoriously resistant to ordinary 
remedial measures. However, the question is one that merits careful study. 



718 DISEASES OF THE BLOOD 

Recent studies by Warthin have led him to the following conclusions regarding 
the effect of this treatment: "Prolonged irradiation of the hematopoietic organs 
in leukemia causes first a degeneration of the young and maternal cells, leading 
to a great decrease in the output of leukocytes, particularly in myelemia. After 
this destructive effect there follows a reaction in which cells of a more resistant 
type are formed, and the essential leukemic process remains unchecked, although 
altered in character." 

Excellent temporary results have accrued in some cases by the use of 5 to 10 
minims of benzole (not benzine) three times a day given in capsule after food. 
The best cases have also had the x-rays during or before the benzole was employed. 

Benzole does more good in the splenomedullary type than in the lymphatic 
form of the disease. 

CHLOROMA. 

Under the name chloroma is recognized a condition characterized by the forma- 
tion of greenish lymphoid tumors, especially in the cranial bones and periosteum, 
and the occurrence of a profound anemia which Dock and Warthin regard as, 
in some if not all cases, a malignant type of leukemia. Exophthalmos and lymphoid 
infiltration of the cornea and of the conjunctiva may be present. Later the perios- 
teum of the bones of the spinal column become affected. Localized paralysis, from 
pressure exerted by these growths upon nerve trunks, may arise. Another char- 
acteristic of chloroma is the peculiar green hue of the new growths; the cause of 
this coloration is unknown. 

The latest study of this remarkable and rare disease is that made by Dock and 
Warthin. These investigators conclude that the disease consists in a neoplastic 
hyperplasia of the parent cells of the leukocytes which develops primarily in the 
red bone-marrow and secondarily affects the periosteum. Typical and atypical 
leukocytes are, therefore, developed, set free in the blood, and may appear as large 
lymphocytes or as neutrophiles or eosinophile myelocytes. On the other hand, it 
is not essential for the diagnosis of chloroma that these leukocytic changes be 
present, for sometimes they fail to appear. Chloroma may, therefore, be regarded 
as a malady lying midway between leukemia and lymphosarcoma. The essential 
point of differentiation is the development of the green masses of lymphoid tissues 
which are distinctly neoplastic in character. The prognosis of chloroma is invari- 
ably fatal. 

ANEMIA INFANTUM. 

Definition. — Lender this term von Jaksch has described a form of anemia occurring 
in children under four years of age and resembling leukemia in many respects, 
in that there is great enlargement of the spleen, marked leukocytosis, some increase 
in the size of the liver and of the lymph nodes. Von Jaksch believes that this 
malady separates itself from a true leukemia of infancy by the fact that the increase 
in the white cells is never so marked as in true leukemia, that children often recover, 
and because there is never any leukemic infiltration of the viscera. The cause is 
not known. 

The red cells are so much decreased that they number only from 3,000,000 to 
1,500,000. There are also present poikilocytes and usually a large number of 
nucleated red cells. The total leukocytosis rarely exceeds 50,000, the chief increase 
being in the mononuclear corpuscles. Myelocytes are absent, or not present in 
sufficient number to justify a diagnosis of leukemia. The liver and spleen are 
enlarged. The condition is usually met with in rachitic or syphilitic children and 
in those suffering from chronic gastro-intestinal catarrh. 

Treatment. — The treatment is identical with that of leukemia. 



PURPURA 719 



PURPURA. 



Under this term is included all those cases in which, as the result of various 
causes, extravasations of small quantities of blood take place into the skin. These 
extravasations are multiple and often very widespread. It must be borne in mind 
that under no condition is purpura a disease in itself. It is a symptom or mani- 
festation of some disturbance in the nutrition of the smaller bloodvessels or of the 
blood. Thus, it occurs as a manifestation of severe infections, such as profound 
septicemia, scarlet fever, typhus fever, measles, and smallpox, and in infections 
not so well understood, in which micro-organisms, known and unknown, are mani- 
festly the cause of the condition. Various investigators have isolated from cases 
of purpura such micro-organisms as the Streptococcus pyogenes, the Staphylococcus 
pyogenes aureus, the pneumococcus , and the Bacillus aerogenes capsulatus. The 
Bacillus coli communis has also been obtained from the blood. Again, certain 
poisons, as snake venom and poisons from the mineral kingdom, may cause purpura. 
A large number of cases of marked purpura have developed in persons who have 
taken iodide of potassium, and after the use of mercury, copaiba, and the chlorate 
of potassium, and certain acid fruits like strawberries or grape fruit, and foods 
like shell fish may induce an attack. It may also develop as the result of some 
congenital defect in the blood, as in hemophilia. 

Diseases generally called diathetic, such as scurvy, tuberculosis, Hodgkin's 
disease, and chronic nephritis, may cause this symptom. Purpuric extravasations 
sometimes develop after severe neuralgic seizures in locomotor ataxia and along 
the course of certain nerves in hysterical women. It is evident, therefore, that 
while the exact pathology of those various states is obscure the etiological factor 
is in one instance an infection, in another a toxemia, endogenous or exogonous, and 
in the third class due to some inherative or congenital state. In still other instances 
it is the result of some trophic nervous lesion. 

The severity of the lesions may vary from small pin-head spots, at first bright 
red and copious which fade to a dirty yellow, to blebs and bullse with ulcerated 
bases. In other cases the exudate is so largely serous that the lesions partake of 
the character of an urticaria. Such cases also may have edema of the glottis, and 
sharp attacks of abdominal pain which preceding the appearance of erythematous 
patches, urticarial wheals, or true purpuric lesions may mislead the physician into 
a diagnosis of appendicitis, gallstone colic or ruptured tubal pregnancy. Hema- 
temesis may be free and give rise to a diagnosis of gastric or duodenal ulcer, par- 
ticularly in those instances in which the lesions in the skin and mucous membrane 
are scanty or absent. The extravasation of blood into the wall of the bowel may 
cause intestinal obstruction; sometimes extravasations of blood or serum take 
place in the eyeball causing blindness, or in the brain inducing a hemiplegia and 
unconsciousness. 

Under the name "purpura rheumatica," or "peliosis rheumatica," a form of 
purpura develops in which there is a distribution of the spots chiefly about the 
large joints, particularly about the knees. Associated with this eruption there is 
swelling of the tissues about the joints resembling that seen in rheumatism. There 
is usually no fever and little pain, although the joints appear stiffened at times. 
It was this arthritic state that gave the name "purpura rheumatica" to the 
condition. In some instances the joint disorder is due to acute rheumatism but in 
the majority it is some other form of infection. 

Under the name of "Schonlein's disease" a very much more severe type of this 
condition has been described. Many of the joints are affected, so that the patient 
is bedridden, and the extravasations of blood into the submucous tissues and into 
the skin are so copious that great swelling and even sloughing may result. Some 
years ago I saw, in consultation with Dr. Wilson, of Woodbury, New Jersey, another 



720 DISEASES OF THE BLOOD 

physician who not only had the joints of the extremities greatly affected, but the 
inferior maxillary joint was also involved. The buccal mucous membrane was so 
infiltrated that we feared the development of noma, and the whole face was much 
distorted by the infiltration. Notwithstanding the severity of the lesions and 
the intense prostration of the patient, recovery usually takes place. Care must 
be taken that this form of purpura is not confused with scurvy or scorbutus 
(which see). 

"Henoch's purpura" describes a condition characterized by lesions in the skin 
which may be a combination of purpura and erythema multiforma. The joints 
may or may not be affected, and bleeding from the gums may appear. The most 
distinctive symptom, which is not present in all cases, but which may be present 
when the others are absent, is gastro-intestinal crises, in which the child is seized 
with pain, diarrhea, and vomiting. All these symptoms are prone to recur at 
irregular intervals. Recovery usually occurs, except in those cases in which the 
hemorrhagic state affects the kidneys, when a fatal result may ensue. 

A form of fulminating purpura sometimes develops in young girls and causes 
death in a few days, the patient being apparently overwhelmed by some unknown 
infection. 

There are three hemorrhagic affections of the newborn that occasionally occur. 

In children with inherited syphilis, hemorrhage from the mucous membranes 
and from the navel, with intense subcutaneous extravasations, may occur and cause 
death. The autopsy shows hemorrhages into the liver and kidneys, and signs of 
inherited syphilis in these parts as well. 

Under the name of WinckeFs disease a condition of jaundice develops within a 
week of birth, followed by dyspnea, hemoglobinuria, and deep cyanosis. I saw a 
case some years ago in which the child was so cyanotic that parts of its body were 
blue-black. The autopsy in such a case shows swelling of the spleen and fatty 
degeneration of the liver and kidneys. 

A third state called " morbus maculosus neonatorum" develops in newborn 
infants, and consists in hemorrhages from the stomach, intestines, or from the 
navel. It is rarely seen in private practice, and is probably due to some infection. 

Hayem and Bensaude have stated that in purpura hemorrhagica the blood, 
when allowed to stand in a vessel for twenty-four hours, slowly clots, but the clot 
does not contract to any extent, and therefore does not squeeze out the serum as it 
does in normal blood, but Howell was unable to find that the blood of such patients 
lacked prothrombin or antithrombin. 

Treatment. — The treatment of all forms of purpura is based upon the recollection 
of two facts, viz., first, that the condition is due in most cases to an infection or at 
least to a cause which has impaired the health, and therefore every means to aid 
the vital resistance of the body must be resorted to. The food should be easily 
digested and nutritious; the patient, if able to travel, should be removed to some 
place where he can bask all day in the sunshine. Moderate doses of tincture of 
the chloride of iron should be given each day to combat the infection and the 
anemia. 

The second point to be recalled is that certain drugs may be employed to increase 
the coagulability of the blood. Of these, the only ones with any real claim to 
power are the lactate and chloride of calcium, which may be given in the dose of 
20 grains three times a- day to an adult, well diluted with water. Certain cases 
seem unable to absorb calcium salts through the alimentary canal and these should 
be treated by hypodermic injection. The solution should not be stronger than 1 
part in 20 of water and the lactate should be used because the chloride is too 
irritating. The effect of one day's dose of 60 grains lasts three or four days, and 
it should not be too frequently repeated, since, if this is done, coagulability is 
decreased. Turpentine, oil of erigeron, ergot, and sulphuric acid have all been 



HEMOPHILIA 721 

used. Their employment is purely empirical, and there is little reason to rely on 
them. Plenty of nutritious food, fresh air, and a day in the bright sunlight will 
do more good in this state than all the medicines can accomplish, and this, too, 
without damaging the stomach. The use of these remedies in this state is putting 
"drugs of which we know little into bodies of which we know less." 



HEMOPHILIA. 

Definition. — Hemophilia is a condition of the body in which there is an inability 
to arrest hemorrhage by the normal coagulation of the blood, or in which hemorrhage 
arises apparently without cause and persists without any attempt being made by 
nature to arrest it. The disease is essentially hereditary in most cases, and it is 
an extraordinary fact that the hemorrhagic tendency is transmitted to males only 
through the female parent, although the mother is herself usually not afflicted. 

Etiology. — Howell has shown that in hemophilia there is a deficiency of pro- 
thrombin which accounts for the delay in coagulation. 

Pathology and Morbid Anatomy. — There are no changes in the blood cells that 
account for this condition. An examination of the tissues of the various organs is 
also practically negative, save that if the hemorrhage has been profuse the changes 
always met with in marked anemia are present. 

Symptoms. — An active but oozing capillary hemorrhage is the form in which the 
bleeding usually occurs, and it follows in some instances very slight injury. Thus 
the mere blowing of the nose may be sufficient to rupture the fine vessels of the 
nasal mucous membrane and cause a dangerous loss of blood, and epistaxis is the 
most common form in which this condition manifests itself. Another common 
source of the blood is from the gum after tooth extraction. 

In some cases bloody effusions take place into the large joints. 

Prognosis. — The prognosis depends largely upon the severity of the loss of blood 
and upon the ability of the patient to restore the quantity lost before the next 
bleeding comes on. Fully 50 per cent, of bleeders die before the seventh year, but 
some live to old age. Although girls who reach puberty menstruate with their 
entrance upon adult life, and so are exposed to an excessive loss of blood, their 
mortality rate in this disease is not so high as that of boys. 

Treatment. — The treatment, if the hemorrhage is acute, consists in the subcu- 
taneous injection of the blood serum of a healthy human being or of " Coagulose" 
prepared from the serum of the horse. In hemophilia neonatorum this is the only 
plan which will save life, in the building up of the general health by out-door life 
and exposure to sunshine, and in the use of small tonic doses of iron and arsenic 
if anemia is present. If a special tendency to hemorrhage exists at any particular 
time, calcium lactate or chloride should be given in doses varying from 10 to 20 
grains three or four times a day, well diluted, to increase the coagulability of the 
blood, but this must not be used for long periods without intermission, as after a 
certain amount is taken the coagulability of the blood is decreased and not increased. 
The local treatment consists in the use of tampons wet with blood serum derived 
from a healthy animal or man, or with coagulose which is dried horse serum, placed 
on the market for this purpose, with adrenalin chloride, 1 : 1000, or gelatin solution 
of the consistency of thin mucilage may be used for the same purpose. When 
adrenalin cannot be obtained, peroxide of hydrogen may be applied in the same 
manner to the bleeding spot. When the hemorrhage is from the gum, a compress 
made of punk may be used, or a compress wet with a saturated solution of alum, 
with Monsel's solution, or with adrenalin chloride solution, 1 ; 1000, 



46 



DISEASES OF NUTRITION. 



DIABETES MELLITUS. 

Definition. — Diabetes mellitus is a disease characterized by the appearance in the 
urine of glucose, and the development of polyuria, thirst, and excessive appetite 
with impairment of nutrition, and in some cases progressive emaciation. The 
mere presence of glucose in the urine does not necessarily indicate that diabetes 
is present. The glycosuria must be associated with other morbid processes to 
present the symptom-complex of the disease. 

Furthermore, while it is true that large amounts of sugar in the urine are in a 
sense of greater importance than small amounts, it is a fact that the amount of sugar 
is not the real index of gravity. It is the secondary products of perverted metab- 
olism, such as, /3-oxybutyric acid and the proportion of nitrogen in the urine 
which are the gauges of severity. 

History. — Diabetes mellitus has been known since the time of Christ, but it 
was not till the latter part of the seventeenth century that Willis, in England, 
noted that the sweet taste of the urine was probably due to sugar, and not until 
1775 that Dobson, of England, actually obtained sugar from the urine. Since that 
time a host of experimental investigators and clinicians have studied the disease 
from every aspect and have added much to our knowledge of it, but no one has 
as yet been able to give us a clear conception of the causes of the malady. Probably 
there are several causes. 

Distribution and Frequency. — Diabetes occurs in all parts of the civilized world, 
but is much more common in Europe than in the United States. It is frequently 
met with in France, in Sweden, in Italy, in India, and Ceylon, but is comparatively 
rare in Russia, Holland, and in Brazil. Negroes rarely suffer from it, but Hebrews 
are so frequently affected by it that it may almost be said to be the prevalent 
disease of that race. Kulz, of Germany, found that in 692 cases of diabetes 17.8 
per cent, occurred in Jews, which is all the more remarkable when we consider that 
Hebrews constitute only 1.2 per cent, of the population of that country. Frerichs 
found 102 Jews in 400 diabetic patients, and von Noorden 252 Jews in 650 patients 
suffering from this disease. 

It is a disease of adult life, as a rule, but very young children suffer from it 
occasionally, and even nurslings have from time to time been reported as presenting 
well-developed cases of the malady. To emphasize its rarity in children, Stern 
may be quoted in his assertion that only thirteen deaths have been reported from 
this malady as occurring in children under five years of age in thirteen years. It 
is more common in males than in females in the proportion of 3 to 2. 

The statement generally made that diabetes is a disease of cities rather than of 
country districts is not altogether true. Some years ago Purdy showed that, as a 
rule, it was much more frequent in the country districts than in cities. In the 
United States the disease is much less frequent in the Gulf and South Atlantic 
States than anywhere else. 

There can be no doubt that the disease is becoming very much more frequent 
than it was several decades ago. I showed this in a paper published some years 

(723) 



724 DISEASES OF NUTRITION 

since, based upon statistics gathered from the Jefferson Medical College Hospital 
and other large hospitals here and abroad. Since then additional statistics have 
been collected which indicate the correctness of these earlier conclusions. 

According to the mortality statistics of the United States Census Reports for 
six decades, the proportion of deaths from diabetes mellitus in 100,000 deaths from 
all known causes has been as follows : 

From 1840 to 1850 72 From 1870 to 1880 .... 191 

" 1850 to 1860 98 " 1880 to 1890 .... 280 

" 1860 to 1870 170 " 1890 to 1900 .... 470 

It seems scarcely credible that so great an increase could have occurred, and it 
is possible that greater care in examining patients and in regard to correct death 
certificates is responsible for part of the increase, yet the records of the Massachu- 
setts General Hospital from 1824 to 1898 showed that four times as many cases of 
diabetes were admitted to the hospital during the last thirteen years of that period 
as during the first fifteen years. On the other hand, it is only fair to state that the 
statistics of L'Hotel Dieu, Lyons, for seventeen years, which were collected by 
Alix, for Lepine, who attempted to ascertain if diabetes was increasing in a certain 
district of France, do not show any increase in the disease. 

Etiology. — The causes of diabetes are not known, although it is a well-recognized 
fact that lesions in certain portions of the nervous system are followed by glycosuria, 
and that certain alterations in the islands of Langerhans in the pancreas and in the 
circulation of the liver are also followed by the same symptom. (See Pathology.) 
As somewhat indirect causes we recognize severe nervous strain and errors in diet, 
but these alone are not sufficient to cause even glycosuria, much less true diabetes, 
in the vast majority of human beings. 

Certain factors tend to produce the chain of disturbances just enumerated, 
and all these agencies may cause changes which may be mild and continue so, or, 
in another case, become severe and rapidly fatal. These may be mentioned as 
follows : 

1 . Heredity. It is well recognized that a diabetic parent often hands down to the 
offspring certain defects which interfere with the proper utilization of carbohydrates. 

2. Errors in diet, both as to food and drink. It is conceivable that errors of this 
character can so pervert, or overwhelm, the processes of nutrition or elimination 
that primary glycosuria followed by permanent diabetes may ensue. Thus, the 
excessive beer-drinkers of Bavaria often suffer from this disease, probably because 
of the excess of fluid, of alcohol, and of carbohydrate which they ingest. These 
factors pervert the function of the liver, of the pancreas, and of the kidneys. 

3. Profound nervous worry and mental anxiety are undoubtedly followed by 
diabetes in some persons probably because the nervous mechanism governing 
nutritional processes is perverted in function by the stress and strain. 

4. Certain injuries to the central nervous system may so result, for severe trauma 
of the head or the growth of an intracranial tumor may produce glycosuria. 

5. It has been definitely shown that injury to, or a growth in, but not destruction 
of the posterior lobe of the hypophysis may develop glycosuria with pofyuria 
without any associated changes in the islands of Langerhans in the pancreas. 
This deduction is supported by the fact that in animals which have been subjected 
to extirpation of the infundibular portion of the gland there is as great an increase 
in fat and as extraordinary tolerance of starches and sugars, as in individuals who 
have complete destruction of this gland by disease. 

6. Possibly in some cases excessive secretion of the suprarenal glands is present. 
Such an abundance of adrenalin in the blood is supposed to act on the system so 
that glucose cannot be stored or there is set free large amounts of glucose already 
in storage. 



DIABETES MELLITUS 725 

7. Certain infectious diseases may produce temporary glycosuria, which disappears 
with the acute disease, or persists and becomes true diabetes, probably because the 
acute infection has damaged beyond repair nervous centres or glands whose function 
is to control glycogenesis and the utilization of glycogen. 

8. Diathetic diseases such as gout undoubtedly cause, or predispose to, diabetes 
in some cases, but whether this influence is direct or simply a sign of general perver- 
sion of metabolism we do not know. 

All these factors are predisposing causes. We still do not know the actual 
cause. Hale White quotes Sir William Gull as having asked "What sin did Pavy 
or his fathers before him commit that he should be condemned to spend his whole 
life seeking the cure of an incurable disease?" To which White adds "Pavy, 
with steadiness of purpose, probably unmatched, worked at the subject from the 
age of 23 till after his eighty-second birthday, but neither he nor the many hundreds 
of others who have tried to unravel it have yet succeeded in fully explaining why 
sugar is sometimes found in urine, nor have they discovered how to cure 
diabetes." 

Pathology. — Of the pathology, or morbid physiology, of diabetes we are very 
ignorant, although an immense amount of skilled research has been devoted to 
this subject for years. It is a well-recognized fact that in all human beings dextrose 
is prepared from carbohydrate foods, and even from proteids and fats, and deposited 
in the liver and in the muscles as glycogen where it lies, as in a storehouse, as reserve 
food. When needed for nutritive processes it is reconverted into dextrose. Dextrose 
also circulates in the healthy blood stream in the proportion of about 1 : 1000, and 
so is carried to various parts of the body for nutritional purposes. 

There are many conditions which produce loss, or leakage, of this substance 
in the form of glucose in the urine. Thus, glycosuria, or the mere presence of 
sugar in the urine, may follow the ingestion of an excess of either cane-sugar or 
grape-sugar or an excess of carbohydrate food. Under these circumstances it is 
simply an overflow of material which the system cannot utilize. This being true, 
it is readily conceivable that in certain states of disease the system may be unable 
to utilize the ordinary amount of dextrose, and therefore it escapes from the body. 
This view receives support from the theory advanced by Loewi and Kolisch, who 
believe that there is in the organism a body, or ferment, or agent, which binds the 
glucose in the tissues in such a form that it does not appear in the blood in excess. 
If for any reason this binding body (Bindekorper) is diminished in power, an excess 
of glucose passes to the kidneys and so escapes from the body. This view explains 
a considerable number of cases of glycosuria, but by no means all of them. 

It is a well-known fact that injury or disease of the so-called diabetic centre of 
Claude Bernard in the medulla is followed by glycosuria, and that this glycosuria 
is directly due to a disorder of the blood supply in the capillaries of the liver. This 
may interfere with the "binding" of the glycogen in that organ. Again, the admin- 
istration of phloridzin will produce glycosuria, but this condition is quite different 
in its causation from ordinary glycosuria, in that the drug acts upon the kidney 
structure in such a way that it permits a leakage of the normal content of glucose 
from the blood. In other words, in this state the fault does not lie in an inability 
of the body to use its glycogen, but in the inability of the kidneys to prevent its 
escape from the body. 

We find, therefore, that glycosuria and diabetes mellitus are by no means identical 
conditions necessarily, although glycosuria is the predominant symptom in this 
disease. There may be a loss of sugar in the urine for many years without any 
impairment of health, or the glycosuria may not be constant, but recurrent and 
appear only when nutritional process are for any reason jarred or disturbed. In 
true diabetes mellitus, on the other hand, there are associated with the glycosuria 
more or less profound impairment of nutrition, with wasting, emaciation, and the 



726 DISEASES OF NUTRITION 

development in the body of certain poisons which act very deleteriously and may 
cause death. 

These distinctions, which serve to separate in the mind of the student glycosuria 
from true diabetes mellitus, however, like many other distinctions, do not actually 
hold true in all cases, for we frequently see persons who begin with the leakage of 
sugar into the urine and end with true diabetes; and we meet intermediate cases 
in which the degree of emaciation, thirst, and polyphagia is so mild that it is difficult 
to tell whether the patient is a sufferer from an inability to deal with carbohydrate 
food or is really diabetic. 

The question of the pathology of this disease, as far as we know it today, can 
perhaps be summed up in the following words : In certain individuals there exists, 
as a result of congenital or acquired defect in the metabolic functions of the body, 
an inability to utilize for the purpose of nutrition all the carbohydrate material 
which is taken as food. Such persons suffer from simple glycosuria. If the defect 
just referred to becomes more marked they gradually lose the power to retain 
and utilize any noteworthy quantity of the carbohydates ingested. Given an indi- 
vidual who is unable to store, or retain, glucose in his body we have before us one 
who is deprived of one of the chief elements required for nutritional balance and 
he is continually losing a most important source of energy and heat. The more 
carbohydrates he ingests the more he loses, and the greater his polyuria because 
the glucose stimulates the kidneys to secrete urine and therefore the greater becomes 
his thirst. Whenever any individual is deprived of food for a length of time, 
whether it be by ordinary starvation, a rigorously inadequate diet, or by loss of 
sugar as in diabetes, his system attempts to obtain the food necessary for its 
existence by utilizing its deposits of fat and protein, not only utilizing these 
tissues as they are ordinarily used when taken as food but it also forms sugar 
from fats and from proteins in order to obtain its carbohydrate quota. In this 
process of forming sugar from fats it develops a poisonous substance, /3-oxy- 
butyric acid. If the metabolic processes are not seriously disordered the body 
goes one step further and oxidizes this acid into aceto-acetic acid, and by still 
another step changes aceto-acetic acid into acetone, which is not poisonous. As 
another means of protecting itself it utilizes the alkalis in the tissues to neutralize 
these acid substances and to aid in their elimination, and so great may be the 
demand for alkali for this purpose that the ammonia produced in protein metab- 
olism is not converted into urea as it is in health. The urine as the result 
of protein destruction and as the result of this use of ammonia may therefore 
contain an excess of nitrogen but a diminished quantity of urea (see Prognosis) . 

The result of these processes may be summed up as follows: (1) The patient 
is starved by his constant loss of sugar. (2) He is wasted by the destruction 
of his fats and proteins. (3) He is deprived of fluid by his polyuria. (4) He is 
robbed of the normal alkalies in his tissues. (5) He suffers from auto-intoxication. 

But the chain of evils does not cease here for his vital resistance being de- 
creased he falls a ready victim to all pathogenic germs. Bad as it may be to 
lose glucose in the urine this loss is only the first evil which induces infinitely 
worse ones. Indeed it may occur that when a patient is passing little sugar, 
because he is deprived of starch as a food and has largely used up his fats, he may, 
nevertheless, be in an infinitely worse condition than another patient, who is passing 
enormous amounts of sugar. The fact that deprivation of carbohydrate in the diet 
of a healthy man induces acetonuria indicates why it is dangerous to suddenly 
deprive a diabetic patient of all starchy food in an endeavor to decrease his sugar 
loss. (See Treatment.) 

Finally, it must be recalled that of all the organs of the body the liver and the 
pancreas are the viscera which show the greatest morbid changes in true diabetes. 
Not only is the liver the organ which is chiefly concerned with the manufacture 



DIABETES MELLITUS 727 

and storing of glycogen, but the pancreas undoubtedly exercises a very powerful 
influence upon the glycogenic processes; for not only does it secrete digestive 
ferments which act in the intestine, but also a ferment or factor which enters 
the blood stream and is intimately concerned with the utilization of glycogen. 
Thus, if the pancreas is extirpated glycosuria is at once developed, and the same 
condition ensues if the gland is totally destroyed by disease. It would appear 
that the so-called islands of Langerhans are the portion of the gland which exercises 
this influence upon the processes connected with the utilization of glycogen, and 
in many cases these islands are found to be distinctly diseased. While disease of 
the pancreas is responsible for the development of diabetes in some cases of the 
malady, it is also a fact that in many cases of very severe diabetes the most careful 
examination of the pancreas after death fails to discover any lesion that can be 
considered in any way responsible for the malady. It seems evident, therefore, 
that many causes may so pervert nutritional processes that glycosuria or true 
diabetes may result, and in this sense it may be said that diabetes is not a primary 
disease, but rather a symptom complex of some primary lesion which we do not at 
present understand. 

Morbid Anatomy. — The changes found in the islands of Langerhans are various. 
In some cases they manifest capillary engorgement or hemorrhagic extravasation. 
In others there is found a pericapillary or peri-insular sclerosis, an atrophy, a 
necrobiosis, or hyaline degeneration'. The latter is probably always primary, and 
the former conditions usually secondary. Aside from changes of the islands of 
Langerhans in the pancreas, the most notable changes presented postmortem in 
any of the organs of the body are found in the liver. This organ is usually markedly 
hyperemic and darker in color than in diseases which do not affect its functions. 
Microscopically it is found that its capillaries are congested, and that the liver 
cells are enlarged and show a tendency to coalesce. These changes are not, how- 
ever, peculiar to the disease, being found in other states; and it is a fact worthy 
of consideration that when death results in cases of severe disease of the liver, 
glycosuria is rather an unusual symptom. There is however a form of diabetes, 
associated with hepatic cirrhosis and bronzing of the skin called "bronzed 
diabetes/' owing to the color of the skin. (See Bronzed Diabetes.) 

The structure of the kidneys is diseased in a very large number of diabetics. 
These changes are not in any way a part of the disease itself, but result from 
the increased activity of these organs in excreting water and sugar, and by reason 
of the effect of toxic substances, such as diacetic acid and oxybutyric acid, 
which, as they are eliminated, damage the renal tissues. The constancy of renal 
changes in diabetes is proved by the frequency with which these organs are found 
diseased at autopsy when death has occurred from this disease. Out of 121 autop- 
sies, reported by Griesinger, Dickinson, and Seeger, renal changes in diabetes were 
found in 77 cases, and Elliott has collected statistics from European clinicians 
which show that albuminuria is present in 43.68 per cent, of all cases of diabetes. 
The renal lesions may be divided into two classes: In one class, which is usually 
met with in chronic cases, an ordinary chronic nephritis develops in which parenchy- 
matous and interstitial changes both occur. In the second form, which is really 
toxic in origin, there is a hyaline degeneration of the tubular epithelium, the so-called 
"cellular necrosis of Ebstein." A so-called glycogen degeneration of Henle's 
loop and of the straight uriniferous tubules (Ehrlich's lesion) is also found, but it 
cannot be claimed that these changes are pathognomonic. 

The changes in the nervous system are usually of little importance. Peripheral 
neuritis is often present. Probably this is purely secondary. Distinct changes 
have, however, been found in the spinal cord in cases of diabetes mellitus, notably 
by Williamson. Using Van Gieson's method this clinician found an increase in 
connective tissue in the columns of Goll in the cervical area. There was also a 



728 DISEASES OF NUTRITION 

diminution in size of the nerve fibres in these columns, and the myelin sheaths and 
axis cylinders were also diminished in size, although a few of the myelin sheaths 
were distended. When Marchi's method was employed degenerated fibres were 
seen in Goll's columns in the cervical, dorsal, and lumbar regions, and a few degen- 
erated fibres were present in Burdach's columns. So, too, degeneration was found 
in the intramedullary course of the posterior nerve roots, between the posterior 
surface of the cord and the posterior horn of gray matter, and to the median side 
of the posterior horn. These latter changes were most marked in the lumbar and 
cervical regions. In a few instances degenerated fibres were seen in the posterior 
roots just outside the pia mater. These changes are probably secondary and due 
to the altered condition of the blood in diabetes. 

The blood is not only unduly rich in glucose, but sometimes contains an excess 
of fat-globules to such an extent that it may form a cream-like layer on the clot 
when it stands after withdrawal. Fraser has recorded a case in which an analysis 
of the blood showed that it contained 16.5 per cent, of fat and the pleural fluid 
20 per cent. 

The blood in some cases of diabetes mellitus is of a pale salmon color which has 
been thought to be due to the presence of fat, and for this reason this condition 
has been called lipemia. Futcher, however, has shown that this appearance is 
not entirely due to fat, for it is not possible to remove it from drawn blood by the 
use of ether, and the granules do not stain black with osmic acid. He suggests 
that these granules are in part albuminous. More recently Cole, in testing the 
blood in a case for Hale White, reached the conclusion that true fat is not present, 
but that the foreign material seems to be an ester of cholesterin with one of the 
higher fatty acids. Heyl showed in 1880 that this state of the blood could be 
demonstrable in the retinal vessels, and Hale White has more recently recorded a 
remarkable case of this character. 

The lungs are often found to contain tuberculous foci, and may show well-devel- 
oped bronchopneumonia or croupous pneumonia, but these are the result of ter- 
minal infections and not part of the primary disease. Arteriosclerosis and its 
train of associated lesions are of frequent occurrence in diabetes mellitus. 

Symptoms. — The symptoms of diabetes vary very greatly in their severity in 
different cases, so greatly that it is almost impossible to detail any array of symp- 
toms which are common to all cases. In many instances the glycosuria exists for 
a considerable period of time before the patient suffers from symptoms which lead 
him to think he is not well. A very well-known medical writer in London, some 
years ago, first discovered he was diabetic by observing that flies were unduly 
attracted to the vessel in which he urinated, and later by noticing that a few drops 
of urine which accidentally fell on his black trousers left a white stain on drying. 
Later on, all the diabetic manifestations developed, and he died of diabetic gan- 
grene of the foot. 

As a rule, as the disease progresses the patient notices that he passes water more 
frequently and in larger quantity than is normal, he develops more or less thirst, 
and loses sexual desire and power. Later on he begins to feel languid and inert; 
he is usually constipated because of his polyuria, and he may develop an inordinate 
appetite in the endeavor to compensate for the loss of nutriment through his urine. 
The thirst, the polyphagia, and the loss of strength and flesh are usually in direct 
proportion to the polyuria and the quantity of sugar excreted. When the polyuria 
is marked the tongue becomes glazed, dry and raw in appearance, and attacks of 
stomatitis or thrush may develop. The skin is also dry and harsh, and the hair 
lacks lustre and is brittle. The pulse is feeble and the temperature subnormal. 
Pruritus ani and vulvas may be severe. 

Although the disease is often characterized by excessive emaciation, this symptom 
is subject to extraordinary variations in different patients. Marked loss of flesh 



DIABETES MELLITUS 729 

is almost constant in all persons under twenty-five years of age, but after this time 
it is by no means uncommon to meet with patients who maintain their weight for 
years. This holds true in direct proportion to the years of age and the degree of 
polyuria and loss of sugar. Where the tissues are freely drained of fluid or starved 
beyond repair the weight of course suffers. (See Complications.) 

The urine in diabetes mellitus is not only abnormal in that it contains sugar, 
but it not uncommonly contains albumin as well. (See Complications.) Its 
specific gravity is high and ranges from 1.025 to 1.045, and one instance of 1.074 
is recorded by Trousseau. Such a specific gravity, however, is exceedingly rare. 
Notwithstanding its high specific gravity, however, the urine is usually exceedingly 
limpid and clear, it has a sweet odor, and is acid in reaction. 

The quantity of sugar present varies over wide ranges. Sometimes it is found 
in as small an amount as 1 to 3 per cent. ; in others it is found to be present in the 
proportion of 10 per cent. The total quantity passed in twenty-four hours may 
be from one ounce, or less, to a pound and a half. Very rarely even more escapes. 
Dickinson reports a case that passed the incredible amount of fifty ounces of sugar 
a day. 

The quantity of urine is also very great in some cases, while in others it may 
not be much above the normal quantity. As much as six to twelve pints are often 
passed in each twenty-four hours, and cases are recorded in which as much as 
thirty pints were passed in this time. 

Complications and Sequelae. — The complications and sequelae of diabetes mellitus 
are important, and are so constantly present that they may aid materially in the 
diagnosis of the disease. Many of them are dependent upon the fact that the 
constant loss of sugar lowers nutrition and so decreases vital resistance to the 
various infections, or they result from perverted metabolic processes closely 
associated with the inability of the body to properly control the functions govern- 
ing the utilization of dextrose in the economy. 

Sweet has demonstrated that for certain organisms the blood loses its bactericidal 
power in diabetes. 

It not infrequently happens that the first symptom presented by a diabetic 
patient is repeated crops of boils or carbuncles. When the urine is examined sugar 
is found, and it becomes evident that the lowered vitality caused by diabetes 
mellitus has permitted infection of the skin to occur. Sometimes the carbuncle 
becomes malignant and speedily destroys the patient. In still other instances, 
which are not as common as has been thought, diabetic gangrene occurs, the primary 
lesion being some break in the skin of a finger or of a toe resulting from the blister 
made by an ill-fitting shoe, or by wounding a corn. Through this lesion infection 
takes place, and vital resistance is so low that the micro-organism speedily causes 
the local death of the part, and almost equally rapidly may involve the blood in 
a diabetic bacteremia. In such cases the gangrene is moist. In another class of 
cases, which depend upon secondary vascular changes not due to direct infection, 
the gangrene is dry and of the so-called senile type. 

Elliott's statistics, already quoted, show that albuminuria is present in about 
43.68 per cent, of diabetics. This albuminuria may at times possess grave sig- 
nificance, and is worthy of careful consideration. It may be said to arise from three 
causes, namely, from renal congestion, due to cardiac feebleness and impairment of 
the circulation; from degeneration of the kidneys, due to true nephritis, and, finally, 
to severe irritation or inflammation of the renal tissues by the poisons of the disease. 
The first type can usually be relieved by careful treatment of the heart, and the 
second type, with casts in the urine, is to be regarded as a complicating condition 
of gravity superimposed upon one already exceedingly grave. The third or toxic 
type is, however, the form which presents the most serious and alarming aspect, 
for its onset is usually acute; it comes on when the patient is already profoundly 



730 DISEASES OF NUTRITION 

ill, and it often betokens the rapid approach of diabetic coma, which in such a case 
may be said to be partly due to the renal lesions. Many clinicians consider that 
coma never comes on without this associated symptom. The kidney condition 
is therefore to be studied carefully in these cases, as it may give warning of 
approaching coma. 

Although albuminuria is quite a common symptom, particularly in those patients 
who have arteriosclerosis, general dropsy is rare, notwithstanding the enfeeblement 
of the heart and the impaired state of the kidneys, because the urinary flow is so 
profuse that the body is rapidly drained of fluid. 

Dyspeptic symptoms are often very annoying. They depend upon the excessive 
eating and drinking, to which many diabetics are forced by their thirst and hunger. 
Feebleness of the digestion arises from the failure in vital power, or to perversion 
of the digestive functions by the toxemic state often developed as the disease 
advances. Extreme constipation is often a very troublesome symptom. 

Pulmonary complications, such as bronchopneumonia or tuberculosis, are very 
frequently met with in diabetics, owing to the lowered vital resistance which permits 
infection. Such complications are very often the cause of death, particularly 
tuberculosis. 

Callian has especially studied the influence of diabetes on the female genitals ; 
pruritus vulvae is very common; menstrual disturbances are common; the atrophy 
of uterus and ovaries, he thinks, depends on the associated sclerosis of their nutritive 
vessels. 

The nervous complications of diabetes mellitus may be divided into the acute and 
chronic. The acute complications are very serious from a prognostic point of 
view, and consist chiefly of diabetic coma. Many theories have been advanced 
as to its direct cause. It is undoubtedly toxic in origin, and seems to be chiefly 
associated with a state of acidosis, or the presence of one or more abnormal acids 
in the blood, of which one is called /9-oxybutyric acid. The idea that acetone 
and diacetic acid are the causes has been cast aside. In some instances the onset 
of the coma (sometimes called "KussmauPs coma") is sudden, but it may be grad- 
ual, although, even in the gradual cases, it is a matter of a few hours at the most, 
as a rule. 

Diabetic coma may be said to appear in three types : The first, and most common, 
is often met with in young persons, and develops with suddenness in many instances; 
that is to say, its onset lasts but a few hours at the most. The early symptoms 
are those of disorders of digestion, with abdominal pain, vomiting, muscular weak- 
ness, and drowsiness, which soon ends in coma. The breathing in this coma is 
often slow and deep, very much as it is in the second stage of opium poisoning. At 
other times it is sighing. To one type of the respiratory state in this condition 
Kussmaul applied the descriptive word "Lufthunger." The second form often 
comes on after fatigue, particularly in elderly persons, and the symptoms may be 
those of profound collapse. In the third form the early symptoms are those of 
ataxia and confusion of speech. 

Sometimes the unconsciousness is preceded by great restlessness and irritability, 
while in other instances the onset of the comatose state is gentle. 

Of the ocular complications, cataract, optic nerve atrophy, and diabetic retinitis 
are to be remembered. Sudden blindness due to optic nerve or retinal changes 
occasionally ensues and palsies of the ocular muscles may take place. 

Diabetics are also subject to apoplexy. 

Of the subacute nervous symptoms we find painful neuritis, and not infrequently 
a pseudotabes due to this cause, with loss of knee-jerk, Romberg's symptom, and 
even the Argyll-Robertson pupil. Sometimes a true tabes dorsalis seems to develop. 

Diagnosis. — The diagnosis of diabetes mellitus is easily made if the physician 
will carefully examine the urine and will bear in mind the fact that he is not justified 



DIABETES MELLITUS 731 

in deciding that the well-developed disease is present unless some symptoms which 
are characteristic are associated with the glycosuria. It may be said that he who 
has constant glycosuria is in the early stages of diabetes mellitus, and this is par- 
ticularly true if this symptom be constant in a young person. On the other hand, 
it not infrequently happens that a person of fifty-five or sixty years develops a 
mild glycosuria which lasts for years, and does not materially impair the health 
for a long period of time. Even these cases, however, often develop into the true 
disease. In other words, we may say that while glycosuria is not diabetes, it is a 
state that indicates a tendency to this disease or the presence of its early stages. 
The separation of the polyuria of diabetes insipidus from that of diabetes mellitus 
is made by the low specific gravity of the urine in the former disease, and the fact 
that sugar is present in the latter malady. A more or less constant glycosuria 
is met with in some cases of exophthalmic goitre, ultimately disappearing as the 
disease improves, or finally developing into true diabetes, and the administration 
of thyroid gland may induce glycosuria. Glycosuria is sometimes seen in women 
with ovarian cysts. 

It not infrequently happens that diabetes mellitus is overlooked because the 
patient does not complain either of thirst or of excessive urination, and the physician 
fails to examine the urine as a matter of routine. But these patients often present 
symptoms which, while not distinctly urinary, should at once call the attention 
of the physician to the possibility of diabetes being present. Thus, any patient 
who suffers from marked loss of flesh and increasing weakness should always be 
suspected of having diabetes, even if signs of tuberculosis are present, for not 
infrequently the tuberculosis is secondary to the diabetes. So, too, women will 
sometimes complain of pruritus of the vulva or eczema of the genitals, or men will 
state that they are becoming impotent, in all of which cases the urine should be 
examined, since diabetes often produces these signs. So, too defects of vision, 
due to diabetic cataract, or, more rarely, to retinal changes, may be the first symp- 
toms manifest to the patient, and still others complain of numbness or tingling 
in the extremities and present the symptoms of locomotor ataxia. On the other 
hand, as already pointed out, physicians not infrequently are so careless as to 
examine the urine only once, and when they discover sugar consider that the case 
is one of diabetes; or they obtain a reaction with Fehling's test, because of the 
presence of some sugar-reducing substance, as when the patient is taking chloral; 
or, again, they mistake physiological glycosuria for true diabetes. It is evident 
that most of the mistakes in the diagnosis of diabetes depend upon lack of urinary 
examination or imperfect methods of testing the urine. 

As an illustration of how necessary it is to examine a number of samples of 
urine before determining that the patient has or has not diabetes, it may be 
recalled that urine passed during the night or before breakfast is often free 
from sugar; while that passed after breakfast and during the day may contain 
much of it. 

The condition of diabetic coma is separated from the unconsciousness of uremia 
by the cider-like odor of the breath, the presence of glycosuria and acetonuria, 
and the absence of the high arterial tension usually met with in renal disease, for 
in this state the pulse is feeble and of low tension. At the same time, it is to be 
recalled that uremia may complicate diabetes. The patient lies in a condition 
which resembles profound alcoholic intoxication. Deeply unconscious, with half- 
opened eyelids, wandering eyeballs, and dilated pupils, he breathes in a panting 
manner, a deep inspiration being followed by a quick expiration. The respiratory 
rate may not be greatly different from the normal, but sometimes it is hurried, 
and then forms " diabetic dyspnea," with a gradually increasing cyanosis. The 
temperature Is usually normal or below normal. This state almost invariably 
ends in death in from one to two days. 



732 DISEASES OF NUTRITION 

Ueinaey Tests. — For many years the most popular tests for the determination 
of the presence of sugar in the urine have been those which depend upon the fact 
that strongly alkaline solutions of grape-sugar reduce copper oxide to lower grades 
of oxidation. The most frequently employed of these tests is that which is made 
by means of Fehling's solution. This is best made in the following manner: 

Copper sulphate, 34.64 gm., with water enough to make 500 c.c. Mix and keep 
in a bottle by itself. Pure Rochelle salts, 173 gm.; solution of sodium hydrate, 
specific gravity 1.330, 100 c.c, and water enough to make 500 c.c. For use mix 
equal volumes of these two solutions, thereby forming Fehling's solution. About 
one drachm of this solution is placed in an ordinary test-tube and boiled. If the 
solution does not remain clear, it is unsuitable for use. If, on the other hand, it 
does remain clear on boiling the suspected urine is to be added to it, a few drops 
at a time, and the boiling continued, when, if sugar is present, the solution becomes 
opaque and yellow in hue, and soon a dense, yellowish-red sediment falls to the 
bottom. Should the quantity of sugar present be exceedingly small, it may be 
necessary to add urine until the volume of urine and the volume of Fehling's 
solution are equal. But the volume of urine must never exceed that of the Fehling 
solution. 

Trommer's test is performed in the following manner : 

A drachm of urine is placed in an ordinary test-tube, and is treated with sufficient 
quantity of sulphate of copper solution to render the fluid a light-green color. 
An equal volume of liquor potassse is then added. This results in a blue precipitate 
of hydrated copper protoxide, which dissolves upon shaking the tube, so that a 
clear blue solution remains. If the test-tube be allowed to stand for some time 
the copper is gradually reduced, and precipitation of the yellowish-red suboxide 
of copper occurs. If the solution is heated, the tests act more promptly. Care 
must be taken that the fluid is not boiled actively, as under these circumstances 
precipitation may take place without sugar being present. 

It is hardly necessary to add that in making these tests the greatest possible 
cleanliness in the test-tube and bottles should be maintained. 

It is of vital importance to remember that the copper tests for sugar respond 
to other agents in the urine. These reducing agents are glycuronic acid, maltose 
in nursing women, lactose, and alcaptone. 

Occasionally the urine in cases of diabetes mellitus contains acetone in excess 
and diacetic and oxybutyric acids. The appearance of acetone in amounts greater 
than normal (0.008 to 0.027) is always to be considered a signal of danger of diabetic 
coma. The test for the presence of acetone consists in distilling the urine and 
adding to several cubic centimetres of the distillate a few drops of liquor potassse, 
to render it alkaline. Several drops of Lugol's solution are now added, when, if 
acetone is present, the fluid becomes turbid, and iodoform is precipitated in crystals. 
If this fluid is now heated, the odor of iodoform is noticeable. 

Gerhardt's test consists in adding an aqueous solution of chloride of iron to the 
urine, when, if diacetic acid is present in large amount, the fluid becomes a deep 
red; but this test is fallacious if the salicylates have been ingested. 

Prognosis. — The prognosis of diabetes is largely influenced by a number of factors. 
In the first place, as a rule, but by no means always, the outlook is favorable for 
long life in direct proportion to the age of the patient. Thus, it not infrequently 
happens that men and women who develop the disease after fifty or sixty years of 
age live the full length of years usually credited to human beings of that age. Even 
in these cases, however, the possibility of some intercurrent infection, like pneu- 
monia, is to be borne in mind as a constant threat against life. Conversely, the 
disease is rapidly fatal in proportion to the youth of the patient. In young persons 
it runs a rapid course and may destroy life in a few weeks. Great emaciation 
usually develops in these cases; whereas, older persons may maintain their weight. 



DIABETES MELLITUS 733 

The mere presence of glycosuria is not justification for as grave a prognosis, even 
if the amount of sugar be marked, as is the presence of glycosuria with associated 
thirst, hunger, and loss of flesh. For the first state is a leakage, while the second 
shows that nutritional changes are marked, and that true complete diabetes mellitus 
is present. 

The prognosis also depends somewhat upon the manner in which the patient 
responds to the regulation of his diet. Thus, if on the partial withdrawal of carbo- 
hydrates and the use of ordinary amounts of proteid and fatty food the sugar is no 
longer found in the urine, and the urine gives no reaction with perchloride of iron 
for acetone, the condition may be considered as a mild form of the disease. If, on 
the other hand, the quantity of sugar diminishes, but does not disappear, and the 
urine gives reaction with perchloride of iron, the case should be considered as one 
of moderate severity. Again, if the gradual decrease in starchy foods, until the 
patient is taking no carbohydrates, fails to diminish the sugar excretion and if a 
perchloride of iron test gives a Burgundy or port-wine coloration, showing the 
presence of acetone in excess, then the disease is to be considered as severe. 

The degree to which the fats are being broken down, and the danger of acid 
intoxication, are important to determine. The presence of acetone is not as grave 
an indication as the presence of diacetic acid nor is diacetic acid as grave as 
/?-oxybutyric acid, since the latter when present shows that the body cannot oxidize 
it into diacetic acid much less into acetone. The quantitative estimation of these 
bodies is so complicated that it is much better to study the relative and absolute 
output of ammonia which is easy to do and is an accurate gauge of the degree of 
their presence, because these acids would rob the body of alkali were it not that 
the organism produces an excess of ammonia to save the normal alkalies. A 
patient in health excretes daily about 0.7 gram of ammonia, but in diabetes it 
may be so enormously increased as to equal 8 or even 14 grams a day. As much as 
5 grams per day in a diabetic are indicative of grave diabetes which may cause 
death in a year. Brown of the United States Navy recommends the following 
simple method for ammonia estimation: 

"About 60 c.c. of filtered urine are treated with 3 gm. of basic lead acetate, well 
stirred, allowed to stand a few minutes and filtered. The filtrate is treated with 
2 gm. of neutral potassium oxalate, again well stirred and filtered. Ten c.c. of 
the clear filtrate are diluted to about 50 c.c. with distilled water and a few drops 
of 1 per cent, phenophthalein added. The fluid will be slightly alkaline or acid, 
more frequently the latter. Fifteen gm. of neutral potassium oxalate are added, 
thoroughly stirred, and the specimen exactly neutralized with one-tenth normal 
sodium hydroxid or sulphuric acid; 20 c.c. of 20 per cent, commercial formalin, 
previously made neutral, are added and the solution again titrated with one-tenth 
decinormal sodium hydroxid. Every cubic centimeter of one-tenth normal sodium 
hydroxid corresponds to 0.0017 gm. ammonia. The burette reading of the second 
titration multiplied by this factor represents the amount of ammonia in 10 c.c. 
of urine. The quantity is then calculated on the basis of the twenty-four hour 
volume." 

It is also desirable to determine the degree to which the patient is splitting up 
his protein molecule to form sugar and ammonia. This can be theoretically esti- 
mated by determining the quantity of urinary nitrogen, since physiological chemists 
have found that each gram of nitrogen represents the destruction of 6.25 grams of 
protein. In a patient who is so far advanced in the disease that he is absolutely in- 
tolerant of carbohydrates and is starved of carbohydrates until he is carbohydrate- 
free, it has been found that the ratio of dextrose to nitrogen is 2.8:1 and this has 
been called the dextrose and nitrogen ratio. That is to say, if he has no carbohydrate 
from which to make dextrose, he is now making 2.8 grams of sugar out of each 
6.25 grams of protein, as represented by the 1 gram of nitrogen found in the urine. 



734 DISEASES OF NUTRITION 

As comparatively few diabetics are absolutely intolerant of carbohydrate and as it 
is often unwise to make them carbohydrate-free by stravation, this method of 
estimation is not clinically feasible, because of its danger, and it would further 
require that the protein intake should be estimated, but if this ratio of 2.8:1 is 
found it is indicative of an advanced form of the disease. 

Mandel and Lusk have stated the following proposition as to prognosis: That 
if a diabetic be put on a meat-fat diet (rich cream, meat, butter, and eggs), and 
the twenty-four-hour urine of the second day be properly collected, 1 the discovery 
of 3.65 grams of dextrose to 1 gram of nitrogen signifies a complete intolerance 
for carbohydrates, and probably a quickly fatal outcome. They have called this 
the fatal ratio. 

The cause of death in diabetes mellitus is usually one of the acute infections, 
such as pneumonia, tuberculosis, or septicemia, with or without carbuncle. Dia- 
betic coma is another common cause of death. Frerichs found that 150 out of 
250 deaths in diabetes were caused by coma. Of 43 fatal cases observed by Taylor, 
death resulted from coma in 26. Mackenzie found 19 deaths from coma in 87 
fatal cases. 

It may be laid down as a rule, that true diabetes mellitus never gets well, but 
that temporary glycosuria often does so under proper treatment. Diabetes may, 
however, be controlled and life prolonged very materially by resort to suitable diet 
and remedial agents. 

Treatment. — By treatment much can be done for the control of this disease. 
As already stated, simple glycosuria can usually be entirely relieved by proper 
attention to exercise, the regulation of the diet, so that the patient does not overeat 
or overdrink, and particularly by the limitation of the amount of carbohydrate 
food which he ingests. In these cases the appearance of sugar in the urine is to be 
regarded as evidence of the inability of the patient to properly utilize these sub- 
stances in the body. If there is reason to believe that he is too sedentary in his 
habits, it sometimes happens that a moderate amount of exercise causes a dis- 
appearance of the glucose. Again, if he is a thin, spare individual, who naturally 
worries much about business or professional duties, absolute rest from these causes 
of stress must be insisted upon, in order that the nervous system may recover its 
equipoise. 

When true diabetes mellitus is present, it is even more essential that these etio- 
logical factors should be controlled. Indeed, it may be well said that to attempt 
treatment by a diet and drugs is useless in a case of diabetes mellitus, unless the 
patient can be properly controlled in regard to his manner of life, provided that 
manner of life is deleterious. In other words, it is futile, in the majority of in- 
stances, to regulate the diet and to give drugs if the patient is to be continually 
exposed to causes which are more potent for evil than the remedies are for good. 

There can be no doubt that the dietetic treatment of diabetes is far more im- 
portant than that by drugs, and it is essential that this fact be borne in mind, since 
physicians are often careless in regard to the question of dietetics, and patients 
are still more so, even after the importance of a proper diet has been conveyed to 
them. Quite frequently they follow the directions of the physician for a short 
time, and then, wearying of being deprived of favorite articles of food, take these 
articles surreptitiously, or openly declare that whether it does them harm or good 
they do not intend to be deprived of things of which they are fond. For these 
reasons the dietetic treatment of diabetes is much the more difficult part of the 
care of these cases. 

1 "The urine should be collected so that an early morning hour (before breakfast) terminates the period 
for one day. Tin's is necessary, because the sugar formed from eaten proteid is eliminated before the 
nitrogen belonging to the same. The long period between the evening meal and breakfast allows for 
the elimination of both constituents." 



DIABETES MELLITUS 735 

As diabetes is a condition in which the body is unable to properly utilize car- 
bohydrates and their educts, it is manifest at once that an excess of carbohydrates 
must be forbidden; but what is an excess to one individual may not be an excess 
for another, for an excess is that quantity which is more than the body can use. 
For this reason it is usually wise, when placing a patient upon an antidiabetic 
diet, to diminish the quantity of carbohydrates which he receives, by a very gradual 
process, and to watch the quantity of sugar in the urine from day to day, since by 
this means the quantity of carbohydrate material which he can utilize may perhaps 
be approximated. A second reason for carrying out this gradual diminution in 
the quantity of starchy food lies in the important fact that not infrequently cases 
of diabetes are plunged into diabetic coma by the institution of a diet practically 
free from carbohydrates, perhaps because the system is in such a condition that 
no sudden variation in the character of the food can be permitted, and also because 
in such cases the organism immediately splits up its own fats and forms poisons. 
Not only is it a clinical fact that coma may be precipitated in this manner, but we 
also know that the quantity of acetone in the urine is greatly increased by severe 
restrictions of carbohydrates. For this reason the physician, when restricting 
diet, should always examine the urine, not only as to its content of sugar, but as to 
content of acetone as well, and if this latter ingredient is present in an amount 
in excess of that which may be considered normal, for a minute trace is sometimes 
present in non-diabetic persons, it is absolutely essential that he shall at once 
restore the full carbohydrate diet, since by so doing the quantity of acetone is 
diminished and the condition of acidosis which produces coma is diminished. 
This is more important if the urine contains, as it often does, diacetic acid and 
iS-oxybutyric acid, particularly the latter, since its presence indicates that the 
patient cannot convert /3-oxybutyric acid into diacetic acid or diacetic acid into 
acetone. (See Treatment of Coma.) The elimination of more than one gram of 
acetone in twenty-four hours is to be considered an excess. 

Patients will often resent the total removal of carbohydrates from their diet 
list, and yet yield to their gradual removal. On the other hand, it is not to 
be forgotten that in some diabetics a certain amount of carbohydrate food seems 
to be essential, in order that they may not manufacture dextrose from other articles 
of food, or from the fat of their own bodies, and in order that acidosis be not 
produced. That is to say, the administration of starch in moderate quantity may 
compensate for their loss of dextrose. 

Sugars should always be excluded. They are unnecessary articles of diet, and, 
aside from the fact that the body is unable to utilize them, they are apt to disturb 
digestion. 

Because carbohydrate food cannot be utilized, it has come to be well recognized 
that the patient must subsist largely upon the different forms of meat, both salt 
and fresh, excepting liver, which contains glycogen, and which, therefore, ought 
not to be given. It has come to be a generally accepted fact, however, that more 
than a very moderate ration of animal proteid is disadvantageous. Eggs are more 
desirable than meat and vegetable albumen more permissible than eggs or meat. 
So, too, butter, cheese, and the various oils and fats may be used. 

It has already been pointed out that diabetic patients whose supply of car- 
bohydrate material has been cut down should be provided with an amount of fat 
over and above that usually ingested, provided, of course, that the individual can 
digest and assimilate fats. It is evident, however, from a series of investigations 
made by von Noorden and others, that butter, when taken in excess of five ounces 
a day, may cause an increase in the quantity of oxybutyric acid in the blood. Von 
Noorden has pointed out, however, that this deleterious effect of large amounts 
of butter can be diminished if the butter is first washed with cold water in a most 
thorough manner, since by this means we remove the lower fatty acids which are 



736 DISEASES OF NUTRITION 

chiefly concerned in the production of acidiosis. Under these circumstances, 
von Noorden tells us that as much as seven ounces of butter can be taken daily 
without difficulty. 

Most of the shell-fish are useful, but oysters contain too much glycogen. 

In the way of fresh vegetables, the patient may receive the various greens, such 
as lettuce, spinach, dandelion, cabbage, cauliflower, Brussels sprouts, string beans 
celery, watercress, tomatoes, onions, cucumbers, olives, and the various kinds of 
pickles, and practically all of the nuts which are commonly employed as foods, 
except chestnuts, which contain too large a proportion of starch. 

Not rarely the patient does best when he is placed upon a diet which varies in 
carbohydrates from week to week; that is to say, he is given a very small quantity 
of carbohydrate one week, and a fairly large quantity of it the next. 

In those instances in which the acetone reaction persists in the urine, whether 
carbohydrates are removed or allowed, vonNoorden has strongly recommended what 
he calls " the oatmeal cure." In this cure the patient eats nothing but oatmeal gruel 
for from one to two weeks, save that in addition to the eight ounces of oatmeal he is 
given a similar quantity of butter and some vegetable albumin. Often this mixture 
is administered as frequently as every two hours. Von Noorden asserts that 
on this diet the excretion of sugar falls to a point far below that excreted on a mixed 
diet from which all carbohydrate has been removed. At the end of a week or two 
it is always necessary to return to other foods temporarily, as otherwise the patient 
rebels against the pursuance of a pure oatmeal diet; but even with these frequent 
returns to an ordinary diet, excellent results are reached. 

For some reason, no better understood than the tolerance of oatmeal, potato 
starch is often well utilized when other starches are not. 

The ability of the patient to utilize carbohydrates can be at times distinctly 
increased by subjecting him to a "starvation day." This consists in giving little 
or no protein and no starch whatever on one day and in allaying his sense of hunger 
by feeding " greens" such as spinach, celery, lettuce, etc. 

Tea, coffee, and cocoa may be employed, provided they are not sweetened by 
cane-sugar, but by saccharin. Dry wines which contain little sugar may be given 
to those who are accustomed to alcoholic drinks, although Scotch whiskey, rye 
whiskey, and dry gin are better than most wines. The various simple mineral 
waters may also be given, and of these both the natural and artificial Vichy waters 
are excellent, because of the quantity of bicarbonate of sodium which they contain. 
The old idea that because the patient urinates in excess he should be deprived of 
water is no longer followed. These patients should be allowed water freely, in 
order that the system may be flushed of toxic materials. When constipation is 
present, the mild saline purgative waters may be given, varying from Apenta, 
Carlsbad, and Hathorn water, to the more powerful saline purges. 

Theoretically, gluten provides a source of nourishment for diabetic patients, 
but practically it is almost impossible to obtain a satisfactory gluten bread which 
does not contain a very considerable quantity of starch. There are upon the 
market a few samples of biscuits made from gluten flour which contain a very 
small percentage of starch, and these may be freely given to these patients. The 
difficulty in the majority of instances is that patients get exceedingly tired of 
a diet from which all forms of bread are excluded, and for this reason it may be 
impossible to entirely exclude bread from the diet list. Most of the biscuits which 
are made from substitutes for wheat flour, such as that of the soya bean, are so 
oily that patients find it difficult to digest them. Almond meal, which also contains 
a very large percentage of oil and no starch, may be given. But here, again, the 
difficulty in digesting the fats it contains is often marked. Perhaps the most 
satisfactory bread is that which is known as aleuronat, and which has been highly 
recommended by von Noorden. Williamson gives the following formula for its 



DIABETES MELLITUS 737 

preparation: Mix 2 ounces (62 gm.) of desiccated cocoanut powder with a little 
water containing a small quantity of German yeast. Make the mass into a sort 
of paste, and put in a warm place for half an hour or longer. The small amount 
of sugar contained in the cocoanut is almost entirely decomposed by the fermenta- 
tion produced by the yeast, and the cocoanut paste becomes spongy. Add 2 
ounces (62 gm.) of aleuronat, 1 beaten egg, and a small quantity of water, in 
which a little saccharin has been dissolved, and mix well until a dough is formed. 
Divide into cakes and bake in a moderate oven for twenty or thirty minutes. The 
great difficulty is to obtain cocoanut fibres sufficiently desiccated and powdered. 

Among the articles which are to be carefully avoided are all the sweet fruits, 
such as melons, grapes, peaches, and those vegetables which contain a very large 
amount of starch and sugar, such as sweet potatoes, beets, beans, peas, and 
carrots. 

The medicinal treatment of diabetes mellitus has narrow limits. It is true that 
a host of drugs have been recommended by various clinicians at various times, the 
statement being made that they were capable of materially decreasing the quantity 
of sugar which was lost in the urine, but further experience has almost universally 
proved that they possess little power. Furthermore, very few of them have been 
shown to possess any influence upon the symptoms associated with the glycosuria. 
In other words, at the best they affect only the one symptom of loss of sugar, and 
in no way correct the underlying cause of the malady. 

Without doubt opium is the most valuable drug in the treatment of diabetes 
mellitus in the majority of cases, for it exercises a more potent influence in diminish- 
ing the elimination of sugar in the urine than any other drug. Its alkaloids, 
morphine and codeine, are also exceedingly valuable, and may be employed when 
they prove capable of controlling the glycosuria and when the opium increases the 
constipation, but neither of these alkaloids is the equal of the crude drug. 

There are several important points in regard to the employment of opium, or 
its derivatives, in diabetes : First, patients of all ages seem to be able to take large 
quantities of opium in this disease without developing the evil manifestations of 
the opium habit. Second, these patients usually have to take ascending doses 
of the drug until they reach a dose which controls the glycosuria more or less 
completely. Third, opiates possess the advantage that they diminish to a large 
extent nervous irritation and stress. Not only do they protect the nervous system 
from external causes of irritation, but by producing mental quiet and diminishing 
worry they indirectly cause good results. An endeavor should be made from time 
to time to diminish, at least temporarily, the quantity of the drug which is taken. 
Ordinarily denarcotized opium is the best preparation. Patients may start on \ 
grain once, twice, or thrice a day, and gradually increase it, if necessary. Or, 
J to J grain of morphine may be given at these intervals. In other instances \ to 1 
grain of codeine may be used as a beginning dose. Some patients get so much 
comfort and such a diminution of glycosuria under moderate doses of these drugs 
that the size of the dose does not have to be increased. Thus, I have had under 
my care for nearly twelve years a woman who has taken but 3 grains of codeine 
a day during all that time. She has never had any desire to increase the dose 
beyond this amount, and it has kept her glycosuria within bounds, besides giving 
her a great deal of comfort. 

In cases which do not possess marked nervous symptoms, but which are rather 
phlegmatic in type, and have a gouty tendency, the salicylate of sodium or salicylate 
of strontium may be given in full doses varying from 10 to 20 grains three or four 
times a day; or, in their place, we may employ some of the new coal-tar products, 
such as antipyrin, acetanilid, and phenacetin. These drugs, however, must be 
given in full doses to have any effect, and they so greatly increase the susceptibility 
of the patient to cold that they must be used with great caution. In cases which 
47 



738 DISEASES OF NUTRITION 

have a syphilitic history, or which seem to be gouty, the iodide of potassium, in 
the dose of 10 to 30 grains or more three or four times a day, often does good. 
When the patient can digest it, cod-liver oil is an exceedingly valuable alterative 
and nutrient. 

With the idea that the alkalies aid oxidation processes in the body and so neu- 
tralize acid poisons, various alkalies, as the potassium and sodium salts, have been 
largely employed. Thus, potassium or sodium bicarbonate may be given in 30, 
40, or 60 grain doses three or four times a day. They aid, too, in the elimination 
of acids. 

Another remedy which is of value in some cases, particularly if anemia is present, 
is Fowler's solution in doses varying from 1 to 3 minims three times a day. With 
some clinicians it has a great reputation" in this disease. 

In the treatment of the various complications of diabetes we must first consider 
diabetic coma. After coma is once established, we have no method of treat- 
ment which promises permanent recovery. I have repeatedly seen a temporary 
return to consciousness follow the intravenous injection of one quart of normal 
saline solution, and Continental clinicians have employed and strongly recom- 
mended the injection of carbonate of sodium in solution. (See below.) 

When the presence of an excess of acetone or diacetic acid or oxybutyric acid 
in the urine, or of the early symptoms of intoxication, indicate that diabetic coma 
is not far distant, two plans of treatment should be promptly instituted. One of 
these is directed to the prevention of the further formation of acidosis. The 
other is designed to deprive these substances of their poisonous properties. As 
already pointed out, the addition of liberal amounts of starchy foods to the 
diet results in the decrease or disappearance of acetone from the urine — acetone 
being the symbol of intoxication. This may increase the glycosuria but this is 
nothing as compared to the danger of coma. If this cannot be done by the use of 
remedies by the mouth, because the stomach is unfit to deal with food, then one of 
the monosaccharids, such as levulose or dextrose, should be dissolved in sterile salt 
solution and injected subcutaneously or into a vein. Ordinary sugars (disaccharids) 
cannot be used in this way, because they require the action of the digestive juices to 
be disintegrated. The quantity of fluid used should be a quart with 10 per cent, 
of dextrose. Not less than 50 to 100 grams of levulose a day should be given by 
the mouth. A 5 per cent, solution of glucose may be given by the rectum, using 
Murphy's drop method. If neither of these can be had, glycerin may be given 
by the mouth. Another point of importance is to cut down the fats given to these 
patients, who before the onset of these symptoms have been subsisting largely 
upon fats and proteids, because the poisons of coma are derived from fats and 
fatty acids. 

For the diminution of the poisonous properties of the toxic substances already 
formed everyone is in accord that alkalies should be freely administered. Vichy 
water should be taken in large quantities, and 60 or 120 grains of bicarbonate of 
sodium may be given every two or three hours dissolved in Vichy water, thereby 
fortifying it. Water to the extent of 5 quarts in twenty-four hours should be 
given to help in the elimination of poisons and, to avoid gastric distention, the 
amounts given each time should not be too large. Salt solution may be used 
by hypodermoclysis. Stadelmann has advised the intravenous injection of car- 
bonate of sodium in order that it may combine with the acids in the tissues, 
and aid in their elimination. The quantity of acetone in the urine may be 
temporarily increased by this plan of treatment. Naunyn uses 35 to 40 grams 
of carbonate of sodium (not bicarbonate) dissolved in a quart of water. This 
must be given very slowly by intravenous injection. Even this plan, if insti- 
tuted after coma is present, rarely does more than restore consciousness tem- 
porarily. If the bowels are confined they should be opened by some saline purge, 



DIABETES INSIPIDUS 739 

but active purgation should not be resorted to, since by this means concentration 
of the poison may take place if the bowel is not active in the process of eliminating 
poisons from the blood. 

BRONZED DIABETES. 

Bronzed diabetes is characterized by cirrhosis of the liver, a peculiar pigmen- 
tation of the skin and viscera (see Hemochromatosis), fibroid changes in the 
pancreas and constant glycosuria. The term "bronzed" is probably an unfor- 
tunate one as the pigments of the skin are more earthy or leaden in hue. The 
color is most marked upon the parts exposed to light, as the face, hands, and neck, 
and it is very unevenly distributed. Occasionally there is considerable somnolence, 
not due to diabetic coma, with great emaciation and feebleness. It is held by 
some that iron which is deposited in the tissues and which is responsible for the 
pigmentation is not derived from the breaking down of red blood cells but from a 
failure to excrete iron taken in the food or set free by the breaking down of iron- 
containing tissues. The prognosis is hopeless, and aside from measures directed 
against the conditions which are common to this rare malady and ordinary 
diabetes mellitus, there is no efficient treatment known. (See Hepatic Hyper- 
trophic Cirrhosis.) 

DIABETES INSIPIDUS. 

Definition. — Diabetes insipidus is a condition in which a person passes excessive 
quantities of urine containing no abnormal constituents and of a low specific gravity. 
This term is sometimes applied erroneously to a fleeting attack of polyuria due to 
nervousness or fright and to profuse diuresis following the ingestion of excessive 
amounts of water. It is also to be separated from the inconstant polyuria some- 
times seen in hysterical women. 

Etiology. — Diabetes insipidus is most commonly met with in persons under 
thirty years of age and may occur in early childhood. It is more common in males 
than in females. Very rarely it is definitely hereditary, and occasionally there is 
in the history of the patient a statement that it developed after some severe injury, 
as a railroad accident or fall. It has also followed sunstroke and prolonged fevers 
of an infectious type, and it has been met with as a symptom in cases of brain 
tumor, particularly if it involves the fourth ventricle. Within the last few years 
a number of investigations have shown that irritation of the posterior lobe of 
the hypophysis, either reflexly through the nervous system or directly in operations, 
causes a very marked polyuria and this perhaps explains this condition in nervous 
and hysterical persons. It is increasingly evident that a large proportion of these 
cases are due to dyspituitarism, since polyuria often results from injury to the 
pituitary body in operations on animals and man. Furthermore, an increasing 
number of cases of polyuria are being reported in which lesions of the pituitary 
body have been found at autopsy. In every case associated with any signs of 
dyspituitarism (see Dyspituitarism) or of brain tumor, as choked disk or hemi- 
anopsia, the sella turcica should be studied by the aid of the z-rays. 

Morbid Anatomy. — Aside from changes in the hypophysis no distinct lesions 
have been found at autopsy. Sometimes the kidneys are found to be swollen 
and congested. 

Symptoms. — The dominant symptom of diabetes insipidus is, of course, a profuse 
urinary flow. Next to this symptom is the constant thirst suffered by the patient, 
who no sooner provides his system with fluid by drinking than it escapes from the 
kidneys. The third symptom of importance is the annoyance caused by the neces- 
sity of emptying the bladder many times a day and the loss of rest at night by 
reason of the same condition. Closely related to these symptoms in its causation 
is dryness of the mouth and excessive dryness of the skin. Partly because of the fact 



740 DISEASES OF NUTRITION 

that the condition develops usually in nervous patients, or in those whose nerves 
have been shattered by accident, persons suffering from diabetes insipidus are 
often very irritable and peevish, an irritability which is maintained by the necessity 
of frequent micturition. The body temperature may be normal or subnormal. 
Tyson states that some cases can take inordinate quantities of alcohol without 
intoxication, but that others are unduly susceptible to the cerebral effects of this 
drug. 

The quantity of urine passed by some cases of diabetes insipidus quite equals 
that passed by well-advanced cases of diabetes mellitus with free polyuria. As 
much as eighty and ninety pints a day have been excreted but the usual quantity 
is rarely above ten or twelve pints. The specific gravity is almost as low as ordinary 
water, and rarely exceeds 1.003 or 1.005, owing to the fact that the normal urinary 
solids are dissolved in such an exceedingly large quantity of fluid. At times the 
total urea is greatly in excess of that normally excreted. Albumin is rarely present 
except in very small amount. 

Diagnosis. — Before deciding that a patient has true diabetes insipidus it must 
be determined that the condition is not a fleeting polyuria, but a constant state. 
Tests as to specific gravity of the urine and for sugar will reveal diabetes mellitus. 
The state of the cardiovascular system and the eye-grounds may reveal chronic 
contracted kidney. 

Prognosis. — Prognosis so far as life is concerned is good. Recovery is by no 
means rare, and even if it does not take place death from the malady rarely, if 
ever, occurs. The celebrated case of Willis lived fifty years with this condition 
present. It is only when the diabetes insipidus depends upon a serious nervous 
lesion that the prognosis is bad, and then because of the lesion and not because of 
the polyuria. 

Treatment. — No treatment for diabetes insipidus which has yet been instituted 
has proved satisfactory. It is quite true that a large number of remedies have 
been spoken of in terms of praise by various practitioners, but the very number of 
them indicates that no one of them gives results which are definitely curative. The 
use of vegetable astringents, such as gallic acid, with the idea that by this means a 
diminution in the secretion of urine may be brought about, sometimes produces 
favorable results. The dose must be large, from 5 to 20 grains three or four times 
a day; but even when such large doses are used as to disorder the stomach, it not 
infrequently happens that no decrease in the quantity of urine is brought about. 
In other instances good results are said to accrue from the employment of an active 
fluidextract of ergot given in the dose of 20 to 30 minims three or four times a day, 
alone or with the bromide of sodium in the dose of 20 grains. The ergot is supposed 
to act by contracting the capillaries in the Malpighian tufts. When the polyuria 
causes much restlessness and insomnia, the remedies already named may be aided 
by the simultaneous administration of codeine, which will probably not decrease 
the quantity of urine, but which usually acts as a nervous sedative with sufficient 
power to prevent the bladder from waking the patient more frequently than is 
absolutely necessary. The bromides may also be used for this purpose. In those 
cases which are associated with neurasthenia or which follow prolonged nervous 
strain, the "rest cure" or a vacation where the patient is not annoyed by business 
or family cares will probably give better results than will drugs. 

GOUT. 

Definition. — Gout is a disease which depends for its existence upon a disorder 
of metabolism, as a result of which deposits of biurate of sodium take place in the 
joints and in the fibrous tissues surrounding them. It is characterized by associated 
changes of a fibroid and calcareous character in other parts of the body in many 



GOVT 741 

instances, and in its acute exacerbations it frequently causes severe inflammation 
and pain in one or more joints. The joint of the big toe is very commonly the 
chief seat of the articular disorder. Gout is sometimes called "podagra." 

Etiology. — The precise cause of gout is unknown, but certain etiological factors 
in its development are universally recognized as being active. The first of these is 
undoubtedly heredity, but while it is true that the tendency to the disease is often 
inherited it is also true that the descendants of gouty persons often fail to develop 
the disease, and that other persons who have no gout in their family history suffer 
from the malady. It is interesting in this connection to note that younger children 
of gouty persons more frequently fall victims to gout than the children of their 
earlier years, probably because the gouty diathesis is better developed in advanced 
years in the parents than in youth. 

A second factor in the production of gout is mode of life as to exercise and mental 
labor. There is universal accord that great mental and nervous stress with little 
physical exercise frequently produces a gouty diathesis and often precipitates an 
acute attack of the malady in those already gouty. Duckworth states that political 
life in England is notoriously conducive to gout, and that lawyers are very prone 
to it. In the case of the country squire who is so often gouty, high living and drink- 
ing, with a long heritage of dietetic indiscretion, probably overcomes all the good 
effects of an active out-door existence. In those who live chiefly out-of-doors, as 
farmers, soldiers, and sailors, the disease is rare. 

A third factor of some importance is age. While cases of well-developed gout 
are met with in young children and, very rarely, even in infancy, the malady com- 
monly does not develop till after the thirtieth year, but rarely waits till the fifth 
decade of life before at least beginning its early manifestations. 

A fourth factor is the abuse of alcohol, not in the sense of going on sprees, but 
in such a manner that the system is all the time engaged in oxidizing or destroying 
this drug. Ales and beers — that is, malt liquors — are more prone to cause gout 
than are whiskies and other distilled liquors. Sweet and sour wines are also provo- 
cative of this disorder, particularly champagnes. 

A fifth factor is overeating. There is an increasing number of persons in America 
who do not eat to live, but live to eat, and who stimulate the digestive organs to 
greater activity by the use of highly seasoned dishes, with the result that they 
ingest and absorb more food than the system can use, stifling oxidation and clogging 
elimination. 

Finally, a very powerful factor in producing gout, in those who are exposed to 
the metal, is lead poisoning of the chronic type. 

We find, then, that the chief causes of gout are heredity, lack of exercise, nervous 
stress, and the ingestion of more food or drink than the body can properly deal with. 

Frequency. — True gout in its frank forms is far less common in England than 
it was in the early part of the last century or in the eighteenth century. In America 
it is certainly very rare. On the other hand, both in England and in this country 
"lurking," "lateral," or masked gout is certainly greatly on the increase. The 
disease is more common in men than in women. 

Pathology. — When we come to a study of this disease from the standpoint of 
perverted physiology or pathology, we encounter a task over which the profession 
has toiled unceasingly year after year with little advance in our understanding of 
gout, but great advance in our knowledge of the metabolic changes in the body. 
When Sydenham wrote, after being a sufferer from gout for years, that it is due to 
"the impaired concoction of matters both in the parts and juices of the body," 
he expressed himself as clearly and correctly as do many modern writers on this 
subject. So late as October 1913, Walker Hall concludes a paper on this subject 
in these words: "It is a slow progress along the zigzag which leads to the centre 
of the gouty maze, but the researches of the last decade have opened up many 



742 DISEASES OF NUTRITION 

new and possible pathways thereto. Further advances, however, wait for progress 
in chemistry and physics, especially in connection with fermentative processes." 

The pages of a text-book are not suitable for a discourse in which a multitude 
of researches are analyzed and judged, yet it is proper to take note of several theories 
as to the cause of gout that have been strongly advocated by one or more investiga- 
tors, with some basis for their views. 

One theory is that when the blood and lymph are saturated with uric acid the 
urates are precipitated by a slight lowering of the temperature, such as is apt to 
occur in an exposed joint. This theory is not adequate to explain the disease, 
because it has been proved that the fluids are not saturated with uric acid or urates 
in cases of gout, and the disease affects parts which are not chilled. 

Again, Kolisch advanced the view that the so-called xanthin bases are the cause 
of gout. This investigator believes that the nucleinic bodies are broken up into 
xanthin and hypoxanthin, and that in the healthy kidneys these are in turn changed 
into uric acid. In gout he thinks that the kidneys fail to perform their function 
properly, that the xanthins are not transformed into uric acid, and that this results 
in the retention of xanthins, which straightway proceed to cause gout. This view 
has been impaired by the fact that his methods of research were faulty and by the 
fact that other investigators, using more accurate methods, get different results. 

His believes that the uric acid of the gouty is a product of the disease, and that 
it is capable of causing evil effects in the body. It is not the prime factor, in other 
words, but a secondary factor, just as the bacillus of diphtheria is the prime factor, 
and the toxins which it produces cause widespread lesions as secondary factors. 
In the normal body uric acid is in large part destroyed; whereas, in gout it is per- 
mitted to exist and induce secondary evil effects. Any cause which prevents the 
destruction of uric acid predisposes the patient to its deleterious influences, and 
these causes may be inherited, acquired, or due to poisons, such as lead. Here, 
again, we are met by the contradictory fact that in a number of diseases an. excess 
of uric acid develops without any signs of gout appearing. Thus, in leukemia, 
pneumonia, and chronic kidney disease this acid circulates in the blood in excess 
but no gout is produced. 

The view of Ebstein is that there is a primary nutritional disturbance in the 
affected joints, and in other tissues, which results in tissue death within those parts, 
and that in these devitalized areas urates are deposited. Finally, von Noorden 
believes that a special ferment acts to produce these local nutritional changes and 
that the deposit of urates then ensues. 

The most popular theory as to the cause of the symptoms has been that there 
is present in the body an excess of uric acid. This is the theory of Garrod, and 
in more recent times has had its most enthusiastic advocate in Haig. Garrod 's 
theory that the decrease of uric acid in the urine at the time of an attack is due 
to its retention in the body, and that this retention causes an outbreak, is now held 
to be erroneous, or at least is regarded with grave doubt, as is also his view that a 
decreased alkalinity of the blood causes a precipitation of the urates, for Magnus- 
Levy, Luff, and W. His, Jr., have all proved that the quantity of uric acid in the 
blood is not increased during or before an attack, nor is the alkalinity of the blood 
decreased. Still others have shown that the decrease in the excretion of uric acid 
just before an attack of gout is due, in part at least, to a decreased ingestion of food. 
These researches do not prove, however, that uric acid-producing substances are 
not present in excess, and it is entirely possible that the scanty elimination of uric 
acid in many of these patients in the interval between attacks is due to the failure 
of the body to change these substances into uric acid, with the result that they 
cause an attack, at which time the percentage of uric acid excreted often tempor- 
arily rises. I confess that this view seems the more attractive. 

When we consider that the injection of uric acid into the blood does not cause 



GOVT 743 

gout, that it is present in leukemia, pneumonia, and nephritis without causing 
gout, and that no excess of uric acid is found in the blood in gout, it is hard to 
believe that uric acid causes gout. While Kolisch's theory may be imperfect in 
detail, and while the kidney may not transform xanthin into uric acid, it is entirely 
possible that an excess of xanthin may be present in gout. This view is supported 
by several facts, which indicate that uric acid is an end-product derived from 
nuclein breakdown, and that it is not this healthy end-product, but by-products 
which are morbid in effect. From nuclein we can obtain albumin and nucleinic 
acid; from neucleinic acid we can obtain phosphoric acid and a substance which 
in turn may be split up into xanthin bases and uric acid. If oxidation is complete, 
uric acid is the chief end-product, if it is incomplete, then xanthin is the chief 
product. Bain and Futcher have both shown that when there is an increase in 
uric acid excretion there is an increase in phosphoric acid secretion, and they believe 
that this throws a side light upon the relation of uric acid and xanthin to gout. 
Thus, in one of Futcher's cases there was a marked fall in both phosphoric acid and 
uric acid immediately before an attack, followed by a very great increase at the 
time of the attack, and this again by a fall. The phosphoric acid curve was far 
greater than the uric acid curve. 

It would seem, therefore, that the destruction of nucleinic bodies may be per- 
verted in gout, and this is what Futcher' s study proves, namely, that as phos- 
phoric acid and uric acid are both derived from nuclein, and as they are greatly 
disturbed in amount in relation to the attack, it is fair to assume that some relation 
exists between nucleinic bodies, their derivatives, and gout. 

At the present time it would seem probable that we may divide this question 
of the pathology of gout into two sub-questions, viz. : 

1. Is there present in the body at the time of an attack of gout an excess of 
uric acid, or, rather, of material capable of producing uric acid? The answer is 
"Yes." 

2. What is the reason that this condition develops? The answer is that we do 
not know, but that it is dependent upon a perversion of metabolism not yet under- 
stood, whereby in health uric acid, a primarily harmless body, is produced, and 
in disease a by-product is found, which causes an attack, before, or during, which 
urate of sodium is deposited in the tissues. 

Morbid Anatomy.- — Gout may produce morbid changes in every tissue of the 
body, even to the hair and nails, but the parts which are most frequently impaired 
by its existence are the heart and the bloodvessels, the kidneys and the joints. 
From the standpoint of outward manifestations and early discomfort, the joint 
changes are, of course, the most important, but from the standpoint of the physician, 
whose duty it is to prolong life, the cardiovascular and renal changes are the factors 
which deserve most attention. Because of the wide distribution of gout in the body, 
Sydenham wrote: "Totum corpus est podagra." 

The lesions in the joints are characteristic; the ligaments, tendons, and bur see 
all become affected, and even the articular cartilages are involved. In all these 
tissues deposits of biurate of sodium take place, and they may be so copious that 
the parts are deformed and incapacitated by roughening of the cartilaginous sur- 
faces, or by thickening of the sheaths of the tendons and joints. In typical cases 
the disease first attacks the joint of the big toe, then the finger-joints, after this 
the metacarpal and metatarsal joints, and still later, but much more rarely, the 
large joints. When these are affected, the wrist, elbow, and knee are the parts 
usually involved. The ball-and-socket joints (hip and shoulder) are very rarely 
involved in gout, and the upper extremities are much less frequently affected than 
the lower ones. When the disease is well advanced there is so great a deposit of 
biurate of sodium that it lies under the skin in a white knob, or pea-shaped mass, 
which looks white and chalky. If the skin covering such a deposit is injured, it 



744 DISEASES OF NUTRITION 

not rarely undergoes necrosis, and biurate of sodium exudates from the part, looking 
like wet chalk. Sometimes on the fingers, near the base of the finger-nails, or 
about the first phalangeal joint, there develop small, hard, uratic masses called 
"crab's eyes." It is a remarkable fact that these deposits often take place without 
any other manifestation of gout being present and without any pain, so that atten- 
tion may be called to them only by reason of the disfiguration produced. Gouty 
deposits about the base of the finger or at the second joint are, however, usually 
part of a general gouty outbreak. 

When the articulating cartilages are affected two conditions may be presented. 
If no injury has occurred, and if no cause of irritation has existed other than the 
gout, the articulating surface is seen to be smeared or plastered, to use Duckworth's 
expression, with a uratic deposit looking as white and smooth as fresh white lead 
(Fig. 125). When irritation has been present the articular cartilage may be 
eroded. In this latter form there is often overgrowth of connective or fibrous 

Fig. 125 




Showing urate of sodium deposited on an articulating surface. (Graupner and Zimmermann.) 

tissue in the surrounding parts along with the deposit of urates, as already described, 
and stiffening or distortion of the joint. The changes in the bursa are often note- 
worthy. I have a case now under treatment in which there is a bursa swollen to 
the size of a bantam's egg on the heel at the insertion of the tendo Achillis. It is a 
very dusky red and is exquisitely sensitive, but contains nothing but fluid. It has 
often developed before, and under active treatment for gout has always disappeared 
and left no trace behind it. 

The cardiovascular changes caused by gout do not result from the deposition 
of biurate of sodium in the heart-valves or in the bloodvessel walls. Indeed, 
it is rare for such deposits to be found, although cases are recorded in which the 
cardiac valves and the intima of the aorta have contained the biurate of sodium. 
But while it is true that biurate of sodium is not deposited in the vascular system, 
as it is in the joints, it is also true that gout causes first arterial spasm, then arterio- 
capillary fibrosis, and, finally, advanced calcareous changes in the vessels. The 
result of this is cardiac hypertrophy on the left side of the heart in particular. 



GOUT 745 

The endocardium is never the seat of acute endocarditis as a result of true gout. 
The only endocardial changes are those common to ordinary cases of general 
atheromatous degeneration, in that sclerotic changes take place in the valves, 
particularly those guarding the aortic and mitral orifices. The chordse tendinese 
are also shortened by a similar process and rendered inelastic. 

The pericardium is very rarely affected. 

The venous system is prone to varicosities and calcareous plates may be present 
in the walls of the veins. These in turn may result in thrombosis and phlebitis. 

Gout, cardiovascular disease, and angina pectoris are a wicked trio that bring 
many a noble man to death. 

Whatever the gouty poison may be which causes changes in the general vascular 
system, that poison also damages the renal tissues as well. The bloodvessels of 
the kidneys are, of course, involved in the general vascular fibrosis, and we have 
the small, contracted kidney sometimes called a "gouty kidney," because it is often 
the result of gout. Many years ago Ord and Greenfield showed that in two-thirds 
of all cases examined at autopsy in which there was gout in the great toe there 
was chronic granular kidney, and in the remaining one-third a condition allied 
to it. While it is quite true that deposits of biurate of sodium are sometimes 
found in the kidney structure in the region of the papillse, and extending outward 
along the pyramids toward the periphery of the organ in whitish streaks, such cases 
are very rare when we consider the number of cases of gout and the number of 
cases of renal disease complicating its existence. 

Symptoms. — These are best studied in three divisions: the acute, the chronic, 
and the aberrant types. 

Acute Gout. — In this form the fully developed symptoms are often preceded 
by several hours or days of nervous irritability, of insomnia, or of general wretchedness 
not easily described. In some cases pruritus ani is present, or itching elsewhere 
may annoy the patient and keep him restless at night. The urinary secretion is 
often scanty and the bladder may be irritable. In other cases these symptoms are 
entirely absent and the patient will recall, during his hours of suffering, that he 
has seldom felt as well as he felt for a day or two before the attack came on. 

The attack itself usually consists in the sudden onset of sharp pain and inflam- 
mation in the ball of the great toe. The pain is very severe and stabbing in char- 
acter, often extending upward into the foot. A swelling develops with surprising 
rapidity and the skin over it is red, hot, and burnished. In addition, the part 
affected is exquisitely sensitive, so that the pressure of the bedclothes, much less 
that of a shoe, is insupportable. Not rarely a distinct febrile condition is present, 
the temperature reaching 102° or more. After a few hours the agony diminishes, 
the swelling decreases, and the patient is more comfortable, but within the next 
twenty-four hours the malady may return with fresh severity. This may persist 
for several days, but at the end of that time the patient is not only soon on the road 
to recovery, but feels better than for a considerable time before the attack, although 
the ball of the toe may be swollen and inflamed for some days longer. 

There are three noteworthy peculiarities about these seizures, namely, that 
they usually develop after midnight, waking the patient from sleep; that although 
the inflammatory process in and about the joint seems furious in its severity, the 
part never goes on to suppuration, and the onset and disappearance of the attack 
is followed by little if any disability in the affected part. Only when repeated 
attacks take place is there developed much deformity of the area involved in the 
gouty manifestation. 

Acute gout is nearly always recurrent. Sometimes it attacks the patient every 
few weeks, in other cases every few months, and in others every few years. 

This form of gout is very rare in the United States, but frequent in England, 
although less so than it was many years ago. 



746 DISEASES OF NUTRITION 

Chronic Gout. — Chronic gout as a distinct condition from acute gout does 
not really exist; that is to say, no sharp line separates this type from the acute 
form. Two types of it may be recognized. In one, repeated attacks of acute 
gout are connected with one another by modified gouty manifestations, such as 
stiffness and soreness in various parts, as in the wrists and elbows, or the main- 
tenance of a certain degree of low-grade inflammation in the joint of the big toe. 
In the other form there are no acute outbreaks such as have just been described, 
but a gradual process of gouty thickening of fibrous tissues and an equally gradual 
deposition of biurate of sodium about the tendons, the joints, and in the articular 
cartilages. Similar deposits called tophi are found in the edges of the ears, and 
the "crab's eye" formations in the fingers already referred to are found. 

The urine is scanty, the arterial tension is usually high, and the aortic second 
sound accentuated. (See Morbid Anatomy.) 

In some instances sudden inflammatory attacks of moderate severity, as com- 
pared to the acute attacks in the big toe, develop in one or several of the large 
joints, as the elbow and knee, and may give rise to the belief that acute articular 
rheumatism is present, particularly as a rise of two or three degrees of fever may 
take place. I have seen a patient with severe nodular gout of the hands develop 
an attack of universal articular gout after having his hands baked in a hot-air 
apparatus, probably because the treatment caused the distribution of a mass of 
gouty material in his body. The alterations in the appearance of the joints in 
these attacks has already been described when writing of the morbid anatomy of 
this disease. They may resemble very closely that malady called arthritis deformans. 

After this type of gout continues for years the patient comes to his death as a 
result of renal or cardiovascular disease, or by some acute infection, such as pneu- 
monia, which finds a ready victim in one whose vital organs are already impaired. 
In other words, death is due to a terminal infection. 

Not rarely patients with this type of gout are intellectually brilliant up to the 
moment of their final illness. The presence of the disease seems to be a spur to 
mental activity. 

Irregular Gout. — Without this division of gout some modern physicians 
would be sadly at sea in diagnosis. It affords a loophole of escape when a patient 
insists on a diagnosis, and however much Haig is in error as to facts he deserves 
the gratitude of many practitioners for having popularized the idea of " uric acid 
as a factor in disease.'' There can be no doubt that many patients do present 
symptoms of aberrant or modified gout, but they are by no means as numerous 
as they are thought to be. The gouty poison is capable of producing almost as 
many symptoms and ailments as is hysteria, but not all the symptoms which are 
credited to it, and it is unfortunate that "uric acid" is so often a cloak to 
ignorance which so pacifies the physician and patient that a search for a true 
cause is discontinued. Uric acid is, as already stated, in all probability not the 
cause even in the true gouty cases of many of the symptoms presented, but rather 
the result of the metabolic disorders underlying the illness. 

There can be no doubt, on the other hand, that gout really is responsible in 
many cases for the presence of a very large number of disorders in widely different 
organs of the body, such as eczema and other forms of inflammatory or irritative 
changes in the skin, notably pruritus. Duckworth speaks of a painful induration 
of the ala of the nose in some gouty persons. In the circulatory system the changes 
caused by gout, even in those who have no outward manifestation of the disease, 
may be very notable, as already pointed out. 

In the article on gonorrheal infection it has already been stated that a suppurative 
urethritis may be due to gout, and irritability of the bladder and renal stone may 
arise from this cause. So, too, it is not infrequent for diabetes mellitus to develop 
in gouty persons and to be modified in its course by antigout remedies. 



GOUT 747 

Albuminuria is also frequently present as a result of the high arterial tension 
or of the nephritis produced by the gouty poison. 

Gouty persons often suffer from sudden and severe attacks of acute 'pharyngitis 
or laryngitis, and from acid dyspepsia, and ophthalmologists constantly meet with 
iritis, conjunctivitis, and other inflammatory processes in the eye due to this cause. 
So, too, it often happens that a thickening of the tympanic membrane, which 
causes deafness, has its origin in this malady. 

Finally, and by no means least important, gout or gouty tendencies often cause 
furious attacks of neuralgia and of migraine. Not rarely after such a seizure of 
pain the patient feels unusually well, just as he does after a frank attack of 
gout. 

Retrocedent gout is a condition in which the gouty process suddenly leaves the 
toe or other joint and attacks some one of the internal viscera, producing, it may 
be, violent purging and vomiting, or precipitating an attack of angina pectoris. 
In other cases the patient suffers from an asthmatic seizure. Sometimes a sudden 
uremia makes it appear that a retrocedent gout has gone to the brain. As a matter 
of fact retrocedent gout is not often seen. A letter of inquiry sent by me to several 
eminent English physicians brought replies that they had rarely seen this accident 
occur, although they have frequently met with cases, as we all have, in which a man 
subject to acute gout of the toe has had a gouty angina pectoris after prolonged 
freedom from trouble in the toe. 

Diagnosis. — The diagnosis of gout when it affects the big toe is a simple matter. 
When present in the form of dermal, ocular, otic, or muscular gout, the history of 
the patient and the character of the attack render a diagnosis possible; but when 
the polyarticular form of gout with fever develops, only careful study and the 
absence of heart changes will enable us to separate the conditions if we can find 
no gouty history and no gouty signs, as in tophi in the ears. Again, there may be 
some hesitancy in separating gout from chalky deposits and fixation of joints of 
arthritis deformans in which the articular process is somewhat inflammatory and 
painful, and in which fibroid changes in the connective tissues about a joint are 
present. Arthritis deformans is, however, a more surely progressive malady; 
it causes greater crippling of the patient; it is not characterized by chalky "crab's 
eyes" and tophi in the ears, nor by inflammatory attacks in the eyes or the great 
toe, nor in the tendons and bur see. 

Many of the cases of masked gout can only be diagnosticated by the improvement 
which is produced by proper dietetic measures and the use of therapeutic measures 
known to be beneficial to gouty persons. 

As stated at the beginning of the discussion of irregular gout, remarkably various 
symptoms can be caused by this malady, but all curious symptoms should not be 
credited to it. As Duckworth well says: "Without doubt many morbid states 
have often been flippantly or erroneously set down to irregular gout which owned 
no such designation, and thus a cloak for ignorance has always been at hand to 
throw over careless observation, ignorance, or wilful misinterpretation of symptoms. 
As a consequence of such errors, some have come to regard even truly gouty mani- 
festations, when not articular, as actually non-existant, and to deny the dependence 
of such upon a gouty habit. The latter error is no more to be condoned than the 
former, and it may be fraught with mischief to the sufferer." 

Prognosis. — The prognosis of gout is better when it develops after forty than 
if it appears after thirty years of age. In many cases of frank gout the prognosis 
as to life is better than in the insidious form, for the latter often attacks the circu- 
latory and renal tissues. Much depends upon the vascular system. If it is fibroid 
the outlook is bad, and if it is not the mere existence of gout need not shorten life 
unless alcohol is abused. Gouty persons, however, are not good "risks" in life 
insurance, as has been proved by several sets of statistics. 



748 DISEASES OF NUTRITION 

Treatment. — The treatment of gout is hygienic, dietetic, and medicinal. A 
further subdivision of the subject may be made into that which is devoted to the 
treatment of an acute attack and into those measures which are taken for the 
relief of the more subacute or irregular manifestations. The hygienic measures 
which are to be employed in the treatment of a person suffering from either gout 
with acute exacerbations, or suppressed gout, consist in such exercise as can be 
taken in the open air without at any time producing more than healthy fatigue. 
Exercise taken to the point of exhaustion is of course always deleterious, and par- 
ticularly in those who are gouty, as it is prone to produce an acute attack or reduce 
vital resistance to such a degree that intercurrent maladies may develop. Golf, 
horseback exercise, and similar out-door pursuits are therefore exceedingly advan- 
tageous, but are not to be carried to an excess. These patients should also be 
directed to drink water in as large a quantity as may be taken without overloading 
the stomach at any one time. Many persons can take half a glass of water every 
hour without producing gastric discomfort or interfering with digestion; whereas, 
if they are content to drink only at meal times, but small quantities of liquid may 
be ingested. Water aids in producing a profuse urinary flow, and so helps to 
eliminate impurities from the body. If the heart is not feeble, hot baths or hot 
Turkish baths may be taken two or three times a week with advantage. Often 
such patients are greatly benefited by going to some of the health resorts where 
hot springs exist. 

The dietetic treatment of gout consists in the exclusion of all sweet wines and 
of fatty or rich foods, and in the ingestion of meals which are sufficiently varied 
in character to maintain the appetite and adequate to maintain nutrition. The 
patient should, however, be particularly warned against an excessive quantity of 
food. In many instances gouty persons will be found to take quantities of food 
which are far in excess of those which are required to provide the patient with the 
2500 to 3000 calories per day which he requires for healthy existence. All wines 
and beers are also disadvantageous for this class of patients, and sweet and sour 
wines and champagnes are peculiarly so. In regard to individual articles of food, 
it has been held in the past that red meats were distinctly more harmful than white 
meats; but, as has been pointed out in discussing the dietetics of Bright's disease, 
this view of the relative harmfulness of red and white meat is becoming obsolete. 
Chemical analysis fails to reveal any material difference between them. The 
point of importance is that the patient shall not eat an excessive quantity of meat, 
or meats, which is prepared in such a way that it is difficult of digestion, as, for 
example, larded game birds or larded beef. Of the various beverages cocoa is 
perhaps the best, but rich chocolates are harmful. Coffee is usually considered 
much better than tea. Indeed, Dr. Haig is quite confident that tea is an abomina- 
tion for the gouty. 

In the way of treatment by drugs, there are only three which can be considered 
as exercising an approximately specific influence, namely, colchicum, iodine in its 
various forms, and the salicylates. Of these the iodides and salicylates are most 
useful for the subacute or irregular forms of gout, while the colchicum is of most 
value for the purpose of combating an acute paroxysm. Most patients with con- 
stant, irregular, gouty manifestations do well if they take continuously, over a long 
period of time, 10 to 15 grains of salicylate of strontium three or four times a day, 
or 5 to 10 grains of iodide of potash or iodide of sodium at similar intervals. By 
this means gouty sore throat, gouty iritis and conjunctivitis, gouty stiffness of the 
various muscles, and gouty neuralgia and migraine may be modified or entirely 
relieved. If there is any tendency to acidity of the urine full doses of citrate or 
acetate of potash, 10 or 15 grains three times a day, should be given, well diluted 
with water. In some instances the urine is alkaline, and when it is so the patient 
feels heavy and depressed. These symptoms can often be modified by the use 



ARTHRITIS DEFORMANS 749 

of 10 to 20 grains of benzoate of sodium in capsule three or four times a day. Com- 
paratively recently novatophan has become a popular remedy in the dose of about 
7 grains four or five times a day, given in tablet form. 

Acute paroxysms of gout are to be treated by the administration of full doses 
of the wine of colchicum seeds, repeated in from six to twelve hours, the dose varying 
from 20 to 40 minims, according to the irritability of the stomach and the idiosyn- 
crasies of the patient to the drug. Not infrequently much better results will be 
obtained if before the colchicum a moderate dose of the compound extract of 
colocynth, such as 10 to 20 grains with 1 or 2 grains of extract of hyoscyamus, is 
given to unload the bowels. Colocynth is chosen because experience has shown 
that it seems to exercise a more beneficial influence in gout than any other purgative, 
and the hyocyamus is used because it prevents the colocynth from producing 
griping pain. Not infrequently some relief may be obtained if the inflamed joint 
is wrapped with lint laden with a 50 per cent, ichthyol ointment. Luff has strongly 
recommended the following application for the same purpose: The entire foot is 
surrounded by a warm pack consisting of cotton-wool saturated with the soothing 
lotion, and then lightly covered with oiled silk. 

1$ — Sodii bicarbonatis § iv. 

Linimenti belladonna? f §iv. 

Tincturae opii f Siss. 

Aquae destillatae : f 5 vii j . 

Equal portions of this lotion and hot water should be used to saturate the wool 
which has been rolled around the joint, and the dressing should be changed every 
four hours. 

It is important to remember that no local depleting measures are to be instituted 
under any circumstances. Blisters, leeches, and other forms of bloodletting are 
not only valueless, but dangerous, as they afford opportunities for infection. 

Many cases of acute and chronic gout are also benefited if from time to time 
they receive moderate doses of calomel or blue pill, such as 3 or 4 grains of blue 
mass or a grain of calomel in broken doses. Many physicians at the present time 
also prefer the active principle of colchicum, colchicine, to the wine of colchicum 
root. It may be given in the dose of T ^ to ■%% of a grain every two or three hours 
in a case of acute gout, or four or five times a day in the subacute varieties. 

Although the various salts of lithium are largely employed by some practitioners 
for the purposes of combating the various aberrant forms of gout, it is to be remem- 
bered that the popularity of these salts depends more upon the skilful advertising 
of tablet manufacturers than upon the actual experience of the profession. Those 
who know most about these salts have found that the lithium preparations do 
not act as well in gout as do the salicylates of sodium or potassium, and the idea 
that lithium has a peculiar affinity for the uric acid is, to a large extent, blasted 
by the knowledge that lithium has a greater affinity for the acid sodium phosphate 
in the blood than it has for uric acid ; beautiful test-tube experiments to the contrary 
notwithstanding. 

ARTHRITIS DEFORMANS. 

Definition. — Arthritis deformans is a chronic disease affecting the joints, and 
characterized by trophic disturbances in their cartilages, in the ends of the bones, 
and in the synovial membranes. It is to be distinctly separated from acute rheu- 
matism and from true gout, although in some cases it appears to be a sequel of 
acute rheumatic infection. Sometimes arthritis deformans is called "rheumatoid 
arthritis," or "osteo-arthritis." 

Etiology. — Much discussion has arisen as to the cause of this malady, some 
adhering to the view that it is due to nervous lesions which result in changes in 



750 DISEASES OF NUTRITION 

the joints, and others asserting that it is the result of an infection. Within recent 
years the former view has lost in popularity and the latter opinion is now in the 
ascendant, although as yet no one has succeeded in isolating a specific micro- 
organism. It is probably produced by any one of several micro-organisms and 
the physician should search for a source of infection, however remote, and endeavor 
to isolate the micro-organisms there and in the joints (see Treatment) . The infect- 
ing organisms probably enter by the upper respiratory passages or pharynx and 
the intestines. 

Those who argue in favor of the infectious nature of the malady point to the 
fact that the nearby lymph nodes are often enlarged, as if combating infection; 
that infection of the joints by various micro-organisms is the usual cause of arthritis, 
and that a considerable portion of the cases of arthritis deformans have had at 
some previous time gonorrhea or other disease which is prone to cause secondary 
arthritic lesions. In support of the nervous theory we find that trophic changes 
take place not alone in the joints, but in the muscles and skin near the joints affected; 
that pain is often present in the nerve trunks, as in neuritis, and that diseases of 
the central nervous system not rarely produce lesions in the joints which resemble 
those found in arthritis deformans. Certain French clinicians have claimed that 
definite lesions are demonstrable in the spinal cord, in the columns of Goll in the 
cervical level, and in the posterior nerve roots as well. The difficulty in accepting 
the neural theory is that there is no proof that these changes are primary and not 
secondary, for it is well known that many joint affections are followed by similar 
lesions, at least in the nerves, skin, and muscles. 

Most clinicians divide the cases of this disease into two classes: the primary, 
in which the arthritic state develops without any preceding joint affection, and 
the secondary, in which there is a history of such an infection. The primary 
cases are those in which the disease develops after a prolonged nervous stress or 
severe physical strain, as in frequent childbearing. The secondary form follows 
acute articular rheumatism and occasionally develops after injury to a single 
joint, although in this case the relationship of cause and effect is very doubtful. 
Even in the cases in which acute rheumatism has preceded the malady this 
relationship is in doubt, and there is nothing to prove that there exists any closer 
tie between them than sequence by coincidence. I have seen it develop in cases 
of bronchiectasis. 

Statistics as to the frequency of arthritis deformans in the two sexes differ greatly. 
In Garrod's statistics the disease affected 411 women out of 500 cases. Stewart 
has recorded 40 cases, of which 20 were in women; and more recently McCrae 
has reported 110 cases, of which 55 were women and 55 were men. My own 
experience at the Jefferson Medical College Hospital has been that nearly all are 
women. 

The greatest prevalence of the disease is between twenty and fifty years of age, 
but Moncorvo has collected 48 cases of polyarthritis deformans in patients under 
fourteen years. 

The disease is very rare in the negro race. In a clinic rich in negroes McCrae 
met with this disease in negroes only four times in 110 cases, which is all the more 
noteworthy because negroes are peculiarly subject to other arthritic changes. 

Morbid Anatomy. — What the changes are in the early stages of this malady is 
not known, because patients rarely come to autopsy until after the disease has 
existed for a long period. What little information we have indicates that the 
process is primarily inflammatory, in that the synovial membranes are injected 
and hyperemic. This is followed by the development of fibrous tissue, and this 
again by the absorption of the cartilaginous coverings at the ends of the bones. 
By these means cartilages become eroded and the ends of the bones become ebur- 
nated. Finally, there develops from the periosteum covering the ends of the bones, 



ARTHRITIS DEFORMANS 751 

bony growths or knobs which lock the joints and because of the thickened mem- 
branes and roughened cartilages increase the tendency to immobility already 
present. These osteophytes are called "Haygarth's nodosities." Associated 
with these changes there is marked wasting of the muscles which govern the move- 
ments of the joint, a wasting not rarely met with in all serious joint affections, a 
glossiness of the skin covering the affected joints due to atrophy of the glands in 
its deeper layers and to changes in the epiderm, and not infrequently trophic 
changes in the nails which may be greatly thinned, ridged, or very brittle. 

The changes in the vertebra? consist in overgrowth of the articular cartilages, 
followed by ossification. The ligaments also become thickened or atrophied. 
Bony formations may appear on the edges of the vertebrae, particularly on their 
anterior surfaces, and finally in this way the whole vertebral column becomes an 
inflexible pillar composed of vertebral bodies welded together. 

Symptoms. — The symptoms vary considerably in the manner of their onset and 
in the course of the disease in different cases. The mode of onset may take two 
forms: the slow 'progressive or gradual type and that type in which a series of attacks 
of articular distress occur which leave behind them more and more chronic change 
in the joints. In some patients the first complaint consists in a sensation of rough- 
ness in the knee-joint; the part feels stiff after it has been in one position for any 
length of time, and "cracks" when it is moved. Not rarely this is first noticed 
in going up or down stairs or in rising from a chair. If the joint is flexed by the 
physician who holds the limb, the cracking can be felt by him. The sensation is 
one of distress more than of pain. 

The tissues about the joint are often swollen, but rarely if ever reddened. Usually 
after one joint is affected another becomes involved, and, as the process gradually 
develops, the patient becomes more and more incapacitated owing to the advancing 
changes in the joints and the new areas affected. 

The atrophy of the muscles also increases the inability to move about with 
ease. 

Finally, the disease involves all the articulations, large and small, even the 
vertebral joints being affected, and the patient is as completely paralyzed from 
fixation as if suffering from a widespread multiple neuritis. Such a result, however, 
does not occur in most instances, the malady being less widely distributed. 

It is a noteworthy fact, for which patients with this disease have cause to be 
devoutly thankful, that in the cases with greatest fixation of the large joints the 
small joints of the hand often escape, and when the hands are severely affected it 
often happens that the large joints are not involved. In still other cases the 
disease after incapacitating one part ceases to be progressive. The frequency 
with which pain occurs in these cases is very variable. In some there is none, in 
others it appears only when the parts are used, as in piano-playing, and in others 
the pain is severe and like that of neuritis. 

Free sweating of the palms of the hands and finger-tips often is present. 

Because of the fact that the manifestations of the disease are often limited to 
one part of the body or to one kind of joints, it has been customary to divide the 
cases into those with only one joint affected, the mono-articular form; those in 
which several joints are chiefly affected, the polyarticular type; and those in which 
the spinal column is the chief seat of the disease, the so-called spondylitis type. 
When the joints of the fingers are chiefly affected, so that they are locked by the 
growth of small, bony knobs on the sides, these growths are called "Heberden's 
nodes." An important difference between these nodes and those due to the deposit 
of urates, as in cases of gout, is that they are true bony growths, and not due that 
the deposition of urate of sodium in the fibrous tissues. It is easy to see that this 
classification is purely one of convenience, and has no real pathological reason for 
its existence. 



752 DISEASES OF NUTRITION 

When the large joints are involved, with associated fixation of the spine, the 
patient lies in bed helpless, with the knees flexed and the back so stiff that it has 
been called "poker back." 

Under the name of spondylitis deformans von Bechterew has described a state 
of spinal fixation in which there is pain, compression of the spinal nerve roots, 
and muscular atrophy. Ascending spinal-cord degeneration is also present. It 
is questionable if this can be considered a part of true arthritis deformans. So, 
too, under the name spondylitis rhizomelique, otherwise known as the Striimpell- 
Marie type of spinal fixation, the muscles of the shoulder and hip- joints are involved, 
but severe nervous lesions such as those just detailed do not develop. Osier 
believes that both of these affections are forms of arthritis deformans. This may 
be a correct view, but, if so, they do not present any symptoms common to arthritis 
deformans as it is generally met with. 

A form of general arthritis without exostosis, but with considerable swelling 
of the joints, is sometimes met with in children. The lymphatic glands are dis- 
tinctly enlarged, the mobility of the joints greatly impaired, and the atrophy of 
the muscles well marked. Not only the lymph nodes nearest the joints, but all 
the lymphatics may be swollen. Anemia is marked. To this condition the name 
"Still's disease" has been applied, because it has been carefully studied by Dr. 
Still. Children may also have the polyarticular form of arthritis deformans as 
it occurs in adults. 

Attention must be called to that type of arthritis deformans in which the vertebra? 
suffer alone. In such instances the spine is fixed and immovable, the ankylosis 
producing so much rigidity that the patient in stooping can only bend at the hips. 
When in addition to fixation deformity takes place, the spinal column may be 
deflected laterally or posteriorly, and the arching of the back may be so great that 
the head is bowed till the chin nearly touches the chest and the patient can only 
see a short distance ahead by rotating the eyes upward. Lateral rotation of the 
head in such a case is often impossible. Associated with this form of vertebral 
arthritis there is often a good deal of pain, which may be felt not only in the back, 
but in the hips and even down the course of the sciatic nerves. In those cases in 
which the disease is limited to a small portion of the spinal column the case may 
be considered as one of tuberculous disease, and the only means by which a positive 
diagnosis can be reached is by the use of tuberculin, if no changes in other joints 
point to the malady now under consideration. 

Diagnosis. — When a well-developed, bedridden case of arthritis deformans is 
met with, the patient being "fixed," and the bony knobs locking the joints, the 
diagnosis is not difficult. The difficulty lies in the cases which are in the early 
stages of the malady. This is particularly true of the cases which are of the acute 
or subacute type, and which are ushered in by a somewhat abrupt onset, with 
soreness, stiffness, and pain in the affected parts. The differentiation of such cases 
in the first attack from a subacute form of true articular rheumatism may be 
practically impossible. If an endocarditis develops, the disease is probably rheu- 
matism, for the endocardium usually escapes in rheumatoid arthritis. Another 
point of differentiation lies in the fact that acute articular rheumatism passes 
from joint to joint, often diminishing in the first joints as the others are involved. 
This is also true of arthritis deformans, save that the joints first affected do not 
get well. The pain of rheumatism is greater and the parts affected are more tender 
to touch. Finally, if the articular difficulty persists week after week, in the face 
of the salicylates freely given, if the temperature creeps along at about 99°, and 
if there is crackling in the joints on flexion, the diagnosis of arthritis deformans is 
probably correct. 

Rheumatoid arthritis also must be differentiated from the arthritic changes 
due to gonorrheal infection and those of locomotor ataxia. 



CHRONIC RHEUMATISM 753 

Prognosis. — A well-developed case of arthritis deformans is absolutely incurable 
and the outlook is gloomy as to freedom of movement. The fact that the disease 
is often characterized by very slow progress and by periods of arrest is the most 
encouraging feature of these cases. 

Treatment. — From the stage of onset the treatment consists in the use of gentle 
massage of the joints with 50 per cent, ichthyol ointment, this ointment being 
also thickly smeared over the part between the times at which the rubbing occurs. 
If pain is present acetanilid or antipyrin may be used. If much stiffness is present 
the joint should be baked in a hot-air apparatus every day or two. Luff advises 
the persistent use of guaiacol, 5 to 20 grains, three times a day for months. The 
iodides may also be used. 

It is a vital mistake to give these joints rest as a part of treatment. Barring 
use to the point of fatigue the patient should be told to move the affected parts 
as frequently as possible. 

Fresh air and sunshine are essential factors in controlling the anemia often 
present. If a septic focus can be found, as in diseased tonsils, it should be removed 
and an autogenous vaccine employed, or if the infection is mixed, a mixed vaccine 
or mixed phylacogen. The patient should be well fed to aid him in combating 
the infectious process. A valuable remedy, one of the best we have, is syrup of 
the iodide of iron in 30 or 60 drop doses three or four times a day well diluted with 
water and taken two hours after meals. 

When deformity which interferes with movement is present it may be wise to cut 
contracted tendons, but this does not increase mobility of the joint, for obvious 
reasons. 

Many patients resort to hot springs and hydrotherapeutic institutes for relief 
from this disease. Such a plan of treatment is good for the general health and 
may seem to arrest the process, but it cannot cause a cure, and if the patient's 
means are limited it is useless to let him waste them in such a futile search for health. 

CHRONIC RHEUMATISM. 

Definition. — Chronic rheumatism is a condition characterized by a chronic 
low-grade inflammatory process in the synovial membranes and fibrous tissues 
about the larger joints which results in stiffness, soreness, and disability. It 
may or may not be a sequence of acute articular rheumatism. 

Etiology. — The causes of this state are unknown. In many cases it seems to 
be part of the general fibrous changes which occur in other parts of the body due 
to old age. Exposure to cold and wet, as in the case of soldiers, firemen, and 
policemen, seems to be productive of the affection. The malady is very common 
among old negroes. It often causes great crippling. 

Morbid Anatomy. — The chief change consists in thickening of the fibrous tissues 
about the joints, but there is little effusion, as a rule, and no deformity aside from 
immobility or fixation in an awkward position until secondary muscular atrophy 
ensues, as it usually does in all chronic joint affections. Occasionally the articular 
cartilages undergo changes and some crepitus can be felt on motion. 

Symptoms. — Stiffness and inability to move readily are the chief symptoms 
complained of. These are worse when there is a threatened change of weather. 
If sudden movement is attempted pain is caused. Rest increases the stiffness 
and exercise greatly decreases it, but, on the other hand, sufficient exercise to 
limber the joints is often very painful, either at once or because of the exaggerated 
degree of stiffness that may follow. Occasionally these patients, particularly 
if they be women, become exceedingly obese. 

Treatment.— Unlike arthritis deformans, this malady gives us the best therapeutic 
results, in many cases, if the patient can be subjected to the salutary influence of 
48 



754 DISEASES OF NUTRITION 

the Hot Springs of Arkansas, Virginia, South Dakota, Banff, in Canada, or at 
Bath, in England. The various sulphur springs are useful in many cases. When 
these springs cannot be resorted to the patient should have the affected joints 
baked in a hot-air apparatus, or should take a Turkish bath several times 
weekly. A well-constructed Turkish bath cabinet, such as is widely sold at 
present, may be used at home. A 50 per cent, ichthyol ointment should be well 
rubbed into the joints twice a day. This may be alternated with chloroform 
liniment containing 4 drachms of tincture of belladonna and 2 drachms of tincture 
of aconite in 8 ounces. In other instances iodine ointment diluted one-half with 
lanolin may be used. 

The use of drugs internally is not very satisfactory as to results. Pain may be 
decreased by acetanilid or antipyrin. The salicylates are rarely useful, but the 
iodides often cause great improvement. There is little use in dieting these patients. 
If they eat and drink sensible things the ordinary diet of health is the best. Alcohol 
should of course be used but little, if at all. 

Warm flannel should be kept next the skin, and cold winds avoided if possible 
by residence in a balmy climate in the winter months. 

MUSCULAR RHEUMATISM. 

Under the name of muscular rheumatism there exists a condition in which a 
patient experiences pain and stiffness when attempting to move certain muscles. 
This, condition is most frequently met with in patients who become chilled after 
severe exercise. It sometimes develops when certain portions of the body have 
been exposed to cold and wet, as, for example, the stiff neck which follows sitting 
in a draught of cool air or the lumbago which follows exposure to a storm. 

The exact cause of muscular rheumatism is not well understood. It has been 
claimed by some persons that the liquids of the body contain so large a quantity 
of toxic materials, produced by perverted metabolism, that when a part is exposed 
to cold precipitation of these toxic materials takes place, either in crystalline or 
amorphous form, and this causes stiffness and pain. The findings of Rosenow 
(see Acute Rheumatic Fever) indicate that this affection is a "rheumatic myositis/ ' 
due to streptococci closely related to those found in articular rheumatism. 

Treatment. — The treatment of muscular rheumatism depends somewhat upon 
the condition which has produced it. If it has followed exposure to cold, a very 
hot bath, a Turkish bath, or a hot pack will often serve to dissipate the pain and 
stiffness, particularly if after the bath active massage of the part affected is prac- 
tised. In still other instances, particularly if the onset of the condition has been 
very acute, relief is obtained by acupuncture. This consists in introducing into 
the substance of the affected muscle a long needle, which does good, it may be, 
by relieving tension in the sheath of the muscle, and allowing some of the serum 
to escape. In many cases relief is obtained by rubbing the affected part with 
chloroform liniment, to which may be added tincture of aconite, tincture of bella- 
donna, and tincture of opium. Equal parts of chloral and camphor, which deliquesce 
when they are mixed, may be rubbed over the painful area. Before giving medicines 
internally, the urine should be examined. If it is distinctly acid, the patient 
should receive from 10 to 20 grains of bicarbonate of potassium in water three or 
four times a day. In other instances similar doses of bicarbonate of sodium will 
prove equally efficacious. In still others it may be necessary to administer one 
of the salicylates. Thus, much benefit will often follow the use of 10 or 15 grains 
of strontium salicylate given three times a day. Often it is advantageous to 
combine with this 4 grains of acetanilid or the same quantity of phenacetin or 
antipyrin. In obstinate cases, or in those in which the symptoms frequently occur, 
the use of iodide of potassium or iodide of strontium in the dose of 5 or 10 grains 



RICKETS 755 

three times a day is advantageous, and sometimes the patient requires the additional 
use of jjf-Q of a grain of colchicine three or four times daily. It is not to be forgotten 
that some of these patients, particularly those that suffer from lumbago, owe their 
condition to auto-intoxication from the alimentary canal, which is due to constipa- 
tion, and in such patients permanent relief will not be obtained until the bowels are 
thoroughly moved each day. In some cases the use of one of the saline purgatives 
is all that is necessary. 

RICKETS. 

Definition. — -Rickets, or rachitis, is a nutritional disease of childhood, consisting 
in a general perversion of the processes by which normal growth takes place. It 
is chiefly characterized by imperfect osteogenesis. The ends of the bones are often 
larger than normal, and there is faulty growth in the cartilages, muscles, and 
tendons. 

Etiology. — Two factors are chiefly concerned in the production of rickets, namely, 
dietetic faults and bad hygienic surroundings. Of these the most important are 
errors in diet. On the other hand, it would seem that in some cases at least the 
diet may be correct, yet the faults in nutrition exist because the system cannot 
utilize the materials which are ordinarily employed in the production of normal 
tissues. The majority of children suffering from rickets improve as soon as their 
food is properly adjusted. 

In the article on Scurvy attention has been called to the fact that while rickets 
affects both rich and poor, it is chiefly seen in the latter class, whereas scurvy in 
infancy is frequently a disease of the well-to-do. In many cases, however, scurvy 
and rickets exist simultaneously. 

The most common fault with the diet consists in the use of proprietary foods 
for infants, in the use of condensed milk, and in the carrying on of lactation until 
the period is past when the child can obtain sufficient nutriment from a breast 
which is secreting a poor quality of milk. 

It is interesting to note in this connection that valuable observations have been 
made upon young animals as to the effect of depriving them of ordinary diet and 
providing them with one not suited to their needs. Thus, Bland-Sutton fed lion 
cubs with raw meat and rickets developed. When a diet of milk, cod-liver oil, 
and powdered bones was given them they speedily got well. Experiments made 
upon other animals have given like results. 

Edlessen holds that the disease is of infective origin. Mendel thinks it depends 
on some change (atrophy) in the thymus and has formulated a system of treatment 
based on the thymic origin of the malady. Spillman rejects the chemical theory 
and holds that the deficiency in lime-salts is a result and not the cause of rickets. 
There has been much unprofitable discussion as to the congenital origin of the 
disease. Fede and Finizio found, among 975 newborn, 4 that might have been 
called cases of fetal rickets; but most of the cases of so-called fetal rickets are 
instances of achondroplasia. 

Age and nationality are factors of some importance in the causation of the 
disease. Holt states that it is very common in the children of the poorer class of 
Italians found in all our large cities, and it is certainly very common in negro 
children. In both of these classes the race has not so much influence as poor food 
and bad surroundings. 

The disease is rarely met with in children over three years of age, but the signs 
of its existence often persist in the shape of bony deformities all through life. Cases 
of rickets have been reported in children at the time of birth and as old as twelve 
years. Both sexes suffer equally severely from it. 

Diseases which impair nutrition may predispose the child to the development 



756 



DISEASES OF NUTRITION 



of rickets, but they do not produce it. Thus, congenital syphilis may act as a 
cause, but is not directly responsible. 

Morbid Anatomy. — While it is true that we know little of the underlying cause 
of rickets, we have very clear and definite knowledge of its morbid anatomy. In 
healthy children the bones grow longitudinally by the development of bony mate- 
rials at the space between the diaphysis and the epiphysis, and in breadth by the 
deposition of bony materials by the inner layers of the periosteum. The medullary 
canal is increased in diameter by the gradual absorption of the adjacent bone. 
In rickets the process is abnormal in that although the development of cells at the 
points of growth may be carried on to excess, the deposition of mineral matter 
to form bone is inadequate. The resulting structure is softer in texture and more 
vascular than normal, that is the osteoid tissue is perverted (Fig. 126) . It happens, 
therefore, that while the length and breadth of the bone is being abnormally devel- 
oped, the lamellae adjacent to the medullary cavity are being absorbed, thus leading 
to structural weakness. Under these conditions it is not difficult to understand 
why it is that the bones are unable to bear the normal stress and rapidly become 
deformed if any strain is placed upon them. 



Fig. 126 



Fig. 127 





Rachitic epiphysitis, showing proliferated cells in the 
epiphysis. (Graupner and Zimmermann.) 



Syphilitic epiphysitis. 



Again, the process of development may be so abnormal that areas of bone are 
found in the midst of cartilage and far in advance of the edge of the normal bone 
growth, or the reverse holds true, and in the midst of bone there may be a carti- 
laginous mass with little mineral matter in it. 

Histologically there is excessive proliferation of the cartilages preliminary to 
ossification with irregular distribution of the columns of cells, excessive vascularity, 
and imperfect calcification. These enlargements seem particularly marked at the 
ends of the long bones and at the costal ends of the ribs and consist of this bone-like 
(osteoid) tissue, which later solidifies and perpetuates deformities of which it was 
originally the cause. 

In addition to the deformity of the long bones produced in this manner we find 
similar changes occurring in the bones of the head and pelvis. Not only do the 
fontanelles remain open for a longer time than is normal, but in addition the surfaces 
of the bones are found to be soft and porous and unduly vascular. In some places 
the occipital bone may be irregularly developed and spaces exist which are closed 
by membrane alone. This condition is called "craniotabes." The frontal bones 



RICKETS 757 

are often large and bulging, forming the so-called "bossy frontals" described by the 
English clinicians. 

The actual deformities which result are bending of the long bones, particularly 
in the legs ; the development of pigeon-breast, with an increase in the anteroposterior 
depth of the chest, and the production of spinal curvature. A very constant 
state is the presence of swellings or enlargements of the ends of the ribs where 
they join the cartilages, producing the knobs or the so-called "rachitic" rosary. 
The spleen and liver are increased in size and Mendel thinks this is compensatory 
for the loss of thymic functions. Mettenheimer and Friedleben describe atrophy 
of the thymus in rickets. 

Symptoms. — The symptoms of rickets, when the condition is well developed, 
are very characteristic and can scarcely be overlooked even by the most careless 
observer. In the earlier stages, however, the manifestations of the disease are 
not so evident, and yet they are important in that they should place the physician 
in a position in which he can prevent further advance of the malady. These 
early symptoms consist in sweating of the head, so that the child's pillow is wet 
with the perspiration, and restless sleep, with grinding of the teeth. Partly because 
of the wet pillow and partly because of lowered vitality, rachitic children are very 
prone to colds and often suffer from constant catarrh of various mucous surfaces. 
Constipation is usually a marked symptom. 

In addition to these symptoms a physical examination of the patient will reveal 
in some cases in the early stages beading of the ribs, that is, enlargement of the juncture 
of the costal cartilages and ribs, the so-called "rachitic rosary." The forehead 
may be full and large from the bulging of the frontal bones, the so-called "bossy 
frontals," already referred to, and the belly is bulging and tumid. 

If the condition is far advanced all these signs are more marked, and in addition 
there may be found wide-open fontanelles and soft spots in the skull due to cranio- 
tabes. This state of craniotabes is much more marked in those cases which suffer 
from syphilis, and some observers have asserted that it occurs only in children 
who have inherited this malady. Auscultation over the open fontanelles may reveal 
a humming murmur synchronous with cardiac systole. Anemia may or may not 
be a marked symptom. 

The nervous symptoms consist in laryngeal spasm (spasmodic croup) and great 
irritability. Epileptoid fits or tetany may develop. 

The shape of the thorax is also modified so that the lateral diameter is decreased 
and the anteroposterior diameter increased. This gives it a somewhat bulging 
or "chicken-breast" appearance. In the neighborhood of the ensiform cartilage 
there is seen, in some cases, a shallow depression of the costal cartilages and ribs, 
which extends outward and upward toward the axilla on both sides. This depres- 
sion covers the space of from one to three ribs and is called " Harrison's groove." 
It is chiefly due to protrusion of the lower ribs, which are pushed outward by the 
bulging of the abdominal wall. This deformity is most marked in children who 
suffer from spasmodic croup and obstruction of the upper respiratory passages. 
Palpation of the chest wall may reveal the fact that it is abnormally pliable or 
yielding. 

If the child is old enough to walk the long bones become deformed because they 
bend under the weight of the body. For this reason the bones of the legs may be 
bent and badly curved anteriorly or laterally. There may be posterior curvature 
of the spine. 

Dentition in rachitic children is usually considerably delayed, and is accompanied 
by gastro-intestinal disorders, chiefly because a tendency to catarrh of these parts 
is always present. The teeth when cut are usually fairly well developed and do 
not readily decay. This is in contrast to the history of syphilitic infants, who often 
cut their teeth abnormally early and then promptly suffer dental decay. 



758 DISEASES OF NUTRITION 

Several of the symptoms described, while often found when rickets is present, 
are by no means characteristic of this disease, and occur frequently in other con- 
ditions. These are the craniotabes of syphilis, the laryngeal spasm, the systolic 
cranial murmur, restless sleep, and grinding of the teeth. 

Diagnosis. — Rickets should be separated from scurvy, with which disease it is 
very nearly related, and which may be present simultaneously. In scurvy the 
nutrition of the mucous membranes and of the bloodvessels seems to be chiefly 
involved, hematoma and purpuric rashes often develop, and bleeding gums are 
seen. These lesions are practically never seen in rickets. There is great soreness 
on moving the child, and paraplegia is more commonly met with in scurvy, 
although in both states this palsy may be present. Again, the scorbutic child 
rapidly improves when given fresh orange-juice and beef-juice. Palsy may be due 
to acute anterior poliomyelitis, but if a careful study of the case is made it will be 
found in rickets that the muscular weakness is universal, whereas in poliomyelitis 
it is limited to certain groups of muscles and the associated rachitic symptoms are 
absent. 

Prognosis. — The prognosis as to life is good so far as the rickets itself is concerned. 
That is to say, death is never due to rickets. On the other hand, a child with 
rickets is a fair mark for every infection to which it may be exposed, and so the 
mortality of these cases from intercurrent maladies is high. If marked deformities 
exist they of course persist through life, except they be in the extremities, when 
they can be corrected by surgical procedures. 

Treatment. — From what has been said it is evident that the first thing to be 
done in a case of rachitis is to regulate the diet, and to see to it that the patient 
receives foodstuffs which contain all the ingredients which are necessary for the 
maintenance of normal nutrition. It not infrequently happens that the milk 
which is given to the child is lacking in mineral ingredients or contains such an 
excess of casein that the child's digestion is disordered and assimilation is disturbed. 
The mere fact that the child does not subsist upon market milk, but upon milk 
which is obtained by keeping a cow for the special purpose of providing sustenance 
for the infant, is more indicative of a dietetic cause for the rickets than if the child 
is obtaining milk which is given by a number of cows, for it not infrequently happens 
that the milk of a single cow disagrees with the child or does not contain all the 
materials which are necessary for its proper growth. If the child has been largely 
fed upon proprietary foods, these should be eliminated from the diet list and fresh 
milk and cereals used in their place. In some instances, as already stated, the 
rickets does not depend upon a lack of normal ingredients in the food, but upon 
the inability of the child to utilize these ingredients. This may depend upon 
digestive disorder, or upon a disturbance of trophic function. Under these circum- 
stances it is not only necessary to investigate the diet, but to administer tonics 
which will improve digestion, such as small doses of quinine, J to \ grain, twice or 
thrice a day; minute doses of nux vomica, or small quantities of the hypophosphites 
or the more modern elixir of the glycerophosphates. Of the latter 10 to 25 minims 
may be given twice or thrice a day. In other instances y^o g ram of phosphorus 
given in a sugar-coated pill may be used twice or thrice a day ; or in its place we may 
administer drachm doses of cod-liver oil, or cod-liver oil in the form of a well-made 
emulsion. 

If anemia is present 5 drops of the syrup of the iodide of iron may be given to a 
child of two or three years of age two or three times a day. As constipation is 
often a troublesome symptom in rickets, careful attention must be paid to the 
state of the bowels. They may be moved either by the use of a little calcined 
magnesia and followed by a few teaspoonfuls of orange-juice, or by one of the non- 
bitter preparations of cascara sagrada, such as aromatic cascara or cascara cordial. 

It is important that a child suffering from rickets should be allowed to have 



SCURVY . 759 

exercise without bearing weight upon its long bones. Such a child should not be 
encouraged to walk, but should be placed upon a rug on the floor, where it can 
crawl and roll about. An endeavor on the part of the parents to teach such a child 
to walk when its bones are unable to bear its weight results in deformities which 
may be so severe as to require operative measures for their relief. 

It is hardly necessary to add that fresh air and sunshine are essential in the care 
of such children. A few weeks at the seashore will often cause a remarkable 
change in nutrition; whereas the most skilful dietetic and medicinal treatment, 
if carried out with unfavorable hygienic surroundings, may produce no results 
whatever. 

In families in which rickets is prone to occur it is often wise to administer to the 
mother during the later months of pregnancy the hypophosphites or the glycerophos- 
phates, and other nerve and bone tonics, as by this means the antenatal nutrition 
of the child can be materially influenced. In a well-known case in Philadelphia 
the first three pregnancies resulted in the destruction of the mother's teeth and 
in the birth of children who speedily showed rickets; whereas, the last three 
pregnancies, during which a diet rich in mineral ingredients was provided, resulted 
in the birth of children who remained perfectly healthy. 

SCURVY. 

Definition. — Scurvy, or scorbutus, is a disease characterized by more or less 
profound nutritional changes in the body which are largely dependent upon the 
use of certain forms of unsuitable food. There may be extravasations of blood 
into the subcutaneous tissues, under the mucous membranes, and about the joints, 
and there is often great spinal tenderness when the disease occurs in infants. 

Etiology. — There can be no doubt that scurvy is due entirely to the use of food 
which fails to provide all the substances needed for the perfect nutrition of the 
body. Not only does it follow the continued use of food which is bad in the sense 
that it is unwholesome, but it arises in those who are subjected to a very limited 
diet of certain kind for long periods of time. Prior to the introduction of steamships 
it was a prevalent disease upon vessels in both the navy and in the mercantile 
marine, often disabling the crews and rendering impossible commercial and explor- 
ing expeditions. The use of steam now causes short voyages, and the better method 
of preserving foodstuffs provides a change of diet almost daily, if it be needed. 

In certain parts of Russia scurvy still occurs in epidemics and is thought to be 
infectious. If this be true it is probably only because lowered vital resistance 
permits an infection to take place. 

Some investigators have believed that the disease arises from a lack of vegetable 
acids found in fruits and vegetables, others that the condition is due to an excess 
of sodium chloride in the blood, and still others that it is due to the presence of 
certain toxic substances developed in the food. Albertoni has recently shown that 
in scurvy there is a complete absence of free hydrochloric acid in the gastric juice, 
that intestinal putrefaction is marked, and that the absorption of fats and car- 
bohydrates is impaired. 

Pathology and Morbid Anatomy. — Anatomically there is nothing characteristic. 
The condition of the blood in scurvy resembles that of the blood in ordinary 
secondary anemia with a decrease in the color-index which is quite marked. If 
the case is studied at autopsy hemorrhages into the internal organs and upon the 
serous surfaces of the abdominal and thoracic viscera are found and ulceration 
of the small and large bowel may be present. Swelling of the gums, loosening of 
the teeth, enlargement of the spleen, and degenerative changes in the heart, liver, 
and kidneys are found. Subperiosteal hemorrhages may detach the periosteum 
over the shafts of the long bones and hemorrhage into the joints may also occur. 



760 DISEASES OF NUTRITION 

Symptoms. — The symptoms of scurvy in adults begin with a sense of general 
wretchedness, pallor, and feebleness. These are followed by sivelling and sponginess 
of the gums, which may bleed if pressed upon, and which may partly cover the teeth 
by a process of granulation. The teeth become loosened, the mouth becomes foul, 
the salivary glands swell, and. petechia? appear over the surface of the body. The 
skin is dry and badly nourished, and extravasations of blood may take place into 
the sheaths of the muscles and joints or beneath the periosteum of the long bones. 
These lesions at times cause patches of hardness or induration in the muscles of 
the thighs or calves. I saw this well developed in an adult patient whom I had in 
the wards of St. Agnes' Hospital many years ago. 

Infantile scurvy, sometimes called "Barlow's disease," is an interesting result 
of modern life. As seamen have escaped the disease by a better diet, babies 
have fallen victims to it as a result of feeding them with artificial foods, and 
these babies are not, as a rule, the children of the poor, but the offspring of 
the rich. 

It is only within the last decade that the possibility of scurvy occurring in young 
children has been generally recognized by the profession. During this period, 
however, evidence has been presented which shows very clearly that scurvy is by 
no means a very rare affection in early life, and that it often manifests itself in 
such a way as to lead the physician to make a very erroneous diagnosis when the 
patient is first brought to him. 

Perhaps the most frequent error in diagnosis under these circumstances is that 
the child is suffering from muscular or articular rheumatism; this decision being 
reached by reason of the fact that the child seems to suffer great pain upon move- 
ment, and sometimes has a moderate degree of fever. 

The characteristic symptoms of scurvy in a young child, when they are well 
developed, are so pathognomonic that it is difficult to see how an error in diagnosis 
can be made if the physician is acquainted with the possibility of the occurrence 
of this disease. Like all diseases, however, instances are met with in which many 
of the characteristic symptoms are entirely absent, and it is not uncommon for 
the painful manifestations spoken of to be the only evidence of the malady. In 
still others, we find a peculiar spongy state of the gums, which tend to bleed when 
lightly touched, and which are frequently so swollen that teeth which have recently 
broken through the gum are speedily covered by the overgrowth of the mucous 
membrane, the edges of which, about the teeth, frequently look as if they were 
composed of tiny blebs of blood of a dark color. Another symptom of scurvy, which 
is by no means as constant, and yet which is equally characteristic, when it occurs, 
is the development of petechias in different portions of the body, very frequently 
about the ankles and feet. In still other cases subperiosteal hematoma develops 
with surprising rapidity, and as pain on movement and the development of great 
swelling are frequently first noticed after a fall or a blow, it not rarely occurs that 
the physician is led into the belief that traumatism is the cause of the illness, 
without recognizing the fact that it has played but a small part in causing the 
sudden development of a state which really indicates grave systemic conditions. 
It is true that these subperiosteal hematomata have been chiefly reported by French 
clinicians, and have been rarely seen in this country; whereas, on the other hand, 
considerable extravasations of bloody serum have been met with in the loose tissues 
after exposure to injuries which in the healthy infant would produce no symptoms 
whatever. Such a hematoma may have great medico-legal importance. Paraplegia 
may also be present. 

The peculiar characteristics of scurvy in infants are the very grave appearance 
of the child when suffering from the disease in its severe froms, the rapidity with 
which it improves under proper treatment, and the rarity with which death occurs 
as the direct result of the malady, since a fatality is usually produced by some 



SCURVY ■ 761 

intercurrent disease. Reinert has, however, recorded a fatal case with red cells 
at 976,000 and hemoglobin at 17 per cent. 

Scorbutus in infancy is distinctly a disease of the children of the well-to-do in 
distinction from rickets which, on the other hand, seems to be a disease of the 
poor. Clinical experience, I think, indicates that scorbutic cases are rarely brought 
to hospital dispensaries while rachitic cases are constantly seen. On the other 
hand, scorbutic cases are not uncommonly met with in private practice. This 
clinical fact seems to carry out certain theories which have been advanced in regard 
to rickets in a way which is interesting. It is not many years since everyone 
believed that rickets was due to a deficient quantity of bone-forming material in 
the food of a child, but since that time other clinicians have stated their belief 
that more commonly it depends upon inability of the child to assimilate and utilize 
the ingredients in its food which it needs for proper bone growth. Or, in other 
words, the fault lies not with the food, but with the child. Among the poor this 
inability is probably due to unhealthy surroundings and a general lack of sanitation 
which interferes with development. On the other hand, such influences. are not at 
work among the children of the well-to-do, but these children often receive, for 
long periods of time, the various artificial foods which, in many instances, they are 
incapable of digesting; and not only this, but no change is made in their diet for 
months, either in the quantity of the various ingredients which it contains, or in 
their quality. These children, therefore, suffer from the nutritive changes which 
come on as a result of a limited and fixed diet with no variation; whereas, the 
children of the poor, who often have too great a variation in their diet, rarely 
present scorbutic symptoms and often do manifest distinct rachitic symptoms. 

Diagnosis. — Physicians, in the presence of obscure illness occurring in early 
childhood, should remember the possibility of either one of these affections being 
the underlying cause for the manifestations of disease, and thoroughly investigate 
the question of diet before administering remedies, such as the salicylates for 
rheumatism, iron for the blood, or bromides for nervous irritation. 

As has been well pointed out by a number of writers, scurvy is not infrequently 
confused with rheumatism and rickets, and sometimes with various forms of specific 
arthritis. The loss of power may lead to a diagnosis of anterior poliomyelitis. 
So, too, cases are recorded in which a diagnosis of syphilitic epiphysitis, or sarcoma 
of the femur or osteomyelitis or deep abscess has been made when scurvy was the 
cause. The bloody urine of scurvy has given rise to a diagnosis of nephritis, and 
the bloody stools to one of dysentery or ileocolitis. The subcutaneous extravasa- 
tions of blood have also misled the physician into a diagnosis of purpura hemor- 
rhagica, and in one instance, to the writer's knowledge it is quite possible that the 
ecchymoses which were found on a child's body and which were thought to lend 
force to a charge of homicide, were due to this form of malnutrition. When pain 
and bloody extravasations take place in the abdominal cavity, the diagnosis of 
intestinal obstruction may be made if care is not exercised. 

Treatment. — The treatment of scurvy in adults consists in providing good and 
varied food, with plenty of oranges or lemons and green vegetables. Sunshine 
and fresh air are also essentials. Arsenic and iron may be given as hematics. 
If digestion is impaired it should be aided by hydrochloric acid and pepsin or 
lime-juice and pepsin. For the lesions in the mouth a chlorate of potash and myrrh 
mouth-wash (see Stomatitis) may be used. 

If the disease occurs in a child it is to be treated by changing the food and by 
using raw milk instead of sterilized milk. Beef-juice squeezed from a half-cooked 
steak and orange-juice are also very useful. 



762 DISEASES OF NUTRITION 

OBESITY. 

Definition. — The term obesity, or adiposity, is used to describe a state in which 
an individual suffers from an excessive deposit of fat in those parts of the body 
where a moderate amount of fat is found in health. In its advanced forms fat 
is also deposited in parts where it is never found in the normal state. 

Etiology. — It must be clearly understood that the mere presence of an unusual 
amount of fat does not in any way indicate ill-health or that the functions of the 
body are perverted. In many instances a considerable degree of obesity exists, 
because it is the natural state of the individual. In others, however, the deposition 
of fat in excess is a manifestation of disease or at least of perverted function. 

In the first class, of what may be called normally obese persons, the condition 
arises from inherited tendency. It is in this class that we find individuals who 
have never been heavy eaters and who for years have deprived themselves of foods 
of which they are fond, but still gained weight. In another class it develops from 
overeating and lack of exercise, and in the third class it is due to disorders of metab- 
olism, whereby foodstuffs are not properly dealt with by the economy after they 
are ingested. 

These three types are worth recalling, because when a patient seeks relief from 
obesity much depends upon the type to which he or she belongs, as to advice, 
prognosis, and treatment. 

Symptoms. — It is not necessary to describe all the symptoms of obesity, for the 
manifest increase in the size of the patient determines the diagnosis of an excess of 
fat. There are, however, certain other symptoms which are of importance, not 
only because they are part of the symptom-complex of obesity, but also because 
their presence determines the degree to which the excess of fat is really annoying 
or harmful. A symptom usually complained of by the patient is dyspnea on 
exertion, which arises from the fact that the heart and lungs are put under stress 
because great muscular activity is needed to move the heavy body. This dyspnea 
is also due to the fact that the vascular network is greater in the obese than in 
those who are lean, and therefore the heart has to drive the blood through a greater 
number of bloodvessels. Thirdly, the heavy deposits of fat on the chest walls, 
in the omentum, in the mesentery, about the diaphragm, and around the heart 
interfere, mechanically, with the free action of the respiratory and cardiac muscles. 
In many cases of severe obesity the layers of fat are projected between the cardiac 
muscular fibres, and thus seriously impede its movements, forming the so-called 
" fatty heart of the obese," which is, of course, a very different state from the true 
fatty heart of myocardial degeneration. The pulse is often small and rapid. The 
arterial tension is also lower than normal, as a rule. 

While many of these patients are mentally and physically slow and somewhat 
somnolent, others are active and restless and even unduly wakeful. 

Next to the dyspnea the chief complaint is of constipation or indigestion and 
excessive sweating. Some cases of obesity, however, have a digestive system all too 
good. 

In some cases, too, there is an excess of urates in the urine, and these cause 
vesical irritability, chiefly because the larger surface of the body and the free perspi- 
ration cause a great loss of fluid, and this in time results in a scarcity of urinary 
flow with consequent concentration of the urinary solids. 

Treatment. — The first point in treatment, as von Noorden has said, is to determine 
whether we shall diminish the fat already present or content ourselves with the 
prevention, if possible, of an increase in the obesity. As a rule, the patient is 
not content with a plan of treatment which does not actually diminish the fat, 
partly because he has delayed consulting a physician until the condition is far 
beyond what he desires. This is particularly the case with women who have 



OBESITY 763 

arrived at middle life and who begin accumulating weight at the time of late child- 
bearing, or in other cases immediately after marriage. These patients are often 
normally fat — that is to say, their condition is physiological — and they should be 
content in the majority of cases to try to prevent further obesity, rather than to 
remove fat already in existence. Such patients are often not unduly fat, and in 
their desire to maintain a " girlish figure" are willing to resort to almost any measure 
to become thin. Indeed, women in the fashionable walks of life, with little to 
think about, often make their lives miserable and destroy good health of mind and 
body by endeavoring, on the one hand, to get thin, or, on the other hand, to get 
stout. 

In such cases the physician should advise against severe measures, point out 
that the plumpness is natural, and, if need be, assert that it is better to be in good 
health, and a little more weighty than the average woman, than to be in bad health 
and slender. I have seen many splendid specimens of healthy womanhood made 
physical wrecks by ill-advised efforts to get thin. 

The great difficulty with all plans of treatment for the reduction of fat, in those 
women who desire to be slim for the sake of vanity, is that no plan can be so nicely 
adjusted as not to remove fat from where its presence is needful to good looks. 
With the decrease in the bulkiness of the hips and waist a hideous leanness of the 
chest and mammary glands ensues and leaves these parts covered with a skin 
thrown in wrinkles by disappearing fat, so that a well-preserved woman of middle 
age is soon converted into a hag. Further than this, pads of fat keep organs in 
place, and those who wilfully remove these pads may subsequently suffer from 
floating kidney, gastroptosis, uterine disorders, and constipation. 

There is a sad lack of knowledge on our part as to the metabolism of obesity and 
nutrition in general, and the patient and physician must be careful how they 
attempt to disarrange processes so intricate and important. 

On the other hand, it is often necessary to arrest a process which is manifestly 
excessive and in need of control. 

In young persons whose nutritive processes are still in a formative stage and 
who are obese, we should not reduce weight already present, but simply try to 
prevent an abnormal increase. This holds true of those persons in later life who 
give a history of having always been fat. It is very unwise to ignore this rule if 
advanced years are already upon the patient, for under these conditions the effects 
of age and the efforts at reduction may produce disastrous nutritional changes. 

The most favorable period of life for reduction in weight is from twenty-five 
to forty years of age. 

Before ordering a diet and mode of life the patient should be subjected to a 
very careful physical examination; the urine should be repeatedly examined, and 
the state of the heart and vascular system carefully noted. If the urine contains 
albumin and sugar a reduction treatment is contra-indicated, and if the heart is 
weak from myocardial degeneration and if the vessels are fibroid it is dangerous 
to institute a plan of this sort. 

When it is determined that the patient is in normal health as to his vital organs 
the treatment for the prevention of increase is to be instituted, the patient being 
informed that a good result cannot be reached by a sudden and rapid process, 
and that patience and persistence are necessary for really valuable results. 

The first factor is exercise taken to the degree of moderate fatigue. Many 
patients take it to excess, and then not only eat and drink heavily, but lie down 
and rest while the nervous system lazily permits vital oxidizing processes to go on 
too slowly, and so more weight is gained than lost. 

In many cases no material reduction in fat can be attained unless the patient 
can be treated in a sanatorium, or at least in some place where an absolute diet 
can be maintained for a long period of time. It is not sufficient to order a reduced 



764 DISEASES OF NUTRITION 

diet and but little to drink and much exercise. Such aids to reduction in weight 
will not in the ordinary case produce much improvement, because the patient is 
not willing to persist in the annoyance of such a strict diet for a sufficient length 
of time to establish a new nutritional abscissa. Unless the state of reduced weight 
is maintained for a long period the patient often gains more flesh on returning to 
the ordinary diet than if no attempt at reduction had been made. 

The order for actual reduction of weight consists in cutting from the diet list 
all sugars and sweet articles, all fats and richly prepared foods, and in the prescribing 
of lean meat, and of vegetables which are bulky but contain little starch. Celery, 
lettuce, string beans, spinach, cabbage, cauliflower, and limited amounts of tomatoes 
may be permitted; whereas potatoes, bread, peas, and beans are to be forbidden. 
All alcoholic drinks are to be avoided, because the alcohol has to be oxidized in 
the body and so prevents an active oxidation of the foodstuffs and tissues. Alcohol 
is also contra-indicated, because it stimulates the digestive organs and so increases 
the desire for food. 

If the avoidance of the fattening foods named above does not prevent an increase 
in weight, then a more rigid diet must be arranged. The patient is not to be given 
all the food he desires, but must suffer from privation and hunger. Instead of 
ordering an amount of food which will give the 2500 to 3000 calories necessary 
for comfortable existence, an amount calculated to allow about 2000 calories or 
less must suffice. 

For breakfast the patient is allowed 3 ounces of lean meat, 1 ounce of bread 
with no butter, and a cup of tea or coffee with no milk and no sugar, the sweetening 
being done by the use of saccharin. At an early luncheon a single soft-boiled egg 
may be given with an ounce of bread. At dinner a cup of clear soup, such as 
consomme or Julienne (but no thickened soup or puree), may be allowed, followed 
by 2 ounces of fresh or salt fish, and this by 2 or 3 ounces of lean meat. At this 
meal small quantities of the various green vegetables already named may be taken. 
The dessert should consist of some fresh fruit, such as an apple, an orange, a grape 
fruit, or a pear. In the middle of the afternoon a glass of milk or a cup of tea 
with a thick water cracker may be given, and at supper-time 3 ounces of lean meat, 
some lettuce with oil and vinegar, celery, 2 ounces of toasted bread or zweibach 
or crackers may be given. At bedtime a biscuit and a glass of milk may be allowed. 
While excessive drinking of water is unwise, the patient should not be deprived 
of water to such extent that he suffers from thirst or has not sufficient liquid in 
his body to carry out to the full every physiological function. Although overfilling 
the tissues with water will make the patient appear fat, a certain amount of fluid 
is necessary to healthy life. 

In the way of drugs there is but one remedy which exercises a great influence 
in reducing flesh, and that is the thyroid gland. This substance does not reduce 
the weight of all cases of obesity, and often fails unless it is given in doses which 
are so large as to cause distinct cardiac feebleness. The doses usually given vary 
from 2 to 6 grains of the extract of the gland once, twice, or thrice a day. It is 
important to give a large amount of nitrogenous food at the same time, for the 
thyroid causes a loss of nitrogenous tissue in the body as well as a loss of fat. Small 
doses of strychnine and of digitalis are also useful to protect the heart from depres- 
sion. The patient should be warned against severe exercise while using this drug, 
and often will do best if confined to bed and given massage and electricity. 

ADIPOSIS DOLOROSA. 

Under the name of adiposis dolorosa my colleague, F. X. Dercum, first described 
in 1 889 a condition in which masses of fat are deposited in different parts of the 
body, chiefly on the chest, arms, buttocks, and legs. These formations are usually 



SCLERODERMA 765 

symmetrical, and, as the name implies, are accompanied by neuralgic pains which 
vary from slight dartings to severe suffering. The disease is of unknown origin, 
and affects women in or past middle life, as a rule. The deposits on the extremities 
are usually firm and even brawny, but they may be so soft as to be pultaceous in 
character. So far the best results in its treatment have been obtained by the use 
of thyroid gland to the point of tolerance. The condition is quite uncommon, 
but a considerable number of cases have been reported. 

OSTEITIS DEFORMANS. 

Osteitis deformans is sometimes called "Paget's disease." It is characterized 
by enlargement and softening of the shafts of the long bones, by pain and deformity. 
The bones of the face are not affected, but the bones of the rest of the head are 
often involved. A careful examination of the long bones in a case of this kind 
reveals the presence of a rarefying osteitis associated with the development of 
new but imperfect lamellae in the bones. The face has a curious triangular appear- 
ance because of the broadening of the upper portion and the narrowness of the chin. 
By the yielding of the bones under pressure, not only the tibiae but the femurs 
also undergo great deformity, so that an extreme degree of bow-legs develops. 
Occasionally, the bending of these bones is forward or backward. There is also 
some spinal curvature. Osteitis deformans rarely develops before the fiftieth 
year. No treatment which has yet been discovered is of any value. 

HYPERTROPHIC PULMONARY OSTEO-ARTHROPATHY. 

This is a condition first recognized by Bamberger, but the name was given by 
Marie. It does not affect the bones of the head or of the face, nor the long bones 
of the arms or leg. In every instance it develops in association with chronic 
pulmonary disease, such as chronic bronchitis, bronchiectasis, fibroid lung, and 
chronic emphysema. • 

The symptoms consist in the enlargement of the hands and feet, particularly 
about the small joints. The growth of the nails is often influenced so that they 
are thickened and incur vat ed. 

LEONTIASIS OSSEA. 

Leontiasis ossea is a disease in which there is a development of multiple osteo- 
phytes or symmetrical enlargement in the bones of the cranium, and sometimes 
in those of the face. It is a very rare affection. 

SCLERODERMA. 

Scleroderma is a chronic disease characterized by localized or general stiffening 
or rigidity of the skin, which is usually pigmented, and which seems to be bound 
over the tissues beneath it in much the same manner that a leather cover is 
sometimes placed over a wooden or metal object. In some instances the scleroder- 
matous process is sharply circumscribed. In other cases it shades off into the 
surrounding tissues, and may have a slightly reddened edge. 

The first symptom usually noticed by the patient is stiffness of the part affected, 
which gradually increases until movement may become almost impossible. The 
skin undergoes atrophic changes, and becomes silvery and shiny in appearance, 
with a certain amount of yellowish or light-brown discoloration. When the disease 
affects the skin of the extremities, it may cause much interference with the move- 
ment of the large joints, and be followed by atrophy of the muscles underlying 



766 DISEASES OF NUTRITION 

the area involved. The lesions most commonly take place in the skin of the neck, 
in the neighborhood of the shoulders, and over the back and chest. It not infre- 
quently attacks the skin of the face. The general health is not seriously impaired. 
There may be some local discomfort, with a sense of formication, or tingling. The 
skin is exceedingly dry, and rarely sweats. 

Treatment. — In the way of treatment thyroid extract has been highly recom- 
mended by certain clinicians. Locally the parts should be treated by massage 
and the local application of oils, which should be of a sedative character. Occa- 
sionally, however, if the process is exceedingly chronic, it may be advisable to 
apply turpentine diluted with six times its amount of sweet oil. Even with the 
best of treatment the prognosis is anything but favorable as to cure, although the 
spread of the malady may be delayed. 



OCHRONOSIS. 

Ochronosis is an extremely rare disease characterized by the development in 
the sclerotic coat of the eyes of a semilunar patch of black pigment which does 
not, however, involve the entire sclera. A somewhat similar discoloration of the 
cartilage of the ears and of the tendons of the hands also occurs, and the urine is 
dark in hue at times, but by no means constantly. Sometimes there is an associated 
arthritis. The disease does not shorten life, nor impair the health, but in the 
presence of alkaptonuria, the copper-reducing substance, may mislead the physician 
into making a diagnosis of glycosuria or diabetes mellitus. Occasionally intense 
black patches develop in the skin and are distinctly limited in outline. 



AINHUM. 

Ainhum is a peculiar trophoneurotic disease, commonly affecting the feet of 
negroes and other dark-skinned races. It is widely distributed in Africa, particu- 
larly along the west coast, and it occurs in India, and Brazil. It is a rare affection 
among negroes in the United States. The disease usually begins in the little 
toe of one foot or both feet, as a narrow fissure or groove, on the plantar surface 
at the junction of the toe and foot. The groove surrounds the toe and slowly 
deepens until eventually it is amputated. Microscopic examination shows that 
the constricting band consists of dense fibrous tissue. As it tightens, the toe 
becomes very much enlarged, and disorganized before it finally separates. As a 
rule, the disease is confined to the one toe, although other toes may be successively 
attacked and the disease may even appear in the leg. 

The cause of this condition has not been determined. It has been ascribed to 
traumatism, such as frequent cuts from blades of grass. By some writers it has 
even been regarded as an expression of a very much attenuated form of leprosy. 
It is evidently a trophic disturbance. 

Treatment. — The treatment is surgical, and consists in free division of the con- 
stricting bands in recent cases and amputation in advanced cases. 



BERIBERI. 

Definition. — Beriberi is sometimes called Endemic Multiple Neuritis, and is a 
disease occurring in nearly all tropical and subtropical countries. The disease is 
associated with marked evidences of peripheral neuritis, with sensory and motor 
palsies, and profound alteration of the motor mechanism of the heart. 



BERIBERI 767 

History. — The recognition of beriberi as a distinct morbid entity is almost as 
old as recorded medicine. The first mention of it was made by Strabo, who de- 
scribes the development of this disease in the Roman armies operating in Arabia 
(24 B.C.). It is also described in the medical writings of the Chinese of the second 
and seventh centuries. It has occupied an important place in the histories of all 
colonizing powers. Dutch and, later, British observers recognized its peculiar 
nature in the beginning of the nineteenth century. Our later knowledge of the 
disease, particularly the recognition of the specific pathological lesions, is due to 
the labors of the German teachers, Scheube and Baelz, in Japanese universities, 
and of Wright and Durham, in the Malay Peninsula, and Herzog, Vedder, and 
Chamberlain in the Philippines. 

Distribution. — Speaking generally, the centres of greatest intensity of beriberi 
are the Malayan and in all rice-eating countries. It devastates the coolie mining 
camps and the plantations of the Malayan peninsula. It is always present in 
Japan, and in portions of the Philippine Islands it is very common. It has occurred 
in widespread epidemics throughout the whole tropical and subtropical zones. 
Within recent years it has been observed among Chinese fishermen from the Alaskan 
coast; by Currie and by Bailey in a settlement of Japanese at Cumberlands, British 
Columbia. 

Etiology. — The studies of Fraser and Stanton in 1909 in the Federated Malay 
States, and more especially those of Strong and Crowell in the Philippines, have 
definitely proved that the cause of beriberi is due to starvation of the body of 
certain substances found on the surface of rice grain and which is lacking in polished 
or cleaned rice. If non-polished rice is used it does not occur, nor does it take 
place if meat and potatoes are added to a diet of polished rice. 

Heiser points out a ready method of determining whether rice is polished and 
therefore lacking in P 2 5 , namely, that grains of rice which are polished and contain 
less than 0.4 per cent. P 2 Oo will stain deeply with Loeffler's methylene blue or 
Churchill's iodine, whereas, if not polished they stain only slightly. 

Frequency. — Beriberi is observed much more frequently in males than in females; 
not because there is any greater susceptibility in the male, but because women form 
a comparatively small number in coolie camps, jails, prisons, and ships. With 
respect to age, beriberi may be said to be a disease of early adolescence and adult 
life, but it occurs in infants who are at the breast of mothers suffering from this 
malady. The great majority of cases occur between the twentieth and fortieth 
years. 

Beriberi is chiefly a disease of the yellow races, occurring principally in prisoners. 
At the present day beriberi is very rarely observed in Europeans and North Ameri- 
cans. The white races enjoy a nearly complete immunity, due in part to the better 
nutritional conditions under which they live. 

Pathology and Morbid Anatomy. — When death occurs rigor mortis is usually 
severe if the disease has been rapid. In slow cases it is often slight. If the case 
be recent and acute, or if death be due to cardiac paralysis, the cadaver bears all 
the evidence of intense dyspnea and cyanosis. The eyes are staring, the conjunctiva 
suffused with blood, the cervical veins tumid and full, the lips covered with bloody 
froth. In the atrophic cases there is very considerable wasting. In the dropsical 
cases the effusion is commonly associated with huge thoracic, pericardial, and 
abdominal dropsies and edema of the lungs. In acute cases marked congestion 
of the pyloric end of the stomach and of the duodenum with punctiform hemor- 
rhages is found. The duodenal glands are swollen and congested. Wright con- 
siders this to be specific lesion of the disease, and states that it is always found when 
the case ends fatally within three weeks of the beginning of the disease. 

The liver and kidneys are enlarged, hyperemic, and show cloudy swelling. The 
spleen is enlarged, but otherwise shows no characteristic changes. The heart is 



768 DISEASES OF NUTRITION 

enlarged, the principal changes being found in the right side. The ventricle is 
both hypertrophied and dilated. Microscopically there is usually marked fatty 
degeneration of the myocardium. Chicken-fat clots are commonly found in 
chronic cases. The intrinsic nerve cells of the heart show marked atrophic changes. 
The terminations of the vagus are also atrophied. The trunk of the vagus is 
not involved in early cases, but in later cases the trunk of this nerve as well as the 
splanchnics and phrenics are profoundly degenerated. The peripheral nerves 
show striking and constant changes. These begin with degeneration of the terminal 
branches of the nerves. Not only the muscular but also the cutaneous twigs, 
and in advanced cases the main nerve trunks, may be involved. The nerve changes 
are present in proportion to the extent and intensity of the paralysis during life 
but they are always degenerative and not inflammatory in type. 

The voluntary muscles show distinct changes in the distribution of the degenerated 
nerves. The muscle fibres undergo fatty degeneration, the striations disappear, 
the nuclei are enlarged, and the interstitial connective tissue may be increased. 
The central nervous system shows congestion of the brain meninges and cord, with 
increase in the cerebrospinal fluid. Degenerative changes can be found in the 
posterior ganglia, and sometimes atrophy of the posterior columns is present. 

Symptoms. — Clinically, several types of the disease are recognized. There are 
atrophic cases (paraplegic or dry beriberi), dropsical cases (wet beriberi), acute 
pernicious cases, and mild or rudimentary cases. These classes represent not only 
variations of type, but variations of intensity. 

The disease is usually ushered in by marked prodromata. There is loss of 
appetite, with severe pain in the epigastrium and oppression in the chest. With 
these symptoms there is a slight febrile rise. In a few cases rigors, lassitude, 
mental disturbances, and head pains are observed. 

Atrophic Cases. — After a few days or weeks the patient notices a slowly increas- 
ing weakness of the legs, with pain and tension in the calf muscles. There is next 
a loss of sensation in the soles of the feet. The patient does not "feel" the floor, 
or feels as though a soft insole had been placed between the foot and the shoe or 
sandal. This increases until the patient becomes bedridden. As a rule, the palsies 
are confined to the legs and trunk, sometimes invading the arms, and very rarely 
affecting the head and neck. The paralyzed limbs rapidly atrophy and areas of 
anesthesia and hyperesthesia develop. Examination shows the superficial reflexes 
preserved; the deep reflexes lost. The calf muscles and extensors of the legs are 
extensively wasted. The palsy is nearly always flaccid, may be quite profound, 
and is more marked in the extensors than in the flexors, resulting in wrist-drop 
and paralytic equinovarus. The electric muscle reactions are markedly altered. 
From the beginning there is marked diminution, going on to total loss of reaction 
to both galvanic and faradic stimulation. 

The sensory symptoms closely parallel the distribution of the motor symptoms, 
and are even more constant. Spots of anesthesia and paresthesia are formed on 
the feet, calves, legs, trunk, and arms. Recovery from the condition is extremely 
tedious. Gradually the areas of hyperesthesia disappear, sensation and motion 
return, and in the course of ten to twelve months the atrophied muscles regain 
their contour. 

Dropsical Cases resemble the atrophic cases plus marked cardiac phenomena 
with dropsy. Sometimes the dropsical cases develop from the atrophic. The 
dropsy begins in the feet and legs and spreads until the whole body is affected. 
The face and lips are puffy and heavy. The arms, legs, and trunk are pudgy. 
With this there are marked evidences of cardiac distress. There are cyanosis of 
the lips and fingers, dyspnea, and a marked sense of oppression in the precordium. 
Usually the patient is quite helpless, or, if he can walk, the slight exertion is attended 
by breathlessness and palpitation, these symptoms being very much increased 



BERIBERI 769 

by effusion into the serous cavities. The urine is greatly diminished, but contains 
no albumin. After persisting for weeks or months the dropsy may rapidly dis- 
appear, with an enormous increase in the urine. As a rule, these cases do not 
present the extreme grades of paralysis and atrophy that are found in the first 
type. Yet the absorption of the dropsical fluid will reveal marked wasting that 
may have been completely masked by the semisolid appearance of the 
effusion. 

In both types of cases the cardiac changes are marked. The pulse rate is usually 
increased and slight exertion serves to further increase the rapidity to 120 to 140 
beats per minute. The heart is enlarged, particularly on its right side. The caro- 
tids pulsate violently and in the severe cases pulsation is seen in the jugular veins. 
Systolic and diastolic murmurs are heard, the murmurs being propagated very 
widely, sometimes even into the bronchial and femoral arteries. Reduplication 
of the sounds is frequently heard, and there is equal spacing between the sounds. 
Despite the forcible cardiac beat and the violent pulsation in the vessels of the 
neck, the peripheral pulse is remarkably small and weak. All these cardiac pheno- 
mena are exceedingly fugitive. Even the most pronounced murmurs and evidences 
of dilatation come and go with rapidity. 

Acute Pernicious Beriberi. — This form attacks, as a rule, the more vigorous 
adults. It may appear as an acute type from the very beginning, or it may repre- 
sent a sudden, fatal episode in mild or convalescent cases. Beginning in the ordi- 
nary way, the disease advances with great rapidity, so that the man becomes bed- 
ridden in a few days. The symptoms of cardiac involvement begin early and are 
marked. When this type develops from the milder forms of the disease the change 
is very sudden. Palpitation and dyspnea become more and more severe. The 
patient gasps and struggles for breath. He complains of extreme pain in the pre- 
cordium. He breathes with tremendous, laboring, gasps. The vessels of the neck 
pulsate violently. The eyes are suffused and staring. A blood-flecked foam 
collects on the lips ; unless speedily relieved the patient dies a most dreadful death. 
In these cases the urine is notably diminished or even suppressed. Nausea and 
vomiting are common toward the end. 

Mild and Rudimentary Beriberi of all degrees are observed. These cases 
usually complain of pain and tension in the legs, with weakness and numbness. 
The anesthetic areas may be very small and sharply marked. The patient usually 
develops some degree of cardiac irritability and palpitation. There may or may 
not be edema of the legs. These cases are important because here and there a very 
mild case may suddenly develop an acute pernicious cardiac attack. As a rule, 
however, they clear up completely, rarely lasting over the cool season. 

Special mention should be made of the skin symptoms. Petechia? and herpes 
of the lips are very common in beriberi, as is also a diffuse or blotchy redness in the 
arms and legs. After the very beginning of the disease there is no fever. A 
marked rise of temperature means a reinfection or the development of some 
complication. 

The blood shows no characteristic nor, indeed, any marked changes in beriberi. 
As a rule, there is a very moderate diminution of the red cells. In severe and long- 
continued cases the anemia may become more marked, with some considerable 
loss of hemoglobin, the color index being minus. In the average cases there is no 
change in the white corpuscles. In severe cases a moderate leukocytosis is found. 
The bacteriological findings are negative. 

The urine shows very little change. The urea is diminished, and, as a rule, 
the specific gravity is also decreased. Sugar and albumin are not found. Indican 
is present in large amounts (Baelz). The urine is diminished in quantity in the 
pernicious cases, even to complete suppression. In the cases of wet beriberi the 
urine is greatly diminished. The secretion is re-established when the exudations 
49 



770 DISEASES OF NUTRITION 

begin to be absorbed. Under these circumstances an unusually large amount of 
urine may be passed, and this re-establishment of the renal function is a very 
favorable prognostic symptom. 

Diagnosis. — When the cases occur in groups of rice eaters, the symptoms of 
peripheral neuritis point to nothing else. In isolated cases, however, the diagnosis 
is not by any means easy, and the distinction between arsenical or alcoholic neuritis 
and beriberi may be difficult. The presence of edema is significant of beriberi. 
The earlier and more decided alterations in the deep reflexes and the palpitating 
and irritable heart also point to beriberi. 

Prognosis. — The percentage mortality of beriberi depends on the pernicious 
cases. The latter are almost always fatal and furnish certainly 90 per cent, of 
the total mortality. In the remaining cases the mortality varies widely in different 
epidemics. Ten per cent, would be a very fair average mortality, although it 
may run as high as 40 per cent. There is, however, no disease in which prognosis 
is so uncertain and hazardous. Again and again cases considered practically well, 
certainly out of all danger, die with rapidity in the appalling cardiac crisis of this 
disease. The prognosis is favorable, without regard to the extent of the paralytic 
lesions, in proportion to the integrity of the innervation of the heart. Increase of 
the urine is a favorable sign. So, too, are return of appetite and sexual desire. 
On the other hand, increasing irregularity of the heart ; equal spacing of the cardiac 
intervals, the short and long pause becoming equal or nearly so; increasing cyanosis, 
paralysis of the diaphragm, and diminishing urine are very unfavorable signs. 
The presence of bronchitis, pneumonia, dysentery, alcoholism, and icterus are 
unfavorable. Vomiting is as sinister a symptom in beriberi as is black vomit in 
yellow fever. 

Treatment. — The main point in treatment is to provide an ample diet, easily 
digested, of barley, unpolished rice and meat or meat extracts. Chamberlain 
and Vedder have shown that in infantile beriberi 20 drops of extract of rice polish- 
ings a day produced remarkable betterment. Vedder and Williams of the United 
States Army in the Philippines have found rice polishings to contain a neuritis 
preventing substance, or vitamine, which when given to persons ill of beriberi 
produces a cure. The unhydrolyzed extract is a specific in wet beriberi and also 
in cardiac cases. This extract does the paralytic cases little good but these cases 
are in time cured by the use of a crystalline base from the polishings. Apparently 
the polishings contain at least two protective or curative substances. 

For cardiac cases, particularly those with dropsy, digitalis is the best remedy. 
It must be given freely in large doses. This remedy should always be readily 
accessible in beriberi wards. If the symptoms of cardiac failure become severe, 
the patient should be bled. It will frequently be found impossible to bleed 
at the elbow, under which circumstances the patient should be bled from the 
jugulars. About 400 c.c. should be drawn. The relief from this measure is prompt 
but evanescent, but, as Manson says, " the patient is for the time being tided over 
an acute danger and given another chance." 

The patient should be put on a liberal diet scale in which nitrogenous foods 
and fats form a conspicuous part. He should be kept in a dry, sunny room, and 
whenever possible should be out of bed in the open air. 

The treatment of the residual palsies is the same as that of any other form of 
severe polyneuritis. 



INTOXICATIONS. 



ALCOHOLISM. 



Definition. — By alcoholism is meant a condition in which the patient suffers 
from the effects of alcohol when taken in sufficient quantities to act as a poison. 

Etiology. — An idea exists among the laity that chronic alcoholism is a manifesta- 
tion of an inherited tendency in many instances, and this is sometimes offered as 
an excuse by a patient for his unlimited libations. There is no such disease as 
alcoholism, nor does an alcoholic have any justification in this excuse. The ten- 
dency to consume alcohol is not an inheritance. The inheritance is a lack of self- 
control, a cowardly inability to meet the hard sides of life, and a willingness to 
escape, if only for a time, by drowning sensation in the stupor of a narcotic. In 
many cases, therefore, we may not only have to combat a habit, but a state of 
degeneracy which permits a habit to exist. 

Symptoms. — Alcoholism may be divided for readiness of consideration into the 
acute and chronic form. 

Acute Alcoholism. — The symptoms of the acute form are familiar to everyone 
who sees life in the town or city, and consist in disorderly conduct due to removal 
of the inhibitory functions of the brain, so that every silly thought or foolish idea 
is carried out in action. Later, as the drug affects the muscle sense, and conse- 
quently disorders co-ordination, the individual staggers and perhaps falls, and finally, 
if the quantity of the drug is adequate, passes into a deep sleep, or coma, from which 
he wakes more or less confused, with depression of the nervous system and a dis- 
ordered digestive tract. In cases where the dose has been very large, death may be 
caused by depression of all the vital functions, of which the one most involved 
is bodily heat, the death being in part due to cold. In the majority of cases, 
however, in which death follows acute alcoholism, it is due not directly to the 
depressing effects of the alcohol, but to the fact that the lowering of temperature 
and the disorder of vital function in the various organs permits infection by the 
pneumococcus to take place so that pneumonia causes death, or some complication 
such as acute nephritis is developed. 

The symptoms of profound acute alcoholism are pallor of the face, dulness of 
the eyes, widely dilated pupils, profound unconsciousness, stertorous breathing, and a 
temperature several degrees below normal. Occasionally convulsive attacks may 
develop. 

Although the symptoms of acute alcoholism are so familiar, there is no state so 
often confused with conditions of disease or with the results of injury. This is 
due to the fact that the symptoms of acute alcoholism are much like those of cerebral 
congestion, apoplexy, uremia, or hemorrhage from a meningeal artery, or fracture 
of the skull. It is also due to the fact that alcohol often causes all these states 
directly or indirectly, and as there is a history of alcoholism or an odor of alcohol 
on the breath, it is natural to make a diagnosis of alcoholism without recognizing 
that another condition is present. Again, it not rarely happens that an alcoholic 
takes a poisonous dose of opium, and so suffers and dies from the effect of this drug. 
The raised temperature in apoplexy is in contrast to the lowered temperature of 

(771) 



772 • INTOXICATIONS 

alcoholism, as is also the full-bounding pulse as compared to the rapid-running 
pulse of alcoholic poisoning. Again, apoplexy is characterized by hemiplegia 
and facial palsy. Opium poisoning is characterized by pinpoint pupils, slow 
breathing, and a warm skin, as opposed to the normal or relaxed pupils, the cool, 
moist skin, and the normal or rapid breathing of alcoholism. 

Treatment. — The treatment of acute alcoholism consists in the administration 
of an emetic to empty the stomach of any alcohol still unabsorbed. Apomorphine 
is probably the best drug for this purpose, as it can be given hypodermically, acts 
promptly, is sedative in its influence, and is safe in a moderate emetic dose of f 
grain. In other cases, or after the emetic has acted, an active cathartic, such as 
30 grains of compound jalap powder or 15 grains of compound extract of colocynth, 
may be used to unload the bowels and portal system, and decrease cerebral conges- 
tion. If circulatory feebleness is present, the aromatic spirit of ammonia in drachm 
doses, diluted with water, may be given. In other cases the physician must give 
full doses (yV grain) of strychnine by the mouth, or by the hypodermic needle if 
depression is marked, and hot bottles must be applied to maintain body heat. 
Strong black coffee by the mouth or by the rectum may be given if active stimula- 
tion seems needful. The effects manifested on the next day are to be removed by 
the use of calomel, followed by a saline purge and the administration of elixir 
of celery and guarana, or, if the patient is very nervous, by the use of guarana and 
bromide of sodium, 5 grains of the extract of the former and 30 grains of the latter 
at a dose. 

Subacute and Chronic Alcoholism. — Chronic alcoholism is divisible into three 
classes. In one the patient suffers from a prolonged alcoholic debauch lasting 
over days, or even weeks, during which time he is never completely sober. In the 
other type he is never drunk, but always under the influence of the drug to an 
extent which eventually produces a train of symptoms even more grave than those 
which follow a debauch. Those who have made a special study of alcoholism 
also recognize that there is a certain class of persons, of the first division just named, 
who take no alcohol for a comparatively long period, varying from weeks to months, 
and then go on a terrific debauch, the so-called "periodical drunkard." It is the 
individual who takes alcohol up to the stage of intoxication for several days consecu- 
tively, and who has often used alcohol in large quantities for weeks before the acute 
exacerbation, who most commonly develops delirium tremens; while the constant, 
moderate "soaker" is more prone to hepatic cirrhosis and affections of the periph- 
eral nerves. Delirium tremens is very prone to develop in persons who are the 
subjects of subacute or chronic alcoholism if, perchance, they suffer from a severe 
injury, surgical operation, or great shock. Not rarely the onset of an acute illness 
may precipitate an attack. 

Morbid Anatomy. — The morbid changes produced by the continuous use of 
alcohol in excess are chiefly found in the organs by which the drug gains access to 
and egress from the body; that is, the stomach, the liver, and the kidneys. Next 
to the effect of the drug upon these organs it expends its deleterious influences 
upon the circulatory system. The passage of alcohol directly to the liver from 
the stomach through the portal vessels causes congestion, irritation, and finally 
atrophic cirrhosis of this organ. (See Hepatic Cirrhosis.) By reason of the direct 
effect of the drug upon the stomach, and the indirect effect produced by the impair- 
ment of its blood supply, which arises from the hepatic changes, chronic gastric 
catarrh develops. The changes found in the kidneys in very chronic alcoholism 
consist in a condition practically identical with that found in contracted kidney, 
and with this state an arteriocapillary fibrosis develops, just as it does in cases 
of cardiovascular changes arising from other causes. The most common change 
in the kidneys, however, consists in a hypostatic congestion, or stasis, which causes 
them to be swollen, cyanotic, and to be functionally inactive. Not rarely these 



ALCOHOLISM 773 

patients develop acute tuberculosis, because of their lowered vital resistance. 
An alcoholic multiple neuritis may develop, and atrophy of the optic nerve may 
occur. 

Symptoms. — The symptoms of delirium tremens are great nervous restlessness 
and apprehension with anxiety, and finally delusions of persecution and terror. 
The delusions are largely those connected with vision, and all sorts of hideous 
objects are described as crawling about the patient. Because of these delusions 
the patient is often violent and difficult to control, but is rarely offensive unless he 
believes that the attendant is in league with the "objects of evil" about him. The 
pulse is usually rapid and feeble, the skin relaxed, and the tongue exceedingly foul. 
The bowels are constipated and the urine scanty. Hypostatic congestion of the 
lungs and congestion of the kidneys are very commonly developed, and these states 
often contribute to the death of the patient. 

It is not to be forgotten that acute croupous pneumonia at the apex not rarely 
is associated with an acute delirium not unlike that of delirium tremens. 

In that form of chronic alcoholism in which the patient is never drunk, but 
always has alcohol in his body, the chief symptoms are irritability of temper, 
gradual mental deterioration, localized sensory and motor palsies, and finally 
dementia. 

Treatment. — The treatment of this state consists in the use of an active cathartic, 
as already advised for acute alcoholism, and the use of full doses of morphine 
hypodermically, if the kidneys are not diseased, to produce nervous rest if the 
patient is becoming exhausted by his lack of sleep or struggling. Care must be 
taken that more than a few doses are not given, for such a patient may become a 
morphine habitue very quickly. Strychnine and atropine are to be used hypo- 
dermically if any signs of pulmonary congestion arise, and they must be given 
boldly. Dry cups should be applied to the back of the chest, and Hoffmann's 
anodyne is useful as a rapidly acting diffusible stimulant. Every measure must 
be taken to disperse and prevent the congestion, which, if it develops in full degree, 
means the death of the patient. 

The question as to the medicinal use of alcohol in these cases is debatable. In 
those who are not accustomed to its constant use, and who may have been intoxi- 
cated for but a few days, it is not necessary to give the drug; but if the patient has 
been in the habit of taking alcohol in considerable amounts prior to his acute 
alcoholic outbreak, whiskey must be used freely in many cases if signs of great 
nervousness develop. Aside from pulmonary and renal complications the most 
frequent one, and a most fatal one, is a state of nervous tension in which the symp- 
toms are those of meningeal irritation with stiffness of the limbs and neck. This 
stage of tonicity in the muscles is preceded by muttering delirium, with periods 
of wakefulness in which hallucinations may make the patient difficult of control. 
The pupils are contracted and the pulse rapid and feeble. The temperature is 
often as high as 103° or even 104°, and not rarely hypostatic congestion of the lungs 
can be found if the bases are examined. Marked hyperesthesia of the skin usually 
exists. Patients with these manifestations usually die, but they may recover 
after a prolonged illness lasting several weeks. My experience is in accord with 
that of Dana, that if there is stiffness of the cervical muscles the patient usually 
dies. This condition is not due to a true meningitis, but to a toxemia with serous 
effusion into the meninges. Dana and others have given the name "wet brain" 
to this condition. 

The diet, if food can be given to the patient, should consist of hot and stimulating 
liquid nourishment, such as highly seasoned beef-tea or peptonized milk, to which 
capsicum and salt have been added to stimulate the digestion to activity. The 
various highly seasoned broths are useful. 



774 INTOXICATIONS 

The treatment of the alcoholic who continually takes the drug day in and day 
out presents grave difficulties. Those who have been wont to take this drug 
every day for many years are rarely willing to put up with the discomfort which 
follows abstinence, and after a few days almost invariably return to the use of 
alcohol. The only treatment which is of any value in such cases is to send the 
patient to some isolated region where he is too far removed from the grog shop to 
be able to obtain alcohol when his desire for it arises, and to take care that he does 
not provide himself beforehand with alcohol to be used during the trip. Usually, 
if the man is well-to-do, several weeks or months of hunting in isolated regions, 
and in the company of someone who does not drink alcohol and has considerable 
mental force, will be the best means of cure. 

For those who take alcohol more or less constantly to the point of intoxication, 
either this measure can be employed or the patient may be placed in a private 
room in a hospital, where he is under absolute control of the nurses and physicians 
attached to the institution, and the alcohol can then be immediately stricken 
off the list of permissible articles, or, if his condition is one of feebleness, it can be 
gradually diminished so that at the end of a week he is getting none of it. In 
the great majority of instances it is utterly futile to attempt home treatment of 
these cases. Even if the family can prevent the man from getting alcohol, home 
life lacks the discipline which is necessary for the control of the patient, not only 
in the sense of preventing him from procuring alcohol, but in the sense of making a 
powerful mental impression. 

In those cases in which removal of alcohol causes nervous excitation and evidences 
of threatened delirium tremens, it is occasionally permissible to administer full 
doses of chloral and the bromides to produce nervous quiet at night. Small doses 
of these drugs practically have no influence whatever, and if the heart is at all 
feeble full doses of chloral are dangerous. Morphine possesses the disadvantage 
that the alcoholic is very prone to develop the morphine habit in addition to his 
alcoholism. This drug is, however, exceedingly valuable if used on those occasions 
when the violence of the patient's nervous symptoms demand sedation. It should 
not be given day after day, but only occasionally, when insomnia is so pressing 
that the consequent exhaustion demands relief. 

Within the last few years very strong claims have been made for the use of 
hyoscine for the purpose of relieving the nervous irritation and craving for alcohol. 
The drug must be given in sufficiently large doses, hypodermically, to place the 
patient deeply under its influence. If necessary as much as yito of a grain every 
two hours may be given hypodermically until the patient sleeps or is resting quietly. 
These doses, of course, produce the full physiological action of hyoscine and often 
cause great dryness of the mouth and talkative delirium. They may be continued 
for several days and then gradually remitted until the patient is no longer taking 
either alcohol or hyoscine. 

If the circulation fails in these cases strychnine and digitalis may be administered. 
For the purpose of combating signs of acute collapse Hoffmann's anodyne and 
strychnine are valuable, as is also the aromatic spirit of ammonia. Another drug 
which has been highly praised in this condition is apomorphine given in the dose 
of ^o of a grain hypodermically as a nervous sedative, the emetic effect of the drug 
not being desired. In some instances larger doses have to be given and may be 
used without producing emesis. 

It must be constantly borne in mind that the most important portion of the 
treatment consists in the isolation of the patient, and in a complete control of 
his methods of life for the period covering several weeks. Drugs are of little value 
except to support him through the period when his system lacks his customary 
doses of alcohol. If the patient is unwilling or unable to resort to this form of 
treatment, the employment of drugs is usually worse than useless. 



MORPHINISM 775 

Careful attention to the digestive system is needful in all these cases. The 
liver should be unloaded by blue mass, followed by a saline puige, every few days, 
and bitter tonics, such as gentian with bicarbonate of sodium, are advantageous. 

MORPHINISM. 

Chronic morphinism, or the morphine habit, is usually acquired as the result 
of the employment of this drug for the purpose of relieving insomnia. Sometimes 
the insomnia is due to neurasthenia, but more frequently the patient is one who 
primarily suffers from sleeplessness due to pain. If the condition producing the 
pain is continued over any considerable period of time, the patient finally becomes 
so dependent upon the use of morphine, as a nervous sedative, that he cannot 
sleep without it, and so even although the pain no longer continues he resorts to 
the drug for the nervous quiet which can be obtained only under its influence. 
Not infrequently these patients continue the use of the morphine long after the 
physician intends that it should be stopped, and so develop the habit of taking the 
drug without the knowledge of the physician who has first prescribed it. Because 
of the possibility of this occurrence he should prescribe only that quantity of 
morphine which is absolutely essential for the relief of pain upon a particular 
occasion, and if he writes a formal prescription ordering the drug from a pharmacist, 
this prescription should contain the words "Do not renew," so that the patient 
will not be able to continue taking the drug after the physician believes that he 
has stopped it. 

In a certain number of cases of morphine habit, the employment of the drug 
rests upon the fact that the patient is a degenerate without the necessary mental 
and nervous vigor to meet the vicissitudes of life. In other words, he is one who, 
in the presence of any condition which produces mental perturbation or distress, 
at once resorts to some sedative to quiet his nervous system, instead of dominating 
it by his will power and conquering the depression with a knowledge that any 
yielding either to that depression or to the desire for a drug is certain in the end 
to wreck his moral and physical condition. This is an important factor to be taken 
into consideration whenever a morphine habitue is to be treated. This condition 
may be hereditary, or it may be acquired. Not rarely, when it is acquired, the 
mental and physical condition of the patient has been impaired by grief, excessive 
business worry, illness, or other cause. When the morphine has been used for 
any length of time this very fact tends to increase the lack of moral stamina on 
the part of the patient. 

Symptoms. — One of the most noteworthy symptoms of morphinism is great 
irritability of the nervous system so that slight causes may produce outbreaks of 
rage, or, on the other hand, a lachrymose state may develop. In some instances, 
where the drug has been used for a long time, there is not only a loss in mental 
power, but the patient develops melancholia or delusions closely resembling those 
seen in an ordinary case of insanity. Before the mental degradation is so complete 
that intellectual processes are greatly impaired, the patient develops a slyness 
quite different from his ordinary frank methods of life when in health. In associa- 
tion with this slyness there is always developed a skill in "prevarication or lying which 
is quite remarkable. Persons who previously have been regarded as eminently 
truthful tell the most skilful falsehoods, and in such a way that the hearer is con- 
vinced of their truth. As a rule, these falsehoods are never so clever as when they 
are intended to result in the obtaining of the drug which is desired, the patient 
resorting to every possible means, honest and dishonest, in order that he may 
obtain the nervous quiet which his system craves. 

Treatment. — It may be asserted with truth that it is useless to attempt to treat 
a patient who is suffering from the morphine habit, with the idea of curing him 



776 INTOXICATIONS 

of his taste for the drug, unless he or she is willing to enter a private room at a 
hospital and be placed under the constant supervision of a night and day nurse. 
This isolation is necessary not only because it is a form of discipline which is advan- 
tageous for the mental condition of the patient, but it is the only way in which the 
physician can be assured that the patient is not surreptitiously continuing his 
daily dose of the narcotic. It must be remembered that the most pious individuals, 
when they become addicted to this drug, develop an extraordinary ability to tell 
lies which are so like the truth that they can deceive the most cautious. In one 
breath, the patient, with tears running down his face, will beseech the physician 
to cure him of the habit which is destroying his happiness, and, at the next moment, 
he will use every form of deceit and cleverness to obtain the drug which he craves. 
Even when the patient is under the observation of trained nurses night and day, 
any sudden improvement in his condition after withdrawal of the morphine, or 
failure to develop symptoms produced by its withdrawal, should make the physician 
believe that in some unknown way the drug has been obtained. In some instances 
the patient enters the hospital with the morphine carefully sewed in the hem of 
the night-dress; in others, a friend or servant is bribed to bring the drug each day 
in some article of food. Nothing but ceaseless watchfulness can possibly prevent 
these patients from obtaining morphine. This being so, it can readily be understood 
that home treatment can rarely succeed. 

Having obtained special control of the patient, the method of treating him would 
consist in one of two plans which have found general acceptance. The first of 
these is the gradual diminution of the morphine so that at the end of three or four 
days, or a week, none of the drug is permitted. If this method is carried out the 
patient usually develops after a few days, or sooner, great restlessness and irri- 
tability, not infrequently active purging, and profound mental and physical depres- 
sion. Cramps in the extremities also add to the suffering. Under these circum- 
stances it is necessary to support the patient by the use of hot, stimulating foods, 
such as broths highly seasoned with pepper and salt, the use of digitalis and strych- 
nine if the circulation fails, and the employment of hyoscyamus or hyoscine to 
diminish irritability of the nervous system. The employment of alcohol, coca 
wine, or similar stimulants for the purpose of aiding the patient at this time is 
is unwise, because he is prone to develop the alcohol or coca habit. If the diarrhea 
is so violent as to require control, aromatic sulphuric acid with a vegetable astrin- 
gent, like the fluidextract of hematoxylon, may be used. Hot compresses may be 
applied about the painful limbs. Great mental excitement may be relieved by 
chloral, but the danger of producing the chloral habit is not to be forgotten. In 
place of chloral, sulphonal or trional may be used. Occasionally nerve quiet 
can be produced by wrapping the patient in a hot, wet blanket, care being taken 
that the hot pack is not continued so long as to produce cardiac depression. 

A second method of treatment is one which has been largely employed in the 
last few years, and for which we are chiefly indebted to a Texas physician, Dr. 
Lott. This consists in putting the patient where we can have him under absolute 
control, and in the administration of full doses of hyoscine hypodermically, giving 
him as much as -^q of a grain every two hours, if need be, until a condition of 
nervous quiet is produced. In the writer's experience these large doses fail to 
produce sleep, and instead cause a condition in which the patient lies awake but 
stupefied, and often mumbles continuously. Curiously enough the mouth does 
not become as dry as one would expect from the administration of such a powerful 
drug in these large doses. Should the circulation seem at all feeble, strychnine 
may also be given. The idea in employing hyoscine is to use that quantity which 
is necessary to keep the patient under control, and to prevent suffering. These 
doses may be continued for a number of days, at the end of which time they are 
gradually diminished and the patient is permitted to return to his normal condition 



ARSENICAL POISONING 111 

as the effects of the hyoscine pass away. By this means the acute mental and 
physical suffering caused by the sudden withdrawal of morphine is avoided, and 
in some instances the patient actually seems to be cured of his malady, although, 
of course, there is great danger in every case of his speedily returning to its use, 
particularly if any nervousness or mental stress is experienced. So common is it 
for the habitue to go back to the employment of this drug habit that many men 
of experience have gone so far as to assert that no case of the morphine habit is 
ever permanently cured. This view is, however, undoubtedly incorrect. The 
writer has seen a number of cases in which permanent cure certainly took place. 

ARSENICAL POISONING. 

Arsenical poisoning occurs in two forms, the acute and chronic. Usually after 
the first stage of acute poisoning, if the patient survives, there develops a second 
stage due to the effects of the arsenic. Acute poisoning usually follows the 
ingestion of "Rough-on-Rats," Paris green, or Scheele's green. The symptoms 
are those of severe gastro-enteritis, with vomiting and purging, followed by death 
in collapse. The antidote is the hydrated sesquioxide of iron with magnesia. 
When the patient survives the acute stage he suffers from secondary lesions in the 
stomach and intestines, kidneys, and liver. Widespread fatty degeneration also 
occurs and peripheral neuritis may be present. 1 

The causes of chronic arsenical poisoning are almost as numerous as are those 
of lead poisoning. It may find its way into the body through the lungs from the 
air of a room the walls of which are covered by a paper heavily laden with arsenical 
dyes; it may enter in beer made from glucose prepared by the use of iron pyrites 
contaminated with arsenic, as in the recent celebrated epidemic in England; or it 
may be given in moderate poisonous dose for a long time with homicidal intent, 
as in a case recently tried in the Philadelphia courts. 

Not very rarely a mild form of chronic arsenical poisoning is met with in cases 
to which a physician has found it necessary to give large doses of arsenic for long 
periods, as in chorea, in leukemia, and Hodgkin's disease. 

Symptoms. — Chronic arsenical poisoning manifests itself chiefly in the form of a 
widespread peripheral neuritis, with the development of a secondary degeneration. 
of the epithelium of the kidneys. The chief symptoms are tingling and pains 
in the limbs, followed, after a time, by paralysis which affects the distal portions 
of the body much more than it does the nerves and muscles of the thighs or arms. 
Atrophy of the muscles supplied by the paralyzed nerves soon takes place. Other 
trophic changes also develop, such as herpetic eruptions resembling those of herpes 
zoster or pemphigus, and glossiness of the skin sometimes supervenes. At times 
curious deposits of pigment take place in the skin. As in lead poisoning, the nerve 
supply to the extensor muscles suffers chiefly, but in addition the small flexor muscles 
are also affected much more commonly than they are in neuritis due to alcohol 
or lead. The lower limbs are affected as much as the upper limbs, whereas in 
lead poisoning it is the upper extremities which suffer most. Again, arsenical 
neuritis affects the sensory and motor fibres, and for this reason pain as well as 
anesthesia is often met with. The pulse is quickened and the mind confused in 
some cases. Because of the involvement of the sensory and motor fibres of the 
peripheral nerves the patient may present symptoms of tabes dorsalis (arsenical 
pseudotabes). The Argyll-Robertson pupil is a useful differential factor, for if it is 
present the cause of the disordered gait is probably due to true locomotor ataxia. 

Prognosis. — The prognosis in such cases depends upon the severity of paralysis 
and the state of the kidneys. If the latter organs are affected the outlook is more 

1 For this train of symptoms see the author's Text-book of Therapeutics, loth edition. 



778 INTOXICATIONS 

grave than if they are intact. Even when the symptoms of neuritis are severe, 
remarkable recovery may ensue if the patient is removed from the exposure to the 
drug. 

Treatment. — The treatment consists in the removal from exposure, the use of 
iodide of potassium to aid in the elimination of the poison, the administration 
of strychnine in full doses if the nerves are not irritable, and in the application of 
massage and electricity to improve the nutrition of the affected parts. Iron may 
be used to combat the anemia. 



LEAD POISONING OR PLUMBISM. 

Acute lead poisoning is not of frequent occurrence. Its consideration is distinctly 
toxicological in character, and for this reason it is not discussed in these pages. 

Chronic lead poisoning, on the other hand, is of exceedingly common occurrence, 
not only in those who are exposed to the poison by reason of their occupation, but 
in persons who have suffered no such exposure but have absorbed the lead from 
sources in which its presence would not be suspected. Further than this, lead 
poisoning in its chronic form may produce the most varied symptoms, which are 
oftentimes so unusual that no thought of lead as a cause is entertained. In speaking 
of the nervous manifestations which are often present, a well-known teacher was 
wont to say: "When you cannot explain a curious train of nervous symptoms, 
always suspect syphilis, hysteria, or lead as the cause." 

Etiology. — It is the insoluble rather than the soluble salts of lead which usually 
cause chronic lead poisoning. The most frequent sufferers are workers in manu- 
factories where paint is made, and house painters who are continually engaged in 
the handling of lead paint. In rarer instances the patient is poisoned by the use 
of water which in passing through new lead pipes dissolves some of the lead; or 
lead is present in a hair-dye or cosmetics and is absorbed by the skin; or, again, it 
has occurred that a miller has filled holes in his grindstones with lead, which has 
then been ground with the flour and eaten in bread. In one instance, in Pennsyl- 
vania, a peddler sold a large number of crocks to farmers' wives. In these was 
placed apple butter, and as the acid in the fruit eroded the lead glazing which 
lined the jars, a widespread epidemic of chronic lead poisoning developed. Perhaps 
the most notorious illustration of how lead may cause poisoning in unsuspecting 
persons is the celebrated "chrome-yellow cases" in Philadelphia, in which a whole- 
sale druggist sold chrome yellow to a number of confectioners, who saved the cost 
of eggs by coloring their cakes with this substance. As a result a large number of 
men, women, and children died, and a much larger number suffered from chronic 
poisoning for months before the source of the trouble was discovered. An extraor- 
dinary cause, however, is the habit of chewing silk thread weighted with lead. 
At least two cases of chronic poisoning from this cause have been met with in 
seamstresses. 

The fact, therefore, that no history of exposure to lead is to be found in a given 
case does not negative the diagnosis of lead poisoning. 

Prevention. — Chronic lead poisoning is to be prevented in workers in lead by 
the exercise of the greatest possible cleanliness as to their hands, which should be 
thoroughly washed before food is touched, as otherwise lead may be taken in 
small amounts and finally cause poisoning. If the workman is employed in grinding 
lead, he must wear a mask to prevent the poison from being inhaled in dust. The 
use of vessels, the glazing of which contains lead, for holding food should be avoided. 
Small amounts of dilute sulphuric acid to form insoluble sulphates in the mouth and 
stomach may be resorted to, and purgation every few days by sulphate of mag- 
nesium is advantageous. 



LEAD POISONING OR PLUMBISM 779 

Pathology and Morbid Anatomy. — There is no other poison from the mineral 
kingdom which taken into the body produces such widespread changes in different 
organs as does lead in the chronic form of poisoning. Even alcohol, that most 
ubiquitous poison, does not cause such a multitude of changes. The nervous 
system is the portion of the body which bears the brunt of the attack, and it is the 
peripheral nerves that suffer most. In them the lead produces a toxic neuritis. 
In advanced cases there is segmentation of the myelin and breaking up of the axis 
cylinder, with a proliferation of the nuclei in the sheath of Schwann. The early 
changes in the nerves affect chiefly the medullary sheath, which is affected in patches 
at irregular intervals — the so-called periaxial neuritis of Gombault. Although 
the lesions are more severe as the distal end of the nerves is approached, Dejerine 
has found them even in the anterior roots. Conspicuous changes in the spinal 
cord are almost never seen, but Oppenheim states that he has found alterations 
in the anterior cornua, and Gowers asserts that in some cases the cells in these 
cornua are degenerated. No constant lesions are found in the brain, even in 
those cases in which severe cerebral symptoms are present, except those dependent 
upon vascular lesions which are part of the general vascular disease produced by 
the poison. 

It is to be especially noted that the sensory fibres of the nerves are not affected, 
and that the musculospiral is the nerve chiefly involved in those cases which have 
peripheral neuritis. As a result of the neuritis, produced by the lead, atrophy 
of a severe character may develop in the muscles supplied by the affected nerves. 
Fatty degeneration of the muscles does not ensue. The second portion of the body 
to feel the effect of the lead is the kidneys, which are not rarely the seat of chronic 
interstitial nephritis, and with this renal lesion a process of arteriofibrosis develops, 
which associated conditions often cause the death of the patient. 

Sailer has recently shown that, in some cases at least, there is an absence of 
hydrochloric acid in the gastric juice. 

Symptoms.— From what has been said of the changes in various organs caused 
by lead, it is evident that the symptoms may be very varied. Paralysis of the 
extensor muscles of the forearm, causing wrist-drop, is the most constant symptom. 
This paralysis is nearly always bilateral, but occasionally but one arm is affected. 
The supinator longus muscle and the short extensor of the thumb, however, usually 
escape, which is curious in view of the fact that the supinator longus muscle receives 
its nerve supply from the musculospiral nerve. In atypical cases Oppenheim 
states that the supinator longus, the biceps, and even the deltoid are involved. 

In the legs palsy is far less frequent than in the forearms, and the muscles involved 
are the peroneal group, but the tibialis anticus is not affected. 

Although motor paralysis is present sensory disturbances are rare. 

Palsy of the ocular muscles producing squint may be due to lead, as may also 
optic neuritis. In very rare cases of severe plumbism cerebral symptoms develop, 
consisting in epileptiform convulsions, or coma. This state is called " encephalopathia 
saturnina." 

Tremor of the forearms is sometimes present in lead poisoning. 

Chronic lead poisoning greatly aids in producing gouty lesions, probably by 
forming a urate of lead in the tissues about the joints. Others believe that the 
lead decreases the alkalinity of the blood and so permits the precipitation of urates 
to occur. 

There still remain to be considered several symptoms of chronic lead poisoning 
which are so constant in their appearance and so characteristic that they are most 
valuable aids in diagnosis. The first of these is the blue line in the edges of the 
gums next the teeth, formed by the deposit of sulphide of lead in the capillaries 
of the part. This sign is often absent in those who are cleanly in the care of the 
mouth. The second is the characteristic pain in the belly, which is exceedingly 



780 INTOXICATIONS 

severe in the region of the umbilicus, and is described as a pain due to twisting 
the bowels around a stick. This is called "painters' colic/' or "colica pictonum." 
The latter term is given to this state because it was frequently met with in Picton 
at one time. A third symptom of chronic lead poisoning is anemia, which is in 
part due to the direct effect of the lead and in part to the renal changes induced 
by this agent. Microscopic examination of the blood will often reveal a granular 
degeneration of the erythrocytes. 

Diagnosis. — In a case in which the blue line on the gum is present the diagnosis 
is easy. When wrist-drop is present it must be separated from that due to pressure, 
as by resting the head on the arm when sleeping or by the pressure of a crutch. 
As a rule, pressure palsy is unilateral and lead palsy bilateral, but this is not so 
invariably, and the history of the patient may be necessary to decide the diagnosis. 
When the palsy is distributed in various parts, particularly if it affects the legs, it 
must be separated from acute poliomyelitis. Lead poisoning is rare in children 
and acute poliomyelitis is common. In adults chronic lead poisoning is more 
frequent than is acute poliomyelitis. Poliomyelitis in its acute form has a history 
of sudden onset with fever, and the onset of lead palsy is rarely so abrupt and is 
usually not febrile. The history of exposure to lead will aid in deciding the diagno- 
sis. In chronic poliomyelitis the only way to determine the question is by the 
history and the frequent examination of the patient's urine for lead. Often lead 
will not be found in the urine unless iodide of potassium is given to set it free from 
the tissues where it has been deposited. 

Saturnine epilepsy must be separated from true epilepsy by the history of the 
patient and by the association of other signs of-plumbism. It must also be separated 
from uremic convulsions, if possible, by the urinary examinations, but this may 
be impossible because the lead may at once cause encephalopathia saturnina and 
uremia through its effects on the cerebral vessels and the kidneys. 

Prognosis. — The prognosis as to the duration of life in chronic lead poisoning 
is good unless cerebral symptoms are present, or renal changes are well marked. 
The prognosis as to the paralysis depends largely upon the general nutrition of 
the patient and the stage to which the neuritis has advanced. If the muscles 
involved have lost all reaction to electrical stimulation, the prognosis must be bad 
as compared with that in a case in which the palsy has lasted for but a short time. 
Even when the reactions of degeneration are present the outlook is not hopeless, 
because if the patient is no longer exposed to the poison recovery sometimes ensues, 
particularly in young persons. 

Treatment. — The treatment of chronic lead poisoning consists in removing 
the patient from continued exposure to the poison. If he is an artisan he must 
cease working in lead. If he has been poisoned by the metal through some accident, 
the source must be discovered and he must no longer be exposed to it. 

The second duty of the physician is to eliminate the lead already in the body 
as rapidly as possible. For this purpose the iodide of potassium should be given 
in full doses, with the object of forming double soluble iodides with the lead. Not 
only have we every reason to believe, from a chemical standpoint, that this medi- 
cinal treatment is advantageous, but it is a well-known clinical fact that chemical 
examination of the urine in a case of lead poisoning will fail repeatedly to show 
lead, and will at once indicate its presence after iodide of potassium is administered, 
proving that by this means lead is carried to the kidneys and speedily passed out 
of the body. It must also be remembered that the liver eliminates lead freely in 
the bile. 

The third indication is to improve the patient's general health not only by 
the use of such tonics as iron and strychnine, but also by ordering an out-door 
existence, with as much sunshine as it is possible for the patient to find in the 
twenty-four hours. 



FOOD POISONING 781 

The paralysis of chronic lead poisoning is to be treated by the administration 
of full doses of strychnine and the simultaneous use of large doses of iodide of 
potassium. The paralysis of the extensor muscles of the arms and legs is to be 
treated not only by the use of strychnine, but by the employment of the slowly 
and rapidly interrupted faradic current. In those cases in which cerebral symptoms 
develop, the patient should receive full doses of iodide of potassium, with the 
object of getting rid of the lead as rapidly as possible. If the symptoms are acute, 
and if a convulsion is already present, the patient should receive a hot pack in 
order that the sedative effect of this therapeutic measure may be exercised upon 
the nervous system, in order that the blood may be drawn away from the congested 
brain, and with the hope that by increasing the action of the skin the kidneys 
may be relieved of some of the work which they would otherwise be forced to 
perform. In other respects the convulsions should be treated, as are all other 
convulsions, by the use of nitrite of amyl inhalations, and by the employment of 
full doses of chloral and the bromides to quiet the brain and spinal cord. 

Painters' colic with its attendant constipation is not to be treated by the use 
of purgatives, but by the use of morphine given hypodermically. This drug, 
which so often causes constipation in the ordinary patient, not rarely produces 
active purgation in these cases, by quieting the intestinal irritation and spasm and 
simultaneously relieving the pain. 

FOOD POISONING. 

Bromatotoxismus. — Symptoms of poisoning produced by the ingestion of food 
which is impure by reason of faulty preparation, or the changes due to decomposi- 
tion, are occasionally met with. It is rather remarkable, considering the long period 
of time during which many foods are kept after they are prepared for the table, 
that more cases of poisoning do not ensue. Much of the information given in 
this article is obtained from the excellent summary of this subject which can be 
found in Vaughan and Novy's Cellular Toxins. 

Poisoning may be produced by the use of grains which have become infected 
by poisonous fungi. Animals may eat substances which may render their milk 
or flesh or both poisonous. The flesh of certain animals also becomes poisonous 
at certain stages of their life history. Foods may also become infected by the 
discharges of human beings; the flesh of animals may suffer from some specific 
disease which may be transmitted to man, and milk may carry the disease of an 
animal to man or may be infected by the discharges of man, and so convey specific 
germs to other individuals. Food may also contain micro-organisms which in 
their process of development produce poisonous symptoms in man. 

Sitotoxismus is applied to poisoning by vegetable foods which are infected by 
moulds or bacteria. 

The most familiar form of poisoning by grains, or vegetable food, is Ergotism 
due to the eating of rye flour made from rye which has been infected by the fungus 
Claviceps purpurea. This ergot is, of course, largely employed in medicine. Several 
poisons are found in ergot, such as ergotinic acid, sphacelinic acid, and cornutin. 
The first of these, however, seems to be poisonous only when it is injected hypo- 
dermically. Sphacelinic acid, on the other hand, is supposed to be responsible 
for the gangrene and cachexia which sometimes develop in persons who have eaten 
infected rye. On the other hand, cornutin seems to be the poison which affects the 
nervous system and produces spasms and convulsions. 

Mytilotoxismus. — Under the name of mytilotoxismus is described the symptoms 
of poisoning which are produced by eating poisonous mussels. These symptoms 
consist in some cases in violent gastro-intestinal irritation with purging, but in the 
majority of instances the manifestations of the poisoning are nervous in character. 



782 INTOXICATIONS 

A rash resembling urticaria and finally becoming vesicular may develop over the 
body, and the eyelids may be so swollen as to prevent vision by extravasation of 
the serum into their tissues. There is often difficulty in breathing, apparently 
due to intense hyperemia of the bronchial mucous membrane. Convulsions and 
coma may develop and death may be due to this cause. 

Treatment. — The treatment of mytilotoxismus consists in the use of an active 
saline cathartic to sweep the poisonous material from the alimentary canal, and 
in the use of ether as a diffusible stimulant. 

Ichthyotoxismus. — When fish produces poisonous symptoms the term ichthyo- 
toxismus is used to describe the condition. As is well known, certain fish are 
unfit to eat, and other fish become poisonous during the season at which they are 
spawning. In still other instances fish suffer from bacterial infections which render 
their flesh unsuitable as food. The ingestion of poisonous fish so seldom occurs, 
at least in this country, that the symptoms produced need not be described. 

Poisoning from the flesh of fish which has undergone decomposition is often 
very violent in its manifestations. The most common symptoms are dilatation 
of the pupils, nausea, vomiting, and severe abdominal pain, followed by the develop- 
ment of a scarlatinal rash all over the body. In such cases a purge to sweep out 
the offending materials and also stimulants are needed. 

Kreotoxismus. — The word kreotoxismus is applied to poisoning resulting from 
the ingestion of meat unfit for food, because of the presence of bacterial or animal 
poisons. Perhaps the most frequent instance of this is in so-called sausage poison- 
ing. Sausages are often made from what may be called the refuse following the 
butchering of animals ordinarily employed as food, and the treatment of this 
material is such that early decomposition changes may readily set in. In most 
instances the process of cooking destroys the poisons, but when cooking is not 
resorted to the symptoms which are induced are exceedingly severe, and death 
may ensue. There is, in many cases of sausage poisoning, difficulty in breathing 
and swallowing, violent vomiting, severe abdominal pain, hoarseness, dimness of 
vision, and delirium. In other cases the mind remains clear. From some of 
these forms of food ptomaines have been isolated. In other instances certain 
bacteria have been found which have been considered responsible, either directly 
or indirectly, for the symptoms. Meat-pie poisoning and poisoning by mince-meat 
are essentially similar to sausage poisoning. 

Tyrotoxismus and Galactotoxismus. — Under the name galactotoxismus is de- 
described the poisoning which results from the ingestion of impure milk. When 
poisoning follows the use of bad cheese it is called tyrotoxismus. This term is also 
applied to the poisoning produced by impure ice-cream. The symptoms are 
sometimes exceedingly severe, and consist in evidences of gastro-enteritis followed 
by collapse. To a substance which Vaughan states he is able to isolate from cheese 
and ice-cream he gave the name of "tyrotoxicon." 



PELLAGRA. 

Synonyms. — Erythema endemicum, Lombardian leprosy, Psychoneurosis maidica, 
Mai de sole, and many other terms. 

History. — Pellagra is a disease which has been recognized for more than 250 
years, but the first authentic study of it was made by Casal, a Spaniard, in 1735, 
although his account of it did not appear until 1762. In 1771 Frapolli of Milan 
gave it the name pellagra which had already been given it by the laity. In the 
United States the first case was not adequately reported until 1902 by Sherwell. 
In the same year Harris, of Atlanta, recorded another case. The first large series 
of cases which called general attention to the malady was reported by Searcy, in 



PLATE XI 




Atrophy of the Skin of the Back of the Hand 
succeeding Pellagrous Erythema. 



Reproduced through the courtesy of Prof. Ludwig Merk, of Innsbruck. 



PELLAGRA 783 

an insane asylum in Mt. Vernon, Alabama, in 1907. Since that time hundreds 
of cases have been recorded and medical literature has teemed with its discussion. 

In Italy in the latter part of the last century pellagra was so prevalent as to 
affect 1 in 19 of the inhabitants, but it has now been largely eradicated. It has 
been reported in nearly all civilized and semi-civilized countries. 

Etiology. — The cause of pellagra is unknown. A large number of investigators 
believe it to be due to damaged corn which is impaired in its nutritional value or 
contains a fungus which is productive of the symptoms. Still others think it a 
result of the growth of some other form of micro-organism in the corn which induces 
an intoxication. Sambon and his followers believe it to be induced by the bite 
of the simulium reptans, sl small insect of worldwide distribution. It is certain 
that care as to corn used as food prevents the disease. 

Pellagra is a non-contagious and non-hereditary disease characterized by great 
variation in its manifestations but chiefly in its early stages by an erythematous 
appearance of the skin of the forearms and hands on the extensor surfaces, and of 
the face, associated with a sense of languor and wretchedness particularly in the 
spring months, at which time the disease nearly always develops. These symptoms 
if mild in many cases disappear to return with the advent of the next spring, and 
by frequent recurrence finally become constant, or in the severe cases there may 
be no such period of immunity. The manifestations of the disease may therefore 
extend over many years and the malady is never acute in the sense of running a 
short, sharp, course as do many acute infectious diseases. In rare instances an 
acute type of pellagra is met with which has its onset in a sharp attack of vomiting, 
headache, and diarrhea., the latter condition being so severe as to resemble dysen- 
tery. Not only is blood in the stools, but bleeding from the gums and tongue 
may occur. Fever as high as 102°, in some cases is present, and emaciation is 
rapid and severe. Death nearly always occurs in these cases after a period of 
about two to six weeks. 

The more severe symptoms of pellagra appearing in those who have the well 
developed type consist in obstinate diarrhea, the tongue is denuded of epithelium 
and sometimes ulcerated. Not rarely a collar-like erythema appears on the neck 
where the collar band of the shirt encircles it (il collar e pellagroso) . 

All parts of the skin exposed to weather are often involved so that, in bare-footed 
persons, the dorsum of the foot may be affected like the back of the hands. Ulti- 
mately the whole leg or forearm on both surfaces may be affected. The erythema 
is red, yet not as bright in hue as in acute sunburn, and disappears on pressure, 
but when the disease is well developed is not altered greatly by pressure, and 
becomes darker in hue or even plum colored. In some cases the early erythematous 
rash disappears after a short time, a fine desquamation of the skin taking place, 
followed by pigmentation. In the dark races the skin may be grayish in hue and 
darker than normal in the affected parts. The patient complains of a sense of 
tenseness or swelling in the affected parts and of heat and burning, but itching 
is not common. In other instances vesicular or bullous eruptions take the place 
of the dry erythema just described ("Wet Pellagra")- Such eruptions are char- 
acteristic of the severe types. After repeated exacerbations and fadings of the 
erythema the skin atrophies, appearing as a thin parchment-like membrane, but 
in the wet type ulcerations may extend as deeply as the tendons of the hand. Even 
these deep lesions may heal. 

As the disease develops into its second stage nervous manifestations take place. 
The languor of the first stages changes into a more or less profound melancholia 
and sometimes there are suicidal tendencies, particularly by drowning. In other 
instances delusions of persecution are met with and finally stupor and coma develop. 
In Italy the mental disorders seem more common than in the United States. 

A third set of symptoms, connected with the alimentary canal, may develop 



784 INTOXICATIONS 

in any stage of the disease, often as early as the erythema. They consist chiefly 
in an intractable diarrhea, often dysenteric in character. There may be also much 
meteorism and pyrosis. 

When the disease reaches its final stages in addition to the stupor or coma already 
described the patient becomes typhoidal in appearance and for the first time may 
have fever. There is profound prostration, marked wasting and a low delirium. 
At the close there may be opisthotonos. 

An examination of the blood does not show any marked changes. The red 
cells are moderately decreased in number and do not show degenerative changes. 
The relative number of the white cells is approximately normal but there may be 
a slight leukocytosis of about 13,000. 

Autopsy shows a general atrophy of the fatty and muscular tissues, especially 
of the muscular coat of the bowel. The liver is enlarged, the spleen shrunken and 
the ribs very fragile. The kidneys are cirrhotic and the large vessels atheromatous. 
The nervous lesions corlsist in hemorrhages into the subarachnoid, and the meninges 
of the brain and cord are thickened by low-grade chronic inflammation. Curiously 
enough the peripheral nerves seem to escape but degenerations of the posterior 
and posterolateral columns of the cord are marked and the nerve trunks show 
degeneration of the myelin sheath. Harris has also emphasized the presence of 
pancreatic atrophy. 

Prognosis. — Much depends on the severity of the symptoms and whether the 
patient's conditions of life can be changed as to habits, food and climate. The 
mortality based on all cases is said to be about 10 per cent., but this includes the 
very mildest manifestations. A more correct percentage is probably about 35 
per cent. 

Treatment. — As far as is known there is no cure for pallagra so far as any drugs 
are concerned, and perhaps not even under suitable dietary and climatic influences. 
Arsenicals have been used in large doses with asserted benefit. The best of these 
is apparently atoxyl or possibly salvarsan. The best diet is milk with rest in bed. 
Drugs do not seem to control the diarrhea. 



DISEASES OF THE NERVOUS SYSTEM. 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE 

BRAIN AND ITS MEMBRANES. 



HEMORRHAGE INTO THE BRAIN, CEREBRAL THROMBOSIS, AND 

EMBOLISM. 

Definition. — Apoplexy consists in the sudden onset of paralysis and loss of 
consciousness from an abrupt intracranial lesion. In its most typical form it is 
due to hemorrhage in the cerebrum, but it may also be due to hemorrhage into the 
cerebellum, into the brain-stem, or into the meninges, and it may result from 
embolism or from thrombosis. When it arises without being accompanied by a 
demonstrable brain lesion, it is spoken of as an " apoplectiform attack." An inflam- 
matory process in the central nervous system, so acute that minute hemorrhages 
occur in the affected area, is also spoken of as apoplectiform, as, for example, 
"apoplectiform bulbar paralysis." 

The term "apoplexy," as commonly employed, is nearly equivalent to the 
popular term "stroke," and is used so indefinitely that it is better to use the more 
accurate terms cerebral hemorrhage, cerebral thrombosis, or embolism when 
describing the condition present. The symptoms produced by thrombosis and 
embolism are almost identical with those due to hemorrhage, and will be found 
discussed in the consideration of the differential diagnosis of the disease. 

Etiology. — As already stated, the usual cause of apoplexy is the rupture of a blood- 
vessel in the brain or its meninges. This is due in the great majority of cases to 
changes in the bloodvessel produced by disease or by injury. These changes are 
described in the article on Arteriosclerosis. The immediate causes which produce 
rupture of an intracranial vessel are numerous, for all factors which cause a sudden 
increase in blood pressure may result in so great a strain on a weakened vessel 
wall that it gives way. Thus, apoplexy not rarely follows a paroxysm of rage, a 
severe nervous shock, a sudden muscular effort, as in running for a car, in straining 
at stool, and during sexual intercourse. The use of alcoholic and other stimulants 
may also cause rupture. 

Frequency. — Men are more frequently attacked by apoplexy than are women, 
because they suffer so much more commonly from arteriocapillary fibrosis. The 
ratio is about as 80 to 20 per cent., according to Starr, but Gintrac puts it at 56.6 
to 43.4 per cent. Of 816 cases of cerebral hemorrhage collected by me from various 
sources, 454 occurred in men and 362 in women. 

The period of life at which cerebral hemorrhage most commonly occurs is from 
fifty to eighty years of age. This is the age period during which the patient is 
actually most liable to this accident; but if the ages of the entire number of persons 
dying of apoplexy in a given series of statistics be added together and an average 
obtained, the largest number of cases is found between forty and sixty years, 
because so few persons live to eighty years that not many persons of that age are 
to be found in such a series. The following table is a combination of the cases of 
50 (785) 



786 DISEASES OF THE NERVOUS SYSTEM 

Gintrac and Breese, and shows the age incidence of cerebral hemorrhage by decades 
from thirty to eighty years : 

Between 30 and 40 years of age 74 

" 40 " 50 " " 98 

" 50 " 60 " " 138 

60 " 70 " " 172 

70 " 80 " " 124 

The question of age in its relation to apoplexy is, however, more dependent upon 
the state of the bloodvessels than upon the actual years of existence, for not in- 
frequently a syphilitic of thirty years of age may suffer more from degeneration of 
the arteries than another man at seventy. 

Available statistics do not show any increase in the frequency of cerebral hemor- 
rhage. Thus, from 1879 to 1884, 12,408 patients were admitted to the medical 
wards of St. Bartholomew's Hospital, London, and of this number 79 were affected 
with cerebral hemorrhage. During the five years from 1897 to 1902, 12,089 medical 
patients were admitted to the hospital, and among them there were 62 cases of 
cerebral hemorrhage. 

Pathology. — The changes which take place in the bloodvessels of the brain which 
result in apoplexy are those of arteriosclerosis as we meet it in other parts of the 
body; the intima becomes roughened and eroded, the muscular sheath undergoes 
fatty degeneration, and the fibrous sheath becomes less elastic than in health. 
Aneurysmal dilatations frequently develop, and these are the parts of the vessel 
from which hemorrhage often ensues. In the article on Arteriosclerosis it was 
shown that the causes of this state are syphilis, lead, gout, renal disease, and, not 
least important, advanced years; but of all these causes renal disease is probably 
the one which most frequently produces vascular rupture, because it is usually 
associated with cardiac hypertrophy and a high arterial tension, which increases 
the stress on the weakened vessel wall. 

Rupture of a vessel occurs very much more frequently in certain areas than 
in others, as already pointed out. This is because certain vessels suffer from arterial 
sclerosis earlier than others, and also because of the anatomical relationship. Thus, 
the blood current reaches the left middle cerebral artery more directly from the 
heart than it does on the right side, where it first passes through the innominate 
artery, which diminishes its force. Durand Fardel states that 75 per cent, of the 
miliary aneurysms which affect cerebral vessels involve the branches of the middle 
cerebral artery which enter the anterior perforated space, namely, the lenticulo- 
striate and the lenticulo-thalamic vessels. For this reason the lenticulo-striate 
branch was called by Charcot the "artery of cerebral hemorrhage." About 50 
to 60 per cent, of all cerebral hemorrhage is from this vessel, and therefore occurs 
in the internal capsule or near it. (See Hemiplegia.) The sharp spurt of blood 
which follows rupture of the vessel wall may break through the corpus striatum in 
either direction, often internally through the caudate nucleus, or it may break 
through the optic thalamus; and when the rupture is large and the blood pressure 
high, the blood thus finds its way into the lateral ventricles (see Fig. 128), into the 
third ventricle, and even into the fourth ventricle, where it causes death by pressure 
on the vital centres, if death has not already ensued from shock and the damage to 
the cerebral tissues. 

When these " capsulo-ganglionic" vessels do not give way the cause of the symp- 
toms is usually rupture of some of the outer branches of the Sylvian artery, produc- 
ing lesions in the cortex. In still other cases, which are less frequent, the hemor- 
rhage takes place into the pons and still more rarely into the cerebellum. 

Cerebellar hemorrhages are especially prone to inundate the fourth ventricle. 

A very much rarer form of apoplexy is that in which by reason of disease of the 



HEMORRHAGE INTO THE BRAIN 



787 



blood, or of the vessels, small oozings or extravasations take place through the 
vessel walls, which on subsequent examination do not reveal any rupture. This 
extravasated fluid finds its way alongside the vessels, and so does damage to a 
wide area without causing any very gross lesion in the brain tissues. Such a state 



Fig. 128 

u qWERLIMB 




Diagram showing the fibres from the cortex forming the corona radiata, which after they are approxi- 
mated pass into the internal capsule. It also shows the decussation of the pyramid of the left side, which 
passes to the right side of the spinal cord, and the direct or uncrossed tract (Ttirck's column). Finally, it 
also shows the secondary degeneration which occurs after cerebral hemorrhage or softening, and which 
follows the course of the motor tracts into the spinal cord. H, site of lesion. The continuous lines are 
fibres going to the legs, the dotted are those going to the arms and motor cranial nerves. The Roman 
numerals refer to the origins of the cranial nerves. (Modified from Van Gehuchten.) 



may develop in the course of purpura or leukocythemia. Extravasations of blood 
into the meninges and cortex also occur as the result of injury. 

In those cases in which the hemorrhage is arrested before it does great damage 
much depends upon the part of the brain which is affected. 



788 



DISEASES OF THE NERVOUS SYSTEM 



If the hemorrhage occurs on, or in, the cortex, and is small in amount, the con- 
vulsions and paralysis which ensue may involve only part of the arm, or leg, or 
face, or one of the special senses, or a particular function controlled by the centre 
that has been destroyed, or such a monoplegia may be due to a small hemorrhage 
in the subcortex cutting off the fibres of the corona radiata descending from the 
cortical centre. But an equally small hemorrhage still lower down, where the 
fibres from the entire cerebral hemisphere come together in the internal capsule, 
will produce a complete hemiplegia (Fig. 128, lesion of ordinary hemiplegia). On 
the other hand, if the lesion occurs still lower down — that is, in the brain-stem, 



Fig. 129 



Lesion of cerebral mo- 
noplegia (brachial) 



Lesion of ordinary 
hemiplegia 



Lesion of cross paralysis 
(face of same side with 
limbs of other side) 



A lesion causing paraplegia 



A lesion causing hemi- 
paraplegia 




Cortical centre for op- 
posite leg 



Cortical centre for op- 
posite arm 



Cortical centre for op- 
posite side of face 



Internal capsule (pos- 
terior limb) 



Motor nerve to face 

Decussation of pyra- 
mids 

Crossed pyramidal tract 



3Iotor nerves to upper 
limb 



Crossed pyramidal tract 



Sensory nerves entering 
cord, and decussating 
soon after entry 



Motor nerves to lower 
limb 



Diagram showing the general arrangement of the motor tract and the effect of lesions at 

various points. (Ormerod.) 



where bundles of fibres are separating from the main paths and crossing to the 
opposite sides to connect with cranial nerves — it will produce crossed paralysis — 
for example, the -face is paralyzed on one side and the body on the other. Ordinary 
"crossed paralysis" indicates a lesion in the lower third of the pons because at 
this point the motor fibres for the face have crossed but the fibres for the limbs 
have not done so (Fig. 129, lesion of crossed paralysis). If the posterior third 
of the internal capsule is affected as well as the anterior and middle thirds, we 
find hemianesthesia as well as motor paralysis on the opposite side (Fig. 130); 
and if the very posterior portion of this limb is affected the optic radiations 



HEMORRHAGE INTO THE BRAIN 



789 



are implicated and hemianopsia is added to the symptoms. (See Fig. 130). 
If the patient survives the attack the extravasated blood coagulates and is sur- 
rounded by a protective wall of lymph, which undergoes organization while 
the clot softens, and contracts as its contents are being absorbed. The per- 
manent lesion of apoplexy is thus commonly a cyst, but sometimes, absorption 
having been complete, only a scar remains. Not only do these changes take place 
at the site of the hemorrhage, when it affects the cortex or motor fibres in the 

Fig. 130 




Cross-section of the brain, showing the lateral ventricles, the cerebellum, and, most important, the cross- 
section of the motor fibres in the internal capsule. (Modified from Fuller.) 



corona radiata or in the internal capsule, but degenerative alterations follow along 
the motor pathways through the peduncles of the cerebrum, the pons, the pyramids 
of the medulla, and so on into the direct and crossed pyramidal tracts of the cord. 
(See Fig. 128.) 

Symptoms. — The symptoms of apoplexy depend upon the site of the lesion and 
upon the suddenness and severity of the hemorrhagic extravasation, as already 
stated. A few cases have some premonitory symptoms such as numbness or tingling 
in the part of the body about to be affected, but most cases are attacked without 



790 DISEASES OF THE NERVOUS SYSTEM 

warning. When the hemorrhage takes place from the middle cerebral artery the 
symptoms are usually as follows: 

An individual who is apparently in his normal health is suddenly seized with 
vertigo, which causes him to stagger and fall. The face is at first pallid and later 
somewhat congested. The respiration is altered almost immediately. At first it 
may be slightly gasping and irregular, but soon becomes full and deep. The air 
is drawn into the lungs with considerable force and then equally forcibly expelled. 
As it enters it causes the relaxed soft palate to vibrate and as it escapes through the 
angle of the mouth, which is paralyzed, it produces a noise to which the term 
"stertorous breathing^ has been applied. The pulse is slow and its tension high 
except for a few moments after the onset of the symptoms, when it may be rapid 
and irregular from the shock. In some cases, too, in which the hemorrhage into 
the brain is very great and death imminent, the pulse may not become full and 
strong. 

An examination of the patient's limbs may show that both sides are almost 
equally relaxed and powerless, but this is usually a temporary state due to shock, 
and in a very short time it will be found that the limbs on one side are moved, or 
at least are not quite powerless, while those on the opposite side are paralyzed. 
In other words, the typical paralysis of cerebral hemorrhage called hemiplegia 
is present. 

The muscles of the trunk are never as completely paralyzed as those of the limbs. 
The muscles of the lower part of the face share in the paralysis, and for this reason 
the features will be drawn away from the paralyzed side because the normal balance 
between the muscles on the two halves of the face has been destroyed. Unlike 
the facial paralysis due to a lesion in the facial nucleus in the pons or in the facial 
nerve itself, the upper muscles escape, and so we find that the muscles of the forehead 
and eyes are not paralyzed; the forehead can be wrinkled and the eyes can be closed. 

In the stage of onset we sometimes find the head and eyes turned sharply to 
one side (conjugate deviation), usually away from the paralyzed side. When 
this occurs it is said that the eyes "look at the lesion." The pupils are sometimes 
contracted, but more commonly are dilated, the pupil on the side upon which the 
hemorrhage has taken place being more dilated than its fellow. 

Pricking or pinching the skin of the paralyzed side is not followed by any reflex 
contraction soon after the onset, though the deep reflexes may be present, but later, 
when the primary shock has passed away, it will be found that the skin reflexes 
as well as the knee-jerk and other deep reflexes are exaggerated, particularly upon the 
paralyzed side. Irritation of the sole of the foot almost invariably causes extension 
of the big toe (Babinski's reflex), a reversal of the normal plantar reflex, which is 
flexion of the toes. Ankle-clonus is also frequently present. 

In cases in which the bladder and the bowel are full at the time of the "stroke," 
the shock of the hemorrhage may result in involuntary evacuations, but in some 
cases the bladder and rectum are not only retentive, in the ordinary sense, but 
fail to empty themselves when they become full. The bladder of an apoplectic 
patient should, therefore, be frequently examined, and if the urine accumulates 
in excess it must be withdrawn by the catheter. If the urine is examined a trace 
of albumin is usually found in it, even if actual renal disease is not present. The 
temperature of the body immediately after a hemorrhage is usually subnormal. 
With reaction from the primary shock, which is often of brief duration, the tem- 
perature rises from one to three degrees, the chief change being on the paralyzed 
side. 

The unconsciousness of the early stage of apoplexy may last from a few hours to 
several days, according to the severity of the lesion. When it persists for any length 
of time the prognosis is correspondingly bad. In some cases the depth of the coma 
decreases and the patient emerges to some extent, only to sink back again into 



HEMORRHAGE INTO THE BRAIN 791 

deep coma and high fever a few days later when a secondary hemorrhage takes 
place, perhaps bursting into the ventricle, or secondary irritation of the brain, 
produced by the presence of the extravasated blood, develops. In other cases 
in which the extravasation of blood has been limited, and the parts damaged are 
not of vital importance, the patient gradually improves in his mental state and 
progresses toward recovery. In most cases, however, the mind never completely 
recovers its previous acuity. 

The persistency of the hemiplegia also varies greatly in different cases. It 
may remain absolutely unchanged, one-half of the body being helpless, or it may 
diminish in severity and even greatly improve to the extent that the patient can 
walk about and write. In most of the cases, however, in which this much-to-be- 
desired result is attained, the lesion has probably been due to embolism or throm- 
bosis rather than to an actual hemorrhage. 

Many patients after an attack of apoplexy not only suffer from a degree of 
mental failure, but in addition become exceedingly irritable or emotional, crying, 
laughing, or getting into a furious temper at slight causes. Distinct loss of emo- 
tional control has been said to be particularly prone to occur when the lesion 
involves the frontal lobes. 

There still remain to be considered several additional symptoms of apoplexy 
which are often present. The most important of these is aphasia. It is most 
common in cases in which the right side is paralyzed, because the speech centre is 
chiefly in the third left frontal convolution. If the patient is left-handed, however, 
the aphasia is present when the left side is paralyzed. The symptom aphasia 
varies very greatly in the time at which it is first evident and in its severity. Not 
infrequently it is one of the first signs of a beginning apoplexy, the speech becoming 
suddenly confused and indistinct. In most cases, however, the aphasia is first 
noticed after the patient recovers from the immediate effects of the stroke. The 
persistency of the aphasia varies greatly. In some cases it remains so severe 
that the patient has great difficulty in making himself understood. In others it 
improves so greatly that it may entirely disappear, or only be present when the 
patient becomes very tired or excited. 

Another special symptom is hemianopsia, which is of the homonymous type, 
that is, the corresponding halves of the visual fields are darkened because the 
temporal half of one retina and the inner or nasal half of the other retina has lost 
its visual function. 

Hemianesthesia persisting after recovery from the primary shock is a rare symp- 
tom and is never complete, thereby differing from the hemianesthesia of hysteria. 
The sense of heat or cold or touch may be impaired, but total loss of the senses does 
not take place. 

When the power of recognizing objects placed in the hand is lost (astereognosis) 
it indicates a lesion in the superior parietal portion of the cortex on the opposite 
side. (See Fig. 131.) 

In some cases of hemiplegia of a severe type bed-sores develop on the heel or 
buttock of the affected side. The tendency to this accident can be greatly decreased 
if the patient is not permitted to lie in one position for long periods of time, and if 
great care is taken as to the cleanliness of the skin in the places where pressure is 
marked. 

As a sequence to an apoplexy we find not only persistent paralysis, but as time 
goes on contractures occur in the affected limbs. The forearm and hand, however, 
suffer far more than the leg. The flexor muscles being stronger than the extensors, 
the hand is usually found in marked flexion upon the wrist, and the fingers are 
turned into the palm of the hand. The leg is usually held in the position of exten- 
sion so that it cannot be bent at the knee, and for this reason it is often swung with 
a lateral movement from the hip when the patient attempts to walk. These 



792 DISEASES OF THE NERVOUS SYSTEM 

contractures are usually much diminished when the patient is asleep, and are due 
to degenerative changes in the crossed pyramidal tracts. (See Fig. 128.) Occasion- 
ally, that curious mobile spasm of the fingers or other members, called "athetosis," 
is a sequence of apoplexy and posthemiplegic chorea may develop. This is most 
common in the hemiplegias of childhood, but occurs in adults. Full doses of 
strychnine may produce spastic contractions in old cases of hemiplegia. Next 
to signs of spasm the most common sequel is muscular atrophy, which is due 
in part to disuse of the muscles in the paralyzed limbs and does not develop till 
some time after the acute stage of the attack. Charcot has reported instances in 
which true trophic joint changes took place, but they are exceedingly rare. 

The symptoms of an attack of apoplexy in which the lesion has been due to 
rupture of a branch of the middle cerebral artery having been described there still 
remain to be considered those additional symptoms which develop when other 
parts of the cranial contents are affected by the giving way of other vessels. 

When a vessel in the dura mater is ruptured, usually as the result of an injury, 
it is the middle meningeal artery or vein which suffers as a rule. The clot which is 
formed is either outside the dura mater (extradural) or beneath it (subdural). 
The noteworthy peculiarity of these cases is that the primary unconsciousness due 
to a blow speedily disappears, the patient may recover his normal mental state, 
and then, after an interval varying from some minutes to several hours or days, 
becomes heavy and dull, and finally comatose. Spasmodic movements of the muscles 
on one side of the body, followed by paralysis, may develop. If the extravasation 
of blood is large, the pupil on the paralyzed side is contracted and that on the side 
of the hemorrhage is dilated. This is called the "Hutchinson pupil." The eyes 
are turned away from the lesion, whereas in the acute stage of an ordinary apoplexy 
they are turned toward it. It is in this form of apoplexy that surgical interference 
is absolutely essential to save life. Such hemorrhages sometimes occur in the 
insane without a history of injury, particularly in paretics and in chronic alcoholics. 

In hemorrhage from a vessel upon the cortex, as one of the branches of the Sylvian 
artery, it is important to recall the fact that muscular spasm, or a convulsion, 
usually ushers in the attack due to the disturbance of the cells in the motor area. 

When the blood finds its way into the lateral ventricles, a general convulsion 
affecting the entire body may develop. Such cases usually pass into deep coma 
and soon die. 

When the lesion is in the pons the temperature is usually soon hyperpyretic, 
the pupils are tightly contracted, swallowing is difficult, and the respiration is very 
slow. Death comes rapidly in these cases as a rule. 

Under the name of "ingravescent apoplexy" a condition is met with in which the 
symptoms develop very gradually, beginning, it may be, by an attack of vertigo 
or aphasia, followed by the slow development of the other symptoms already 
described, so that several days may elapse before the entire symptom-complex 
of apoplexy is present. 

Diagnosis. — An attack of apoplexy, or hemorrhage into the brain, must be separ- 
ated from a number of conditions which may closely resemble it. Two conditions 
which resemble it so closely as to be inseparable in some cases are thrombosis and 
embolism of the cerebral vessels. The symptoms produced by these accidents 
will be found described below. 

An ordinary attack of syncope can readily be differentiated by the pallor, the 
feeble pulse, the weak heart of a fainting attack, and the quick recovery of the 
patient after receiving some rapidly acting diffusible stimulant. 

In epilepsy the peculiar initial cry, the bloody froth at the mouth, the general 
convulsion, and the deep unconsciousness are more constant and severe than 
in apoplexy, even if the hemorrhage takes place in the cortex. Epilepsy is more 
common in the young, apoplexy in those of advanced years, and there may be 



HEMORRHAGE INTO THE BRAIN 793 

scars to indicate previous severe falls in epileptics. A history of epilepsy will 
practically settle the diagnosis, although the epileptic is liable to apoplexy. The 
respiration in the coma of apoplexy continues deep and noisy, the lips and cheeks 
of one side flap in the air current, showing paralysis, and weakness of one arm and 
leg may be ascertained. In the coma of epilepsy the breathing soon becomes 
quiet. Barely in epilepsy weakness of one side of the body or of one limb may 
appear as the patient emerges from the coma; this postepileptic hemiplegia is 
ascribed to exhaustion, for it passes off in a few hours or days, but it may put the 
diagnosis in doubt for a time. 

From the stupid stage of acute alcoholism apoplexy can be differentiated by 
the history of the patient, by the odor of alcohol on his breath, by the fact that 
both legs are moved if they are irritated by pricking, proving the absence of hemi- 
plegia, and by the cool skin as compared to the hot, dry skin of apoplexy. It is, 
however, possible for an apoplectic to have induced an attack by the use of alcohol, 
and therefore the odor of alcohol on his breath is not of great importance from a 
diagnostic standpoint. 

Opium poisoning is differentiated by the presence of contracted pupils, by the 
fact that by shouting the patient can be aroused, by the absence of paralysis, 
and by the presence of the corneal reflexes. 

The coma of uremia and of diabetes may also be mistaken for apoplexy, but 
in uremia there may be edema of the lower extremities, and there is a urinous 
odor about the body and breath of the patient. If the renal disease is of the 
parenchymatous type, the peculiar waxen appearance of the patient and the urine 
heavily loaded with albumin will make the diagnosis clear. If the uremia is of 
the type caused by chronic contracted kidney, these latter signs will not be present 
nor will edema be found, and as apoplexy often complicates this disease the diagnosis 
may be most difficult. Unless the coma is very deep one side may be moved far 
more than the other, revealing the hemiplegia of apoplexy. However, in uremia 
the cerebral condition may be more pronounced in one hemisphere, thus causing a 
hemiplegia ("uremic apoplexy"). In diabetic coma the sweet odor of the breath 
and the presence of sugar and acetone in the urine will make the diagnosis possible. 

In sunstroke likewise hemiplegia may be found, which is not an apoplexy in 
the ordinary sense. 

Finally, it must not be forgotten that apoplectiform attacks not rarely develop 
in the course of general paralysis of the insane. In this disease the speedy return 
to consciousness and recovery of power in the affected limbs, with the physical 
signs of this disease and the mental symptoms, will render a diagnosis possible. 

The separation of the paralysis due to hemorrhage from that due to thrombosis 
depends more upon the history of the patient than upon the symptoms actually 
present. As already stated, hemorrhage usually follows some effort and takes 
place during waking hours, whereas the paralysis of thrombosis develops during 
periods of quiet and rest, as during sleep, so that the patient wakes to find the 
palsy present. In cases of hemorrhage premonitory symptoms are not common, 
but in thrombosis they are nearly constant. Thrombosis is most frequent in 
the aged or prematurely senile, and in syphilitics. Again, thrombosis does not 
cause such violent symptoms nor is the onset of the symptoms so sudden, but 
consciousness is preserved or is not so completely lost, or if moderate coma is 
present it is brief in duration and is followed by mental clearness. Finally, in 
cases of thrombosis, the recovery of power in parts of the paralyzed side may be 
quite rapid, and at the end of a few days only a few mucles, as one arm or leg, are 
affected. Such cases are, however, often mentally feeble, emotional, and forgetful 
after the attack. There is often to be found a history of syphilis, of arteriosclerosis, 
or an infectious disease, which has predisposed the patient to a formation of a clot 
by causing disease in the lining of the bloodvessel or producing changes in the blood. 



794 DISEASES OF THE NERVOUS SYSTEM 

Embolism can be determined by the sudden onset of symptoms during the 
waking hours, as a rule, and by the discovery of some source of clot or foreign 
body, as in an endocarditis with vegetations or a septic "focus elsewhere. Uncon- 
sciousness, when it develops, may be as profound, but is usually more transient 
than in hemorrhage (Mills), and is often entirely absent. The appearance of the 
patient is not so alarming as in hemorrhage, and localized or general twitching 
may be present in the affected limbs. Not rarely, the symptoms improve with 
great rapidity and after a few days may amount to only a partial monoplegia. 
It must be recalled, however, that in some cases of thrombosis and embolism the 
symptoms may be so like those due to hemorrhage that a differentiation is almost 
impossible. 

The chances of the case being one of hemorrhage rather than embolism or throm- 
bosis is as 6 to 1, according to Dana. 

Prognosis. — Many cases of hemorrhage into the brain survive the first rupture, 
but if so they nearly always fall victims to subsequent attacks. Out of 441 cases 
occurring in St. Thomas' and St. Bartholomew's Hospitals, London, 375 proved 
fatal, a mortality percentage of 85. This percentage is, however, far too high 
for private practice, where milder cases are often seen. In the severe cases in 
which the coma is profound, the temperature low and then quite high, the paralysis 
severe, and control of the bladder or bowels impaired, death will probably occur 
in the first attack, and if Cheyne-Stokes breathing is present death nearly always 
takes place within a few hours. If the hemorrhage affects the pons or cerebellum 
death may come on speedily, but when the hemorrhage is small the patient often 
survives. When the hemorrhage is cortical the prognosis is better than in the 
other forms unless the pressure symptoms are severe. The patient not rarely 
dies from pulmonary edema or pneumonia as an intercurrent disease. 

Treatment. — Apoplexy, like other forms of internal hemorrhage, cannot be 
materially benefited by medicinal treatment. If nature does not form a clot to 
plug the bleeding vessel, the hemorrhage must continue until it has done so much 
damage that death is inevitable unless the vessel is on the surface or in the meninges, 
when surgical relief should be given. Again, the pressure with which the blood 
escapes into the soft textures of the brain is so great that if the leak is of any size 
the mechanical injury to the cerebral tissues must be very great, and for this reason 
the organ is permanently disabled. 

Until the researches of Cushing, of Baltimore, in regard to the significance 
of high arterial pressure in cases of hemorrhagic extravasations inside the skull, 
it was universally taught that the presence of a full, bounding pulse in a case of 
apoplexy indicated venesection, particularly if at the same time there was distinct 
venous engorgement, the thought being that by this means the blood pressure 
would be lowered, and that there would be a corresponding decrease in the leakage 
from the ruptured vessel. Cushing's investigations have apparently shown beyond 
all doubt that the high arterial pressure which is so constantly found in persons 
who suffer from hemorrhage inside the skull is an effort of nature to maintain the 
blood supply to the vital centres at the base of the brain, and that if this blood 
supply cannot be maintained because of a fall in arterial pressure death speedily 
ensues. In other words, the maintenance of a high arterial pressure in these 
cases is an advantageous sign, and any marked diminution in arterial tension is an 
indication that the vasomotor centre is becoming paralyzed and that the blood 
supply to the centres at the base of the brain is becoming impaired. If Cushing's 
studies are correctly interpreted hy him, venesection or the administration of 
vascular sedatives, with the purpose of lowering tension, is therefore a distinctly 
harmful method of treatment, and truth demands that we should admit that the 
physician can do little if anything in the way of controlling the escape of blood. 

For the purpose of apparently making an effort to do good for the sake of the 



INFANTILE CEREBRAL PARALYSIS 795 

friends who may demand activity rather than masterly inactivity, a hot mustard 
foot-bath may be given, and some diffusible stimulant like Hoffmann's anodyne 
may be used if the patient is able to swallow or atropine may be given hypo- 
dermically if arterial tension falls and the surface becomes cold and clammy. 

If vomiting occurs, the patient should be promptly turned on one side so that 
free drainage from the mouth may take place, and in order that particles of food 
may not be drawn into the respiratory passages. 

If the tongue falls back in such a manner as to make the breathing difficult it 
should be drawn forward by means of the fingers covered with a towel. If, by 
chance, the patient is convulsed, his tongue should be protected from damage by 
placing between the teeth a penholder or tooth-brush handle wound around with 
a piece of muslin. 

The patient's body should always be put in that position in which breathing 
is most easily carried on. 

The treatment after the hemorrhage has ceased consists in absolute rest, in 
the application of an ice-bag to the head, and attention to the bowels and bladder 
to prevent them from becoming overdistended. Gentle purgation is probably 
advantageous for its influence upon the brain. If any evidence of nervous excita- 
tion exists, it may be controlled by small doses of the bromides or morphine. If 
any tendency to secondary reaction develops in the course of a few days, cold to 
the head and small doses of aconite to quiet the circulation may be administered. 
Later on, with the hope of diminishing the paralysis, iodide of potassium may be 
given in moderate doses in order that it may aid in the absorption of the extra- 
vasated blood and remove products of inflammation. There is little use in giving 
the iodide of potassium for the purpose of causing absorption earlier than two or 
three weeks after the hemorrhage. Strychnine is usually not valuable in these 
cases, as it is very apt to produce spasm or contracture in the parts which are 
paralyzed by irritating the motor tracts in the spinal cord. 

From three to four weeks after the hemorrhage it is often advantageous to apply 
a slowly interrupted faradic current to the paralyzed muscles, with the object of 
maintaining their nutrition by exercise and keeping them in the best possible con- 
dition, in the hope that eventually they may receive a sufficient amount of nervous 
impulse from the cerebral centres to be able to respond sufficiently to permit the 
patient to move his limbs. Massage is another excellent means to combat the 
loss of power. Passive and active movements followed by a course of systematic 
exercises will render valuable service in combating secondary contractures of the 
paralyzed extremities. Great care should be taken that all stimulants which 
increase circulatory activity, and all foods which readily cause indigestion, be 
avoided, as these two factors tend to produce that most unfortunate complication, 
another hemorrhage. 

INFANTILE CEREBRAL PARALYSIS. 

Definition. — As a result of injury or disease of the brain during fetal life or soon 
after birth, it not rarely happens that certain portions of the cerebrum fail to 
develop, and as a consequence a number of very characteristic conditions are 
produced, which depend in their nature upon the site and size of the atrophied 
region. 

These conditions can be grouped in three divisions : In the first there is a spastic 
paralysis which may be limited to one side of the body (spastic hemiplegia), or it 
may be bilateral (spastic diplegia). In spastic diplegia the legs may be affected 
alone or the arms and legs may both be involved. The second class is chiefly 
characterized by mental failure varying in severity from slight intellectual deficiency 
to absolute idiocy. In some instances the defect is manifested by epileptic attacks. 



796 DISEASES OF THE NERVOUS SYSTEM 

The third class presents disorders of the special senses, such as blindness, deafness, 
mutism from deafness, and it may be epileptic seizures as well. 

Etiology. — Acute infectious disease occurring in the mother during pregnancy 
may result in lesions in the fetal brain. Syphilis may also act in this manner. 
It is probable, too, that definite developmental defects may be hereditary, as when 
the parent or parents are epileptics, neurotic, alcoholic, or otherwise degenerate. 
Premature labor is a frequent cause of diplegia. A very large proportion of cases 
develop as a result of injury during birth because of a meningeal or cerebral hemor- 
rhage. In a few cases the damage is due to a fall in early infancy, and in still 
others there develops some time during the first three years of life a cerebral throm- 
bosis, a hemorrhage, an encephalitis, or a meningitis which is followed by the brain 
symptoms about to be described. Such a condition may arise as a complication 
or sequela of any one of the acute infectious diseases of childhood. A convulsion 
may be said to be the cause in certain cases, but it is probable that the lesion in the 
brain is responsible for this symptom rather than that it is the provoking factor. 
Finally, there are certain cases in which it is impossible to discover any cause 
whatever. 

Pathology and Morbid Anatomy. — When spastic paralysis is present it is due to a 
lesion which involves the motor portion of the cerebral cortex and neighboring 
convolutions. The lesion itself in long-standing cases is sclerotic or atrophic 
in character and is associated with similar changes in the motor fibres, which pass 
from the cortex, and occur in the basal ganglia as well. In some cases the sclerotic 
change is limited to these ganglia. When there is diplegia both sides of the brain 
are involved. In that type of case in which mental impairment is present the 
atrophy and sclerosis affect the anterior convolutions of the brain, and when 
disorders of special sense are present it is because the perceptive centres of the 
senses affected are involved in the damaged area. It is readily seen, therefore, 
that as the lesions are distributed so are the manifestations of the disease varied. 

The exact nature of the cerebral lesions has been found to be of several types: 
(1) A localized atrophy, or failure of development, may produce an excavation 
of the surface of the brain, usually due to meningeal hemorrhage at birth, with 
formation of a clot which indents the delicate cortex permanently. This indenta- 
tion is called porencephaly (poros, the Greek word for "hole")- (2) A sclerotic 
process with overgrowth of connective tissue and atrophy of the nervous protoplasm 
may be present. (3) Imperfect development of the cerebral cells may be found 
or arrested myelinization of the nerve fibres of the motor tract. (4) Atrophy 
may follow cerebral softening produced by the closure of a vessel by an embolus 
or thrombus. (5) An inflammatory process in the pia mater may cause an adhesion 
to the cerebrum and so cause atrophy (meningo-encephalitis) . (6) A cerebral 
hemorrhage may not only destroy the cerebral tissue, but cause a cyst to develop. 
(7) A cyst may cause atrophy from pressure. (8) Hydrocephalus, in which state 
the cerebral ventricles may be so distended that the brain tissues atrophy from 
pressure. (9) Rarely an external hydrocephalus may produce the same results. 

Symptoms. — The symptoms in a child affected by this accident, like those of 
ordinary apoplexy, vary greatly in speed of onset, in severity, and in type. When 
the lesion occurs at birth there are often no symptoms for several days or even 
weeks, except it may be an unusual limpness of the limbs and some difficulty in 
swallowing. In other cases unilateral spasms or general convulsions speedily 
develop, but these are not of long duration, and it is- noticed that the child's head 
is not held erect, but falls from side to side, backward or forward. The convulsions 
may affect the entire body, or be confined to the side in which paralysis is about 
to develop. Associated with these convulsions there is a marked rise in temperature, 
the fever sometimes reaching as high as 105°. After the convulsion there may be 
postconvulsive coma, which may last several days. Gradual improvement now 



INFANTILE CEREBRAL PARALYSIS 



797 



Fig. 131 



takes place, and as the child returns to consciousness it is found that there is 
loss of power upon one side of the body. Shortly afterward it is also noticed that 
the arm upon the affected side is not only paralyzed, but that it is in a somewhat 
spastic state. The leg suffers in a similar manner. Later on, club-foot and a sharply 
flexed hand develop from secondary contractures. The paralyzed limbs fail to 
develop as they should, become atrophied, and are often considerably shorter than 
the limbs upon the healthy side. The reflexes are exaggerated and Babinski's sign 
is present. Sensation is not impaired. 

If the child survives, the paralyzed parts gradually become markedly distorted 
and tenotomies may be necessary to prevent the contracture from causing so 
great a deformity as to make any motion im- 
possible. Even these means may not make 
walking possible. If the intellectual portions 
of the brain are not involved, and if the 
patient reaches the years of puberty, it not 
infrequently happens that by prolonged train- 
ing a very remarkable degree of ability is de- 
veloped in the nonparalyzed side so that the 
individual can follow some pursuit which will 
render him self-supporting. In other instances, 
however, the spastic condition of the affected 
limbs is very marked, the hand is sharply flexed 
at the wrist, and athetoid movements of the 
fingers may be present whenever any attempt 
is made to move them. These athetoid 
movements occur very soon after the para- 
lysis is noticed in certain cases. In others 
they do not develop for a long time. The 
state of the legs is even more noticeable, if 
such a thing be possible. Here we find that 
the parts are at once placed in strong exten- 
sion if they are touched, the muscles of the 
calf are tightly contracted and the feet are 
inverted or turned inward. The thighs are 
abducted. When the attack comes on after 
the child has learned to speak, there may be 
marked aphasia for a time, but this symptom 
often gradually disappears. 

Spastic diplegia may affect either the arms 
or the legs, usually both arms and legs, and 
is characterized not only by loss of power in 
these parts, but by rigidity, which is particu- 
larly marked in the lower extremities. The 
symptoms usually develop slowly, not acutely 
as they do in spastic hemiplegia. 

When a hemiplegia develops in a child of 
a year or more it is usually due to hemor- 
rhage or embolism or to the polio-encephalitis of Striimpel rather than to 
meningeal disease. 

Various deformities of the lower limbs occur, and the muscles of the trunk, 
particularly at the back, are so rigid that the child is as if fixed in a plaster cast. 
In other instances where the condition has developed some time after birth, the 
patient can sometimes walk by the aid of a cane or crutches, but in those instances 
in which the lesion is severe the contractures and athetoid movements, the exag- 





• 




' 


fa*. \ *m 1 






P 






\l / 






;f W 






' \ 






.;" % 








" 



Hemiplegia, with contractures. The 
patient had suffered since the age of two 
years. (Curschmann.) 



798 DISEASES OF THE NERVOUS SYSTEM 

geration of the reflexes, and the imperfectly developed muscles all combine to 
make the child absolutely helpless. There is no loss in the control of the sphincters 
nor any trophic disturbances in the way of bed-sores, nor are there any sensory 
disturbances or electrical reactions of degeneration. 

Both of these types not infrequently suffer from epileptic convulsions, which 
may be of the Jacksonian type. In those cases which are due to lesions in the 
intellectual area of the brain, idiocy may be present. In those instances in which 
the defect of mental power is not complete the patient is called an imbecile. Such 
patients are often subject to violent outbursts of anger, to attacks of malicious 
mischief, and are often exceedingly filthy in their habits. 

In the cases in which the posterior portions of the brain are affected, the disorders 
of special sense do not usually make themselves manifest until the child is at least 
a year or eighteen months old. Often prior to the discovery of any symptoms of 
disorder of special sense, epileptic convulsions have called attention to the fact 
that the cerebral development is imperfect. In some instances the disorders of 
vision may amount to nothing more than a hemianopsia. In others there may 
be total blindness, or deafness, or loss of smell and taste. In these cases also 
ordinary epilepsy and Jacksonian epilepsy are often present. In some instances 
minor epilepsy takes the place of major epileptic attacks. 

Diagnosis. — The diagnosis in a well-developed case of infantile cerebral paralysis 
is not difficult. The early development of the malady (after a hard labor it may 
be), the marked arrest of normal development, and the epileptic convulsions, with 
the spastic state of the muscles, all separate this form of infantile paralysis from 
those forms which depend for their existence upon lesions in the spinal cord, for 
in the latter the paralyzed parts are flaccid. There are, however, two forms of 
spinal spastic palsy of childhood with which this condition can be confused, one 
of which is the so-called "hereditary spastic spinal paralysis," but in this disease 
the mental symptoms are lacking and the condition is progressive. The second 
state which resembles this disease is "amaurotic family idiocy," but in this malady 
the paralysis may be flaccid or spastic and blindness is an early symptom. There 
is also a characteristic change in the fundus; a cherry-red spot in the region of the 
fossa centralis, surrounded by a whitish areola. The very rarity of these diseases 
serves to exclude them. 

Prognosis. — It must be evident that the prognosis as to complete recovery in 
severe cases is anything but good. In those cases in which the mental powers 
are feeble and convulsions frequently recur, the outlook is bad both as to recovery 
and a long duration of life. If they live they are hopeless imbeciles or idiots. 
When the affection is confined chiefly to one side of the brain — that is, when there 
is hemiplegia — adult years may be reached and ordinary mental pursuits followed 
in many cases. 

Some of these patients, moreover, can be materially improved by proper training, 
in which instance special centres which are not impaired, or intellectual centres which 
have escaped the wreck, may be developed to such an extent that a fair degree of 
comfort and intelligence may be attainable. The convulsions cannot be cured, 
as they depend upon faulty development, but they may be modified by skilful 
treatment, consisting in the administration of nervous sedatives, the avoidance 
of all causes of nervous excitement and irritation, and the moderate employment 
of the bromides: As a rule, better results can be obtained from hygienic methods 
and from mental training in an institution devoted to this purpose than can be 
obtained at home. At one time it was considered that operative interference might 
be of very great value in these cases, but we now know that little can be expected 
from such a plan of treatment. In those cases in which the skull has seemed 
to be abnormally small it was proposed that the skull should be cut, or bone should 
be removed, in such a way as to permit expansion of the brain. But the smallness 



APHASIA 799 

of the skull is probably more dependent upon the size of the brain than is the size 
of the brain upon the condition of the skull. In some instances the parents prefer 
running the risk of the child's death as the result of such a grave operation rather 
than to have it continue a hopeless invalid, and in such cases, if there are distinct 
localizing symptoms, epileptic or otherwise, the question of cerebral localization 
and operation must be carefully considered. 

Little's Disease. — The name "Little's disease" has heen applied by some writers 
to the cerebral palsies of childhood ; but is probably best restricted to cases- in 
which there is congenital spastic rigidity of the limbs, particularly of the legs, 
tending to improvement. In Little's disease, thus defined, there is normal mental 
capacity and no epilepsy or athetosis. The condition is purely motor from defective 
development of the pyramidal system in the brain or, according to Dejerine, in 
the spinal cord. 

APHASIA. 

Definition and Symptoms. — Aphasia is a condition in which the function of speech 
becomes impaired or arrested as the result of disease involving those parts of the 
brain which are concerned with the expression of ideas in words. For the power 
of speech it is necessary that the individual shall have not alone the motor centres 
which will cause the proper muscular movements which give rise to certain sounds, 
but in addition there must be, in close association with these centres, others in 
which the conception of an idea must originate, and still others in which a sense of 
the appearance of words, or sounds of words, is stored. When a child is learning 
to talk, an object, such as a horse, is pointed out to him, and the word "horse" is 
frequently repeated at the same moment. He therefore learns to associate a 
certain shape and form with the word "horse." For him to do this it is necessary 
that his visual apparatus shall carry to his brain a certain form, and that his brain 
should store up that form as typifying a certain object. It is also necessary that 
his auditory apparatus shall carry to his brain a certain sound or sounds, and that 
his brain shall associate this sound with the form that he has seen. In addition 
it may be that he has touched or stroked the horse, and so his sense of touch has 
conveyed to his brain a certain model, or form, which is associated with those 
received by means of his eyes and ears. When, therefore, he sees a horse a second 
time the memories or imprints derived from these various sources are utilized, and 
he attempts to reproduce the word "horse" by a process which calls into play 
certain muscles which are necessary for making this sound. Speech is therefore 
in one sense a complicated function, closely connected with the organs of special 
sense, of intellection, and with the motor neurones as well. This is perhaps made 
more clear by the following diagram : 




A 

o 

A, pathways for receiving imprints or models; B, centre for storage of models; C, centre for storage of 
motor memories; D, concept centre; E, motor centres for controlling muscles of speech at F. 

A visual impulse, an auditory impulse, a touch impulse, an olfactory impulse, 
or a taste impulse, or all of them together, pass to the centre B, where they are 
received and stored. From B these memories or imprints are transmitted, when- 
ever they are needed, to those centres in the brain which are concerned with the 



800 DISEASES OF THE NERVOUS SYSTEM 

power of the conception of an idea, or they may be transferred directly to C, which 
may transform them into speech by mimicry, without any idea or higher intellectual 
process than that concerned with imitation. If the child thinks of a horse at D, 
he receives memories of the character of a horse from B and sends from D an impulse 
which causes C to send impulses to the organs of speech. It is evident, therefore, 
that if the sensory tracts are diseased before the centres for storing the record 
are developed, or if any part of the mechanism described in the diagram is unde- 
veloped or damaged, the entire chain fails because one of its links is broken. 

This process may, however, be even more complicated than that described. 
Thus, there may be stored in the storage centre not only the model or imprint 
of a horse but also the additional memory of the appearance of the word "horse" 
when in type, and in addition there may be stored the memory of certain move- 
ments which are characteristic of a horse, so that the child can imitate its movements 
or perhaps draw an outline of its appearance. While pantomine and drawing 
are not speech, they are so nearly related to it as to really form part of it. Again, 
it is necessary that there should be stored at C the models or memories of those 
muscular movements which will give rise to the sound of the word horse, for this 
is part of learning how to talk. 

In certain cases in which the brain is diseased the patient may see and feel and 
hear a horse, and his concept centres may know perfectly that a horse is before him, 
or that the word "horse" is in print, but he cannot say the word "horse" because 
the centres concerned with the storage of memories of the muscular movements 
necessary to speak the word "horse" are destroyed. He may write the word 
"horse" or draw a horse, but he cannot say "horse." 1 To this form of motor 
aphasia the word aphemia is applied. If the centre in which the memories of 
how to write the word "horse" are destroyed the condition is called agraphia, 
and if those in which the muscular movements required to describe a horse by 
gesture are diseased it is said to be amimia. When the tracts that associate the 
storage centres for memories of words are interfered with, the patient skips, or 
jumbles, or repeats his words, and this is called conduction aphasia; and if he speaks 
one word when he means another, it is called paraphasia. 

On the other hand, when the sensory portion of the speech mechanism is diseased 
the patient may be able to say the word "horse," but if he sees a horse he cannot 
say that he has seen it because he has lost the memories of the horse; or if he sees 
the word "horse" in print, he may be able to reproduce the letters in writing, in 
their order, but he is entirely unable to read, for he has lost the memory of the 
significance of these letters when so joined. This is called alexia, or word blindness 
an unfortunate term, as blindness would indicate failure of visual power, which 
does not exist. Again, in certain cases there is loss of memory of sounds. The 
voice of a speaker may be heard and even imitated, but the patient understands 
nothing more than if an unknown language was spoken. It conveys no idea to 
his mind. This is called word deafness — another unfortunate term, because hearing 
in the ordinary sense of that word is perfect. Apraxia is still another nearly 
related state in which the patient fails to appreciate the purposes or uses of an 
object. He may see, hear, and touch a knife or a coin, but his mind cannot grasp 
its uses. 

When we come to study the lesions which produce these disturbances in the 
ability to express an idea, we find that when the patient has aphemia or motor 
aphasia the damage has been done to the third left frontal convolution (Broca's 
convolution). In such a case he also cannot write either his own ideas or the words 
that he hears spoken, but he can copy. If the lesion is a severe one, his power of 
understanding words he sees written or hears spoken is usually impaired. In 

1 As a matter of fact, these powers are usually lost. 



TUMORS OF THE BRAIN AND ITS MEMBRANES 801 

other words, he also suffers from word-blindness and word-deafness. When he 
has word-blindness or alexia, the lesion is at the left angular gyrus. If there is a 
pure alexia the lesion is in the subcortical substance of the left angular gyrus. In 
word-deafness the lesion is in the posterior part of the first temporal convolution 
on the left side. Aphasia also develops when a lesion takes place from hemorrhage, 
embolism, or thrombosis in the knee of the internal capsule, for at this point the 
fibres which convey speech impulses are destroyed. 



TUMORS OF THE BRAIN AND ITS MEMBRANES. 

Intracranial tumors arise from the substance of the brain itself or from the 
membranes which surround it. A great variety of these growths have been recorded, 
but by far the most common are tubercle, gumma, glioma, and sarcoma. Cancer, 
fibroma, neuroma, and vascular tumors also rarely occur. Echinococcus cysts 
may develop. 

Etiology and Frequency. — The causes of these morbid growths are not understood 
except in the case of tubercle and gumma. Sex seems to exercise a very distinct 
influence, for we find that males suffer very much more frequently than females. 
Gowers states that out of 650 cases of brain tumor 440 occurred in males to 210 
in females. Dana gives the figures at 644 to 320, and Starr's figures are nearly 
identical in their proportions. This great preponderance in males is not explained 
by either syphilis or injury, for there is no greater frequency of gumma in men than 
in women. On the contrary, tubercle and glioma are the growths that are particu- 
larly frequent in men. Gowers has shown that after the first six months of life 
till old age all ages suffer about equally. Thus, the percentage in the first decade 
is 18.5, in the second 14, in the third 20, in the fourth decade 18.5, and in the fifth 
14. Most of the growths in childhood are tuberculous, and indeed they form 53 
per cent, of all growths at all ages, if gumma be excluded. 

Pathology and Morbid Anatomy. — Tumors of the brain affect its tissues in its 
different areas as follows, according to Gowers: In the hemispheres 297, in the 
cerebellum 179, in the base of the brain 76, in the pons 59, in the central ganglia 
48, in the medulla 31, in the corpora quadrigemina 13, and in the crus 10. 

Tuberculous tumors occur as solid, firm, round masses which are not rarely 
multiple. Their size varies from that of a pea to a hen's egg or even larger. The 
growth starts from the lymphoid sheaths of the vessels, and rapidly obliterates 
them. For this reason it is devoid of vessels and its tissue soon undergoes necrosis, 
so that on section it is cheesy and shows spots of softening. As the surface is soft, 
and the surrounding brain substance is also softened, the mass is clearly outlined, 
hence the name tuberculoma. Finally, the growth may become calcified or undergo 
suppuration. Tuberculous growths are often found in the cerebellum, and they 
also occur in the pons and cerebrum. When in the cerebrum they are usually 
found along the great vessels in the interpeduncular space or in the fissure of 
Sylvius ; not rarely the growth is near a Pacchionian body, but it may be found in 
the depths of the centrum ovale. 

Gummata of the brain rarely reach a size greater than that of a hickory-nut. 
They are also somewhat cheesy in appearance and have an irregular surface, 
which may be gelatinous, or indurated and hard, and enclosed in a fibrous cap- 
sule. These growths are thought to spring from the bloodvessels of the dura 
mater. 

Sarcomata occur as round, oval, or spindle-cell tumors which destroy the tissues 

of the brain as they grow. When they are of the gliomatous type they differ 

greatly from all the growths so far described, for they are not round, but extend 

by a process of infiltration between the nerve cells. They may be soft and mucoid 

51 



802 DISEASES OF THE NERVOUS SYSTEM 

(myxoglioma) , or firm and fibrous (fibroglioma) . Gliomas of the soft variety are 
liable to hemorrhage. A cystic form of glioma due to softening is not rare. Glio- 
mata are usually single. 

The secondary changes produced by these growths are of importance and depend 
chiefly upon the pressure of the tumor upon healthy tissues which in this way are 
destroyed. The very growth of the tumor inside the skull also increases intracranial 
pressure, and if it be so situated that it prevents the free passage of cerebrospinal 
fluid from the choroid plexus in the lateral ventricle through the third ventricle 
and the iter a tertio ad quartum ventriculum, then distention of the lateral ventricles 
or internal hydrocephalus develops. A tumor of the pons, of the corpora quad- 
rigemina of the middle lobe of the cerebellum, or in the third ventricle may cause 
such obstruction. A third result of the intracranial tumor is irritation of the nerve 
cells of the brain and inflammation in them or in the meningeal membranes, and 
lastly it may cause actual thinning of the skull by the pressure induced. 

Symptoms. — By far the most common symptom of brain tumor is headache, 
constant in type like all headaches of organic origin. This headache is usually 
severe and is characterized by sharp exacerbations. In some instances it is dull 
and boring in character. In others it is sharp, stabbing, and tearing. By reason 
of its constancy it prevents sleep, and in its most severe paroxysms, may produce 
temporary aberration of mind. The pain is widely diffused, and is particularly 
severe if it encroaches on the dura which is supplied with sensation by the fifth 
nerve. If the pain is localized it does not necessarily indicate that the growth 
is in that neighborhood, although in those cases in which the tumor is superficial 
the locality of the growth and of the pain is often identical. 

Next to headache in constancy as a symptom is vomiting. The expulsion of 
the stomach contents is usually spoken of as "projectile," and in this respect it 
resembles the vomiting of certain forms of intestinal obstruction. Although the 
vomiting is severe, nausea is often absent. This symptom is supposed to be most 
frequent and severe when the growth is rapidly progressing. Vertigo also occurs 
and varies from slight dizziness to a degree which causes the patient to fall. Not 
infrequently this vertigo causes the patient to walk in the direction in which it is 
not his intention to go. Vertiginous symptoms are more common in tumor of 
the cerebellum than in lesions elsewhere, and often the patient falls to one 
side. Another very important symptom of brain tumor is optic neuritis, which 
occurs in a large proportion of cases and which often enables us to make a 
diagnosis of brain tumor with the aid of the ophthalmoscope when the other 
symptoms are so obscure that it is difficult to determine the nature of the patient's 
disease. 

Optic neuritis is usually most marked in cases of tumor of the cerebellum, of 
the midbrain, and of the great ganglia near the base. It occurs less frequently 
when the tumor is in the cortex or springs from one of the membranes, but the 
localizing value of neuritis is really not great. Nearly always both optic nerves 
are involved, although sometimes the lesion develops in one before it attacks the 
other. Gowers gives three reasons for this optic neuritis: First, irritation of the 
nerve fibres produced by the pressure which finally causes inflammation. Second, 
distention of the nerve sheaths and the lymphatic spaces of the papilla by sub- 
arachnoid fluid, which, perhaps, contains irritating poisons. The third cause is 
thought to be inflammation of the meninges, which is so frequently present, and 
which may extend to the optic nerve. 

Slowness of thought and gradual mental failure are not infrequently present. 
Sometimes aphasia develops. All these three symptoms are prone to occur when 
the tumor affects the frontal lobe, and the symptom of aphasia is, of course, most 
frequently developed when the left frontal lobe is involved. Epileptiform con- 



TUMORS, OF THE BRAIN AND ITS MEMBRANES 803 

vulsions occur in about one-quarter of the cases of brain tumor, and are especially 
marked in those instances in which the growth directly or indirectly produces irrita- 
tion of the cortex. So, too, there may be symptoms which for a time resemble the 
early stages of an apoplexy. Quite rarely actual rupture of a bloodvessel occurs, 
and so the symptoms are really apoplectic. 

Paralysis due to brain tumor may be unilateral or bilateral. When unilateral 
it may manifest itself as a monoplegia or as a hemiplegia. It is usually gradual 
in onset, and when hemiplegic in type is due to the presence of a growth in the upper 
part of the pons, in the crus, or in the internal capsule, or over a wide area in the 
cortex. Localized paralysis, such as monoplegia, may be due to a growth involving 
the cortex or the subcortex before the fibres have come together so closely that 
even a small tumor must affect the whole bundle and produce widespread paralysis. 
Such a monoplegia involving the arm or leg is not infrequently associated with 
epileptiform attacks, limited to the paralyzed part. If the growth is in the lower 
third of the pons the ordinary form of crossed paralysis may be present, the face 
being paralyzed on the side of the lesion, while the arm and leg are paralyzed on the 
opposite side. 

A rarer form of crossed paralysis (Weber's syndrome) may result from tumor 
of one crus involving the third nerve. The eyes are deviated to the side opposite 
the lesion and the pupil dilated on the side of the lesion, while the arm and leg, 
as in ordinary hemiplegia, are paralyzed upon the opposite side. 

Bilateral paralysis due to brain tumor can only occur when the growth is multiple 
and presses upon both sides of the brain, or when it is so situated that it can at 
once cut off fibres from both sides as they approach the middle area, as in the pons 
or in the medulla. Under these circumstances the legs are usually more affected 
than the arms, even though the face as well as the arms be included in the paralysis. 
Contractures, tonic spasms, or convulsions, either generalized or Jacksonian, may 
also occur. They usually indicate that the growth is situated somewhere near the 
cortex, where it produces other irritations. 

If the tumor is in the frontal area and grows forward it may cause protrusion 
of the eyeballs and paralysis of the extrinsic muscles of the eye, while if it grows 
backward it may cause spasm and epileptiform convulsions by the irritation of 
the motor area of the cortex. 

The development of a cortical growth in the posterior part of the frontal lobe 
along the fissure of Rolando produces symptoms which are more definite than 
those which are found in association with growths elsewhere, because it is the 
motor area of the brain. Not infrequently localized convulsions, or Jacksonian 
epilepsy, occur in such cases and paralysis limited to the same muscles may follow 
such an attack. The part in which the convulsion begins and the subsequent 
paralysis indicate the presence of the tumor in or beneath the centre supplying the 
centres controlling these muscles. Disorders of sensation in the affected limb may 
be present, consisting of numbness, tingling, and even hemianesthesia. 

When a tumor involves the parietal region the symptoms are not definite, but 
pertain chiefly to common sensation and "muscle sense." 

If the superior parietal lobule be invaded there is more or less loss of "muscle 
sense," and often the symptom astereognosis is present. When the angular gyrus 
on the left side is involved, word blindness may be present. 

When that portion of the parietal area near the longitudinal fissure is invaded 
we not infrequently have spasms or convulsions in the lower extremities on the 
side opposite the lesion, because the growth begins to invade the part of the leg 
centre which is on the inner surface of the hemisphere. 

Tumors of the occipital lobe, if in the cuneus or otherwise near the calcarine 
fissure, produce lateral homonymous hemianopsia. If the growth in the occipital 



804 



DISEASES OF THE NERVOUS SYSTEM 



lobe is sufficiently far forward to involve some of the parietal area, and so do 
damage to the angular gyrus, word-blindness and hemianopsia may develop, and 




Showing the areas of the brain concerned with special functions. 1. Prefrontal area. 2. Central 
area. 3. Parietal area. 4. Occipital area. 5. Temporal area. (Modified from Fuller.) 

Fig. 134 




6. Corpus callosum. 7. Thalamus opticus. 10. Corpora quadrigemina. 11. Crus. 12. Pons. 
13. Medulla oblongata. 14. Cerebellum. 15. Fourth ventricle. (Modified from Reichert.) 



if the invasion extends still farther, hemiataxia, hemianesthesia, and even some 
hemiplegia due to involvement of some of the fibres of the internal capsule may 
be present. 



TUMORS OF THE BRAIN AND ITS MEMBRANES 



805 



In the first left temporal convolution brain tumor produces word-deafness, 
a form of sensory aphasia. Occasionally large tumors in the temporal area produce 
vertigo. 

Tumors of the corpus callosum are not only very unusual, but produce symptoms 
which are not very definite, being primarily those of mental failure and secondarily 
those due to encroachment upon neighboring parts. In addition to the general 
symptoms of brain tumor, the growth in this region produces hemiplegia, ultimately 
developing into paraplegia, great mental dulness, and finally coma. 



Fig. 135 




10. Corpora quadrigemina. 



11. Cms. 12. Pons. 13. Medulla oblongata. 
(Modified from Reichert.) 



14. Cerebellum. 



When a tumor involves the great basal ganglia or the fibres of the internal capsule, 
hemiplegia is the most prominent symptom, and hemianesthesia and choreic 
movements may be present. 

If the posterior part (pulvinar) of the optic thalamus and nearby tissues, particu- 
larly one of the optic tracts, are involved by the growth, hemianopsia may be 
present, but this hemianopsia may be separated from that which is due to a lesion 
in the occipital lobe by the presence of Wernicke's sign (hemianopic pupillary 
inaction) . 

Having from these several symptoms determined that a brain tumor is present, 
it still remains for the physician to definitely determine its locality, and this can 
only be done by his knowledge of cerebral localization. For this study the 
brain can best be divided into fifteen parts, most of which can be seen on the 
accompanying diagrams (Figs. 133, 134, and 135). 

The numbers in the text refer to the numbers in the figures and show where the 
growth would be situated. 



806 



DISEASES OF THE NERVOUS SYSTEM 



Table op Cerebral Localizing Symptoms. 1 



1. 

Tumors of the prefrontal area . < 
(See Fig. 133.) 



2. 

Tumors of the central area 
(See Fig. 133.) 



Tumors of the parietal area 
(See Fig. 133.) 



4. 
Tumors of the occipital lobe 
(See Fig. 133.) 



5. 
Tumors of temporal area 
(See Fig. 133.) 



Tumors of corpus callosum 
(Very rare.) 
(See Fig. 134.) 



7, 8, 9. 
Tumors of the great basal ganglia 

and capsule. 
(See Fig. 134, for 7 and Fig. 130 
for 8 and 9.) 



10. 
Tumor of the corpora quadri- 
gemina (vermis of the cerebel- 
lum) and spinal gland. 
Additional information as to 
these lesions can be had by- 
studying Figs. 130 and 135. 

11. 

Tumors of eras . . . . 
(Very rare.) 



12. 

Tumors in the pons 



No symptoms, or 

Stupidity. 

Silliness. 

Emotionalism. 

Loss of smell on one side or both sides. 

Hemianopsia and optic neuritis. 

Protrusion of the eyeball. 

Paralysis of the extrinsic ocular muscles. 

Jacksonian epilepsy. 

Sensory disorders, tingling or hemianesthesia. 

Impaired muscle sense. 

Motor aphasia and agraphia. 

Local palsy after spasm. 

No symptoms, or 

Loss of muscle sense if supramarginal gyrus is affected. 

Word-blindness if angular gyrus and inferior lobule are affected. 

Paralysis or spasm of the lower limbs if the upper margin of the 
cerebral area is invaded. 

Perhaps slight paralysis of the sixth nerve if the angular gyrus is 
affected. 

Homonymous hemianopsia if the cuneus or the neighborhood of the 
calcarine fissure and first occipital convolution are involved. 

Failure to grasp meaning of surrounding objects (mind-blindness) if 
cuneus escapes. 

Word-blindness and some hemianopsia if the angular'gyrus is affected. 

Hemiataxia, hemianesthesia, and partial hemiplegia if the internal 
capsule is slightly involved in the posterior part, and also homony- 
mous hemianopsia from involvement of the optic radiations. 

No symptoms if on right side. 

Word-deafness if the posterior part of the first and second temporal 
convolution is involved. 

Vertigo and forced movements, if the growth is low down, due to 
irritation of internal ear. 

Gradually developing hemiplegia followed by paraplegia. 

Dulness and other mental symptoms suggesting paresis. 

Stupor \ and various symptoms due to pressure upon neighboring 

Coma / structures. 

Death. 

Progressive hemiplegia. 

Anesthesia (?) 

Choreic movements if tumor involves optic thalamus (7) and nearby 
part of capsule (8) . Starr thinks that these movements are cortical. 

No localizing symptoms if the tumor involves the caudate or lenticu- 
lar nucleus (9). 

Hemianopsia and the hemianopic pupillary inaction of Wernicke, 2 
if the optic tract or its endings near the posterior part of the optic 
thalamus and adjacent tissues are involved. If this pupillary in- 
action of Wernicke is absent hemianopsia indicates a lesion in the 
occipital lobe involving the cortex or the optic radiations. 

Cerebellar inco-ordination. 

Forced movements. 

Ocular palsies, often symmetrical. 

Hemianopsia if primary optic centres of one side are destroyed; 
blindness if destroyed on both sides. 

Deafness or partial deafness if posterior tubercles of corpora quadri- 
gemina are affected. 

Hemiplegia. 

Hemianesthesia (?) 

Paralysis of oculomotor nerve upon same side as tumor (crossed 
paralysis) . 

Facial palsy on same side as tumor; hemiplegia on opposite side 
(crossed paralysis) . 

Trifacial paralysis on same side as tumor if below middle of pons; 
hemianesthesia on opposite side (crossed sensory paralysis) . 

Hemianesthesia and hemiplegia if tumor is large and above middle 
of the pons. 

Conjugate deviation of eyes away from the lesion. 



1 In the preparation of this table much use has been made of the facts stated by Dana in his work 
on Nervous Diseases. 

2 A ray of light thrown on the blind half of the retina will not produce reflex pupillary contraction, 
though the pupils react normally if the light strikes the other half of the retina. 



TUMORS OF THE BRAIN AND ITS MEMBRANES 807 

fo f Hemiplegia and hemianesthesia with hypoglossal paralysis or other 

m • j 11 J cranial nerve palsy on side of lesion. Glycosuria and vasomotor 

Tumors m medulla { ,. , , * * 

disturbance. 

Symptoms of bulbar paralysis if growth is large. 

Headache 



14. 

Cerebellar tumor 



15. 

Tumor in anterior fossa 



> usually severe. 



Vomiting 

Vertigo 

Optic neuritis 

Reeling gait if in middle lobe. 

Glycosuria and cranial nerve palsies if pressing upon or in middle 

lobe. 
Bulbar symptoms (i. e., cranial nerve palsies). 
Hydrocephalus if tumor presses on aqueduct of Sylvius. 
Same symptoms as prefrontal tumors. 
Loss of smell, sight, and oculomotor paralysis. Acromegaly, optic 

neuritis, and temporal hemianopsia if the tumor is in middle fossa 

and involves optic chiasm. 



Diagnosis. — As already stated, the important symptoms in the diagnosis of 
brain tumor are headache, vertigo, optic neuritis, convulsions, and paralysis. 
It must be remembered, however, that these symptoms are none of them pathog- 
nomonic of brain tumor, and that each of them is often present in other maladies. 
It is the combination of symptoms rather than any one of them alone that indicates 
or establishes the diagnosis. Headache and vertigo are due to a host of causes, as 
convulsions and paralysis are common conditions; it is the localization of the 
convulsions and of the paralysis, pointing to a distinct focus, that is significant. 
Hysteria may, however, cause localized palsies and localized anesthesia, but they 
are not associated with optic neuritis and the hysterical sensory stigmata would be 
conspicuous. Sometimes, too, localized convulsions are not only due to tumor, 
but are symptomatic of a general condition such as poisoning, or of a widespread 
nervous disease such as paresis. The most valuable sign of brain tumor, optic 
neuritis, may be present in chronic contracted kidney, chronic lead poisoning, and 
severe anemia, etc., but these conditions can be eliminated from the case by the 
absence of the other signs and symptoms of these maladies. 

Among the pathological states that may produce symptoms of brain tumor 
is to be mentioned localized meningitis due to tuberculosis or syphilis. (See 
Meningitis.) In tuberculosis the degree of optic neuritis is usually slight; there 
is a primary tuberculous focus existing elsewhere, and, as the case progresses, 
evidences of a general meningeal inflammation may develop. Syphilitic meningitis 
is usually diffuse, not localized, and when localized is to be considered as a gumma 
or tumor. Another cause of such symptoms is abscess. This may be differentiated 
by its rapid development and by the presence of a septic focus elsewhere, as in the 
ear or in other parts of the body. (See Brain Abscess.) 

The question as to the character of the growth is determined by the following 
facts in many cases. Tuberculous growths are frequently met with, particularly 
in children. The presence of tuberculous infection elsewhere also points to this 
form of tumor. So, too, the presence of a malignant growth in some other part 
of the body suggests that the lesion in the brain is of the same character. A 
history or the presence of the scars of syphilis and a positive Wassermann test will 
indicate the existence of a gumma. Gowers states that if the tumor be in the 
cerebellum or pons, there is some probability " of its being tubercle or glioma, and 
if it is in the cortex the probability that it is syphilitic is considerable." "A tumor 
outside the brain tissue is probably sarcoma. " So, too, the disappearance of the 
symptoms under active antisyphilitic treatment point to syphilis as the cause. 
"A tumor which grows rapidly at the onset and then becomes stationary is probably 
tuberculous." 

Prognosis. — The prognosis in all forms of brain tumor is grave. It is least so 
in gumma and next best in tubercle, for in the former active treatment may cure, 
and in the second a long period of arrest may ensue. A growth in the pons or 



808 DISEASES OF THE NERVOUS SYSTEM 

medulla is more dangerous as to life than one in the cortex, but the presence of 
severe symptoms of brain tumor, be the seat of the growth what it may, is always 
of grave omen. 

Treatment. — From what has been said of the etiology and pathology of brain 
tumor it must be evident that medicinal treatment can do nothing more than 
palliate the patient's suffering, unless the growth be syphilitic. For the relief 
of the headache the various coal-tar products, such as acetanilid, phenacetin, or 
antipyrin, may be employed, and their efficiency is usually much increased by 
giving simultaneously 1 or 2 grains of caffeine and 10 or 20 grains of one of the 
bromides, preferably the bromide of strontium or bromide of sodium. In those 
cases in which the headache becomes so severe as to be insupportable, hypodermic 
injections of morphine may be employed, but it is an interesting therapeutic fact 
that this drug gives less relief in the pain of brain tumor than in almost any other 
affection characterized by pain. Excessive vomiting is to be checked by adminis- 
trations per rectum of 10 or 20 grains of chloral with 60 grains of bromide of sodium, 
to which may be added 30 to 60 minims of deodorized tincture of opium. So, 
too, epileptiform convulsions, if they are severe, may be prevented, at least in 
part, by the use of the bromides, or, if an aura is present, by inhalations of nitrite 
of amyl. 

In those cases in which there is the history of syphilis, the administration of 
salvarsan or mercury and the iodide of potassium is, of course, strongly indicated, 
and if a gumma is producing symptoms such as convulsions, which may in them- 
selves endanger the patient's life, the mercury should be pushed as actively as 
possible, being given by the mouth, by inunction, by hypodermic injection — 
that is, by every avenue of entrance — in the hope that it may exercise its influence 
upon the syphilitic growth before a convulsion sufficiently violent to cause death 
ensues. In other instances, when there are no acute symptoms which demand 
immediate interference, protiodide of mercury may be alternated with iodide of 
potassium, iodide of sodium, or iodide of strontium. Salvarsan seems less 
efficacious in these cases than mercury. 

When the growth is due to tuberculosis the administration of cod-liver oil, iron, 
and arsenic, and residence in a climate in which plenty of fresh air and sunshine 
can be constantly obtained, is essential. In such cases great improvement in the 
general health may do something toward arresting the local process. 

In those forms of brain tumor which are not tuberculous or syphilitic, the use 
of drugs, except to relieve pain, is practically useless, and operative interference 
offers the patient the best chance of recovery. Surgical procedures can, however, 
only be resorted to in those cases in which a definite localization of the tumor can 
be made, and where that locality is so situated that the surgeon can reach it without 
doing damage to vital parts. The earlier the operation is performed the better 
is the outlook. M. Allen Starr has collected 400 cases of brain tumor which were 
operated upon. In 154 instances tumor of the cerebrum was successfully removed, 
and the patients recovered. In 52 cases the patients died. In 16 instances in 
which the tumor was in the cerebellum it was removed and the patients recovered. 
In 8 instances death followed removal. It is interesting to note that in 91 instances 
of supposed cerebral tumor the growth could not be found on operation. The 
same failure to discover a growth was met with in 22 instances of supposed cere- 
bellar tumor. 

Of the cases which recovered 52 were sarcoma, 29 were cysts, 8 were gummata, 
19 were tuberculous, and 15 were gliomas. 

The operation of cerebral decompression, consisting in the removal of an area 
of bone, usually in the subtemporal region, is indicated as a palliative measure 
when the swelling of the optic disks threatens loss of vision. 

For the measures which are to be pursued in the removal of brain tumor, the 
reader is referred to the modern works on surgery. 



ABSCESS OF THE BRAIN 809 



ABSCESS OF THE BRAIN. 

Definition. — Abscess of the brain is a condition in which an accumulation of 
pus takes place in the cerebrum, or the cerebellum, or between these parts and their 
covering membranes. In the latter case the brain substance forms one wall of the 
abscess and the membranes the other wall. The latter type of abscess differs from 
purulent meningitis in that the inflammatory process is primarily in the nervous 
tissues, and that it is limited to a comparatively small area. Abscess of the brain 
without involvement of the membranes is much the more common form, and the 
white matter suffers very much more frequently than the gray substance. Abscess 
rarely occurs in the central ganglia, the pons, the medulla, or the middle lobe of the 
cerebellum. 

Etiology. — Abscess of the brain is always due to an infection by some pathogenic 
organism. In some instances the process is excited by an injury which affords 
a nidus in which the organism may develop; in other cases a septic embolus is 
carried from another part of the body in which there is an infected area; in still 
others the infection takes place more directly, as in those instances in which by 
fracture of the skull injury and infection both occur, or, as in the case of abscess 
of the middle ear and mastoid disease, the infection spreads by way of the 
sinus. 

Middle-ear disease is the cause in a great proportion of cases, about 45 per cent, 
arising from this primary focus of infection and 25 per cent, from injury. The 
remaining causes are infection of the other cranial bones than the mastoid or septic 
foci elsewhere. 

Males are affected far more frequently than females, in the proportion of 3 to 1 . 
This is largely due to the fact that males are so much more exposed to injury than 
females. If the cases of abscess due to middle-ear disease are studied by themselves, 
the proportion is almost equal; but if those due to trauma are considered by them- 
selves, the proportion is 5 of men to 1 of women. 

The disease is most frequent between the tenth and twentieth years of life. 
In the second decade ear disease is the common cause, and in the third decade ear 
disease and injury, or a distant focus of infection, are about equal in frequency as 
causes. 

Pathology and Morbid Anatomy. — A majority of cases of brain abscess affect 
the right side of the brain. Out of 71 cases collected by Oppenheim 55 were in the 
temporal lobe, 13 in the cerebellum, 2 in the pons, and 1 in the crus. 

The pathological process which results in abscess consists primarily of an enceph- 
alitis which speedily goes on to the stage of suppuration. This encephalitis may 
be due to any organism capable of causing an active inflammatory process. Thus, 
the Streptococcus pyogenes, the Staphylococcus pyogenes aureus, and the pneumo- 
coccus may be the provoking factors. In other cases the typhoid bacillus may 
be the cause, and even the streptothrix may produce such a lesion, as in a case 
seen by me in consultation with the late Dr. J. H. Musser. The abscess is nearly 
always single, but two or more pockets of pus may be present. The size of the 
abscess varies greatly. In some cases it is so small as scarcely to be recognized, a 
small collection of pus being found in the centre of an area of softening; whereas 
in other cases the quantity of pus may be very large, varying in quantity from 
a drachm to several ounces. 

The abscess may be surrounded by an inflammatory fibrous wall which serves 
to separate it from the neighboring white matter, or it may be contained in a cavity 
without any such well-defined margin, the walls of the abscess being composed of 
softened brain tissue. The latter form is prone t.o spread more rapidly than the 
abscess which has been walled off. On the other hand, the wall of the abscess may 



810 DISEASES OF THE NERVOUS SYSTEM 

rupture and produce sudden death. Not rarely the extension of the inflammatory 
process produces a meningitis if the abscess is situated near the surface of the brain, 
and a septic thrombosis of the nearby vessels may occur. 

Symptoms. — It is of interest to note that cerebral abscess may occur without 
producing symptoms- sufficiently typical to lead to an antemortem diagnosis. 
In the great proportion of cases, however, the symptoms of its existence are well 
developed. The most constant of these is headache, general or localized; it is often 
excruciating when associated with middle-ear disease; next in constancy is mental 
disturbance, the patient being alternately irritable and dull, and often seeming to 
be exceedingly ill. The temperature, unlike that of septic processes elsewhere, is 
usually normal or subnormal, unless the abscess ruptures, when it may be hyper- 
pyretic. A persistent low temperature, associated with a slow pulse rate, is very 
characteristic of the affection. 

The blood may show no change, but usually there is a moderate degree of leuko- 
cytosis with a relative increase of the polymorphonuclear leukocytes to 85 per 
cent, or higher. The surface of the skull is often hypersensitive, and in some cases 
it has been possible to localize the abscess by the dulness on percussion produced 
by its presence. Optic neuritis is often present. None of these symptoms is 
in any sense pathognomonic, since all may occur in other states of disease; but 
when they are taken into consideration in connection with a history of middle-ear 
disease, injury, or the presence of a septic focus elsewhere, they possess great 
diagnostic value. The deafness due to destruction of the auditory centre is masked 
by the deafness due to the disease in the ear. Paralysis of one side of the face is 
not of much diagnostic value, since this symptom is often due to the inflammation 
about the facial nerve as it passes through the stylomastoid foramen. 

The value of localizing symptoms depends, of course, upon the part of the brain 
which happens to be affected. When the infection spreads from the mastoid bone 
after or during otitis media, and infects the temporal lobe, there are no localizing 
nervous symptoms because we are in the dark as to the function of the temporo- 
sphenoidal lobe. In a few cases a lesion in the left temporosphenoidal lobe has 
caused aphasia. When the association tracts between the occipital lobe and the 
speech centre are involved the patient may present the symptom described by 
Freund as optical aphasia. Starr has observed a case of this character. The 
patient knows an object when it is placed before him, but cannot name it. The 
lesion would be in the left temporal lobe, and it may likewise cause hemiplegia or 
hemianesthesia by pressure upon the internal capsule. Hemianopsia may also 
be caused in this manner. 

When the abscess is in the cerebellum the symptoms are those characteristic 
of cerebellar tumor, viz., a staggering gait, vertigo, and, it may be, vomiting, 
diplopia, and nystagmus. In some instances the patient staggers toward the 
diseased side. If pressure is brought to bear by the abscess upon the crus or pons 
there may be paralysis of the oculomotor or facial nerves on the side of the lesion, 
with increase in the knee-jerks on the opposite side. 

Diagnosis. — The diagnosis of brain abscess is not difficult if the symptoms just 
described have been preceded by a history of injury or of a septic process elsewhere, 
near or remote. There are two other states with which it may be confused, namely, 
meningitis and thrombosis of the lateral sinus. In the former condition the onset 
is usually more abrupt, the headache is prone to be more severe in the early stages, 
and a sharp febrile movement is usually present; whereas, as has already been 
pointed out, in cerebral abscess fever is often absent unless the abscess ruptures. 
The pressure of abscess produces a slow pulse like that of cerebral compression, 
but in meningitis the pulse is usually very rapid. Additional symptoms of menin- 
gitis, which are of great value, are the stiffness of the muscles of the neck, the 
muscular twitchings, the early development of squint, a marked leukocytosis 



ACUTE CEREBRITIS OR ENCEPHALITIS 811 

(above 15,000 or 20,000), and, last of all, the presence of a pathological state of the 
cerebrospinal fluid obtained by lumbar puncture. (See Cerebrospinal Fever.) 

When thrombosis of a lateral sinus is present the febrile movement is sharp 
and severe, with marked remissions and exacerbations as in sepsis. There is 
swelling of the jugular vein on the affected side and of the conjunctiva as well, 
associated, it may be, with exophthalmos. Swelling, edema, and pain on pressure 
over the mastoid may also be present. The use of the ophthalmoscope also reveals 
choked disk in many cases as an early symptom. 

Prognosis. — This depends very largely upon the site of the abscess and the ability 
of the surgeon to evacuate and drain it. In all cases the prognosis is necessarily 
grave. That many patients may recover if promptly relieved is shown by recent 
statistics, which show that 60 per cent, of traumatic abscess recover after operation, 
and about 50 per cent, of abscess due to ear disease do likewise. 

Treatment. — The treatment is purely surgical, and for the necessary procedures 
reference must be had to surgical treatises. 

ACUTE CEREBRITIS OR ENCEPHALITIS. 

Definition. — Acute cerebritis, sometimes called "acute encephalitis," is a con- 
dition in which there is an acute inflammation of the brain arising as a primary 
disease not secondary to meningitis. 

\: Etiology. — The cause of acute cerebritis is always an infection due to the entrance 
of a micro-organism into the body, and in most instances the condition arises as a 
complication of measles, scarlet fever, smallpox, or ulcerative endocarditis, or in 
the convalescence from influenza. Acute alcoholism and other forms of poisoning 
may, by diminishing vital resistance in the brain, predispose to this condition. 
Possibly trauma may have a like result. Whatever may be the cause, this con- 
dition as a primary acute disease is very rare. 

Pathology and Morbid Anatomy. — The inflammatory process is not widely diffused, 
as a rule, but is found to exist chiefly in the distribution of one or more nearly 
related bloodvessels. At times it affects the same areas on both sides of the brain. 
In some instances only the cortex is involved, while in others the process chiefly 
affects the white matter. A limited form of this condition is the acute inflammation 
of the medulla, pons, or midbrain (polio-encephalitis inferior of Wernicke or acute 
bulbar paralysis) . 

The changes found in the affected parts are those characteristic of acute inflam- 
mation in all the nervous tissues, and indeed in any acute inflammation, namely, 
hyperemia, out-wandering of blood cells, and minute hemorrhagic extravasations, 
followed by the ordinary degenerative changes in the nerve cells produced by an 
interference with their normal blood supply and the effects of toxemia. The 
nerve-cell body or ganglion cell itself suffers from cloudy swelling, loses its sharp 
outlines, and its nucleus becomes indistinct or disappears. The axones and den- 
drites also undergo a similar change. The interstitial tissues are at first filled with 
small cells, and ultimately there is an overgrowth of the neuroglia cells, so that 
patches of sclerosis are produced. This last result is, of course, permanent, and 
if it takes place to any great extent may seriously impair the function of the brain. 
If the inflammatory process is in the cortex, adhesions to the meninges may take 
place. 

Symptoms. — The symptoms of acute cerebritis depend to a large extent upon 
the portion of the brain which is chiefly affected, although the general manifesta- 
tions of an acute inflammatory process in the brain are present in all cases. The 
patient is seized, after a few hours of general distress, with headache and dizziness, 
followed by a chill and, it may be, vomiting. These symptoms are in turn speedily 
followed by fever and rapidity of the pulse and respirations, and these in turn in 



812 DISEASES OF THE NERVOUS SYSTEM 

some instances by delirium of a violent type. If the case is severe the patient may 
now pass into coma, and then gradually pass to death, or, after several days, or even 
weeks, of these symptoms, consciousness gradually returns, the temperature falls, 
and recovery takes place, although, as already stated, permanent impairment of 
some of the cerebral functions may persist. 

The special symptoms which depend upon the areas of the brain which are 
affected consist in hemiplegia, monoplegia, aphasia, or in word-blindness and word- 
deafness, hemianopsia, or mutism. Any of these may become permanent. In still 
other cases the patient suffers from impairment of the intellectual powers or the 
changes in the motor cortex produce epileptic attacks, and in other instances the 
development of the sclerotic patches already named results in the production of a 
condition identical with disseminated sclerosis with nystagmus, tremor, and peculiar 
speech. The very rare condition called "polio-encephalitis superior of Wernicke" 
is manifested by the presence of ptosis, strabismus, nystagmus, and even optic 
neuritis with vertigo and a staggering gait. In addition there may be difficult speech 
and facial paralysis. 

Diagnosis. — Acute encephalitis may be confused with brain tumor when epilepti- 
form convulsions and paralyses are prominent, but the absence of choked disk 
and the rapid onset will distinguish the former. In its " comatose" and " epileptic" 
forms it may resemble apoplexy or epilepsy, and a close study of the entire clinical 
picture is necessary, with the history, to differentiate such cases. 

Prognosis. — That the prognosis in acute encephalitis in the early course of the 
malady must be uncertain is manifest when we consider the character of the lesions 
which are present. Even after the active stage of the disease is passed the outlook 
as to complete restoration to health is still clouded because it is not possible to tell 
what secondary changes may develop in the brain or its membranes. All cases 
of acute encephalitis are to be regarded as of much gravity. A high temperature, 
convulsions, profound and prolonged coma are all very unfavorable symptoms. 
Even in the very grave cases a remarkable degree of recovery may occur. 

Treatment. — This consists in the application of an ice-bag to the head, and in 
the use of moderate doses of tincture of aconite if there is circulatory excitement. 
If the bowels are confined, an active saline purgative is useful to move them and to 
deplete the bloodvessels. A hot foot-bath may also be used. Phenacetin and 
acetanilid may be employed for the relief of pain, but they usually fail. On the 
other hand, the use of opium or morphine often makes the pain worse. Absolute 
rest in a darkened room is essential. After the acute process is over iodide of 
potassium may be given in the dose of 10 grains three times a day, with the hope 
that in this manner inflammatory exudates and adhesions may be absorbed. 



THROMBOSIS OF THE VENOUS SINUSES. 

Etiology. — Thrombosis of the venous sinuses is due, as are cases of thrombosis 
elsewhere, to an inflammation of the endothelium which lines these vessels. This 
inflammation may be the result of a septic infection in remote or in neighboring 
tissues, as, for example, in suppurative otitis media. Where the cause is sepsis 
the thrombus usually contains micro-organisms. The vast majority of instances 
depend upon suppuration in the ear. 

Pathology and Morbid Anatomy. — The size of the thrombus varies very greatly. 
Beginning as a small clot in one sinus, it may gradually increase in size until the 
sinus is filled, and may even extend to adjacent sinuses and into neighboring veins. 
If septic in origin it may be purulent in character. The longitudinal sinus is very 
rarely affected. The lateral sinus is the one most commonly involved, and after 
it the cavernous sinus. 



CEREBRAL MENINGITIS 813 

Symptoms. — The symptoms of thrombosis of the lateral sinus are congestion 
of the veins in the neighborhood of the mastoid, with swelling of the tissues covering 
it. There is often pain and tenderness on pressure. Not rarely the cervical glands 
are enlarged from infection, and wryneck may be present. Choked disk is frequently 
present upon both sides. With the infection of the sinus there is usually a history 
of a rigor followed by high fever, with headache, vomiting, delirium, and finally 
coma. The fever not rarely follows a septic course, rising and falling sharply. 
Other evidences of septicemia may also be present, such as sweating, diarrhea, and 
the occurrence of infarctions in such organs as the lungs, spleen, and kidneys. 

In thrombosis of the cavernous sinus there is local swelling, congestion of the 
face about the eyes, epistaxis, and undue fulness of the retinal veins. Occasionally 
squint develops as a result of interference with the function of the oculomotor and 
abducens nerve. 

Thrombosis of the longitudinal sinus is manifested by intense venous congestion 
in the scalp, and indeed of the entire head. Choked disk may be present and 
epistaxis may occur. 

Prognosis. — This is unfavorable unless surgical interference gives relief, and 
surgical interference is practically limited to cases of disease of the lateral sinus. 

Treatment. — This is purely surgical, and consists in trephining or otherwise 
opening both the source of infection and the sinus and thus removing the focus and 
the clot. For details as to the method of operation, and as to the statistics of 
recovery following such operations, the reader is referred to books on surgery. 

CEREBRAL MENINGITIS. 

Definition and Etiology. — By meningitis is meant an inflammation of the mem- 
branes covering the brain or spinal cord. From an anatomical standpoint there 
are three of these — the dura mater, the arachnoid, and the pia mater — but from 
the standpoint of the clinician and pathologist these membranes may be divided 
into two parts, the dura mater on the one hand and the arachnoid and pia mater 
(pia-arachnoid) on the other, for the dura is often inflamed by itself, but the pia 
and arachnoid are always affected together. When the dura is alone involved it 
is called pachymeningitis, and when the other membranes are affected it is called 
leptomeningitis. 

Pachymeningitis. — Pachymeningitis may occur in an internal form, when the 
smooth inner layer of this membrane is inflamed (pachymeningitis interna), and 
in an external form, in which the outer layer is chiefly affected where it is in contact 
with the bone (pachymeningitis externa). The latter is the more common type 
by far. 

Pachymeningitis externa is, in the greater proportion of cases, secondary to 
some traumatism or to disease of the bone. Thus, a blow on the head which 
fractures the skull, or necrosis of the skull, may so result. Very much more rarely 
an acute infection arises, as in an infectious and septic malady such as erysipelas. 

Pathology and Morbid Anatomy. — The inflammatory process resembles that seen 
in any inflammation, namely, hyperemia followed by swelling and cellular infiltra- 
tion, and this in turn by the formation of pus which is found between the skull 
and the dura mater, or, in extraordinary cases, between the layers of this membrane. 
When the inflammatory process does not go on to suppuration, the external layer 
of the dura becomes thickened and adherent to the skull. If the inflammation 
is very severe the inner layer of the dura is affected, and the pia mater may become 
involved and adherent to it. 

Symptoms. — These consist in those characteristic of the cause, as the primary 
unconsciousness from a blow, or the pain of bone disease, and in the development, 
as direct symptoms, of headache, confusion of mind, delirium, and in severe cases, 



814 DISEASES OF THE NERVOUS SYSTEM 

convulsive seizures. Fever may or may not be present. If pus collects, symptoms 
of pressure on the brain may develop, and paralysis of the opposite side of the body 
may ensue (hemiplegia) . 

Diagnosis. — The history of injury, of bone disease, or of some focus of infection 
makes the diagnosis possible. 

Prognosis. — This is bad in direct proportion to the severity of the inflammatory 
process and the degree to which the pia mater is involved. External pachymenin- 
gitis is less grave than leptomeningitis. 

Treatment.— This consists in the use of saline purgatives to relieve cranial con- 
gestion, in applying an ice-cap to the head, rest in bed in a darkened room to 
secure perfect quiet, and in the employment of aconite as a cardiovascular sedative 
if the pulse is excited. If symptoms of cerebral compression develop, as coma or 
paralysis, the fluid or pus must be evacuated by operation. 

Pachymeningitis Interna. — Pachymeningitis interna occurs in a purulent and 
in a hemorrhagic form, the purulent being very rare. To the hemorrhagic type 
the terms "hemorrhagic internal pachymeningitis" or "hematoma of the dura 
mater" are sometimes applied. Even this type is rarely met with, and its existence 
is rarely recognizable before autopsy. It affects males far more commonly than 
females (4 to 1, Gowers), and is generally met with after the fiftieth year. It is 
also met with more commonly in the first twelve months of life than in childhood 
or early manhood. As a rule, in adults it develops in the course of some form of 
chronic insanity, particularly in the course of general paralysis of the insane, or in 
cases of chronic inebriety. Very rarely it has complicated the course of one of the 
acute infectious diseases, such as typhoid fever ' or smallpox. In children it may 
complicate scurvy. 

Pathology and Morbid Anatomy. — The exact method or process by which the 
hemorrhagic extravasation takes place is not known. The autopsy reveals a 
bilateral, and rarely a unilateral, extravasation between the layers of the dura 
and between the dura and the arachnoid. Not only is a bloody fluid formed in 
these spaces, but a pseudomembrane is also present; it may be in several layers. 
These layers are at first red and later may be pallid, and, by adhering together 
at spots, form pockets in which the bloody fluid is found. When the condition 
has existed a long time this fluid may be decolorized and contain crystals of choles- 
terin. Very rarely suppuration takes place. 

Symptoms. — The symptoms are in many cases, if the disease complicates chronic 
insanity, so suppressed, or absent, that no suspicion of the state just described is 
harbored. In some cases the patient develops attacks which resemble those of 
apoplexy, which are supposed to be due to fresh extravasations of blood. In 
other instances there are signs of cerebral compression, as shown by stupor, or 
coma, or optic neuritis. Headache and vomiting may be present. Partial hemi- 
plegia may develop. 

The prognosis is very unfavorable. Treatment is almost useless. Quiet and 
rest, with cold to the head, is all that can be done. In cases with strictly localized 
symptoms surgical intervention is justifiable. 

Leptomeningitis. — Leptomeningitis is the form of meningitis which compli- 
cates the course of all of the acute infections, notably pneumonia, erysipelas, 
septicemia, and less frequently variola, scarlet fever, typhoid fever, and measles. 
Measles produces it very commonly because this malady is often followed by 
otitis media, and because otitis media not rarely causes mastoid abscess, and, from 
this focus, infection involves the meninges or the lateral sinus. It is probable, 
too, that a very considerable proportion of cases of leptomeningitis are caused by 
infection which takes place through the nose. It can be readily understood that 
any infectious micro-organism which can gain access to the meninges through the 
openings in the skull or in the blood may cause such an inflammation, and, in 



CEREBRAL MENINGITIS 815 

addition, that the possibility, or probability, of infection is greatly increased by 
any disease which lowers vital resistance, such as nephritis. It must not be thought, 
however, that all cases of leptomeningitis due to the pneumococcus are complica- 
tions of croupous pneumonia, for this micro-organism may produce a meningitis 
by direct infection, without the lung being affected in the least. It is probable, 
too, that the typhoid bacillus may, in a case which has long since convalesced 
from the fever, act in a similar manner. (For the relationship of leptomeningitis 
to pneumonia and typhoid fever the reader is referred to the articles on those 
diseases. Also to that on cerebrospinal meningitis.) 

Meningitis is more common in children during the first decade of life than at 
any other period, but in these cases the inflammation usually involves the meninges 
at the base, whereas in adults that part of the meninges which covers the convexity 
is chiefly affected. 

Morbid Anatomy and Pathology. — The inflammatory process may involve the 
whole membrane or be quite limited. The limited cases are those which arise 
from direct infection from a nearby focus of disease. Thus, in cases which are 
secondary to middle-ear disease the lesion is often unilateral, whereas in those 
cases in which the pneumococcus is the infecting agent the entire convexity on 
both sides is usually affected. In the latter type of case the effusion which develops 
is often large in quantity and purulent. If the cause is tuberculous the base is 
usually affected. (See Tuberculous Meningitis.) The actual lesions found in 
the meninges in these cases are noteworthy. Beginning with hyperemia and 
congestion they pass on to cloudiness of the membranes affected, which is particu- 
larly well marked along the course of the bloodvessels because of the engorgement 
of the accompanying lymph vessels. Smajl spots of purulent material are dotted 
along these vessels which, as they increase in size, coalesce, and so considerable 
areas are covered by pus. When the process is severe the dura mater and the cere- 
bral cortex may be involved by the inflammatory changes. 

Symptoms. — In studying the symptoms of leptomeningitis it must be recalled 
that the manifestations of involvement of the cortical area are by no means pathog- 
nomonic. Every physician of experience has seen cases of typhoid fever or 
croupous pneumonia present apparent evidences of meningitis, yet the autopsy 
has revealed no such lesion present. In other words, as pointed out when these 
diseases were discussed, toxins produced by the specific organisms may cause 
symptoms identical with those of meningeal inflammation. This is exceedingly com- 
mon in the pneumonia of children, and is termed pseudomeningitis or meningismus. 

There are, however, certain symptoms of meningitis which are certainly indicative 
of either inflammation or irritation of the meninges, particularly if they are asso- 
ciated with a disease or an injury qualified to produce meningeal involvement. 
These consist in fever, headache, vomiting, retraction of the head, and rarely convulsions. 
Grinding of the teeth, obstinate constipation, and an excessive hyperesthesia of the 
skin of the arms and legs are also common symptoms. When the inflammatory 
process is basilar the symptoms are much more definite and reliable. In addition 
to those just named we find that optic neuritis is present, and strabismus and ptosis, 
due to the pressure exercised upon the cranial nerves, develop. The pupils may 
be contracted in the early stages because of irritation of the oculomotor nerves, 
and later widely dilated by reason of paralysis of these nerves. Fever may or may 
not be present, and the pulse is usually slow even if the temperature is raised. 
Kernig's sign may be present. (See Cerebrospinal Meningitis.) A rapid loss of 
flesh takes place in nearly all cases. 

Diagnosis. — The symptoms of basilar leptomeningitis, whatever its cause, are 
usually unmistakable. A very useful aid to diagnosis is lumbar puncture, already 
described under Cerebrospinal Meningitis. If the cerebrospinal fluid escapes with 
a spurt from the needle, it is indicative of the presence of tuberculous meningitis, 



816 DISEASES OF THE NERVOUS SYSTEM 

but by no means positive of this condition, for it sometimes happens that a similar 
high pressure exists in cases of purulent meningitis and of spinal tumor. If disin- 
tegrated blood is present in the cerebrospinal fluid it is an indication of the presence 
of pachymeningitis or injury. Fresh blood, on the other hand, is probably due to 
the puncture. If the fluid is perfectly clear, every inflammatory affection of the 
meninges except tuberculosis may be excluded. In tuberculosis it may be clear, 
but is often cloudy, and toward the end of the case even purulent. The normal 
proportion of albumin in it is 0.2 to 0.5 per mille (Quincke), and if more than 
0.5 per mille is present an inflammatory process is probably going on. If the 
small quantity of sugar which is normally present is absent, this is a sign that 
inflammation is present. 

Treatment. — Aside from the employment of rest and cold to the head, if fever is 
present or pain is suffered, we can do little for this condition except we resort to 
lumbar puncture for the purpose of relieving pressure. 

The cerebrospinal fluid may also give us valuable information as to the presence 
or absence of meningitis, if it be examined microscopically and a quantitative 
estimation of its leukocytes is made. As a general rule, there is a marked increase 
in lymphocytes if the inflammatory process is tuberculous, and of polymorpho- 
nuclear cells, if it is non-tuberculous. Exceptions to this rule occur, and therefore 
the presence of either one of these forms of leukocytes in increased number is not 
pathognomonic. 

Microscopic examination of the cerebrospinal fluid may also be made for the 
purpose of discovering tubercle bacilli, or the diplococcus of pneumonia, or other 
pathogenic micro-organisms. The fluid for this purpose should be kept on ice 
for not less than twelve hours, until a small clot is formed. The web-like fibres of 
this clot are transferred to a cover-glass, spread in as thin a film as possible, and 
stained by the methods commonly employed for staining the tubercle bacillus. 
Where the examination must be performed at once, the fluid may be put in a 
centrifuge, and the sediment examined by the staining methods already described. 
As with examinations of the sputum in suspected tuberculosis, the finding of tubercle 
bacilli is a positive sign of great value, but the failure to find them by no means 
proves that the disease is not tuberculous. Reference to the presence of the 
Diplococcus inter cellularis meningitidis has already been made in the article upon 
Cerebrospinal Meningitis. Occasionally the streptococcus and staphylococcus 
are found. In African "sleeping sickness" trypanosomes have frequently been 
found in the cerebrospinal fluid. 

DEMENTIA PARALYTICA. 

Definition. — Dementia paralytica, often called " meningoencephalitis," "paresis," 
or "general paralysis of the insane," is a state characterized anatomically by a 
widely diffused process of degeneration in the central nervous system, particularly 
in the cerebral cortex, with morbid changes in the pia mater. The chief symptoms 
in the early stages are the development of great irritability of temper, forgetfulness, 
carelessness as to habits, and later delusions of grandeur. Clinically it is character- 
ized by a progressive paralysis of the body, associated with certain physical signs, 
and a progressive loss of mental power of a peculiar kind. The most striking 
symptom of this disease is the "delusion of grandeur." 

Etiology. — Without doubt syphilis is a provoking cause in a large proportion of 
cases. This view is supported by the finding of the specific spirochete, the con- 
stancy of the Wassermann reaction in the cerebrospinal fluid, a sign of active 
syphilis, not of the results of syphilis. It is like locomotor ataxia, in that its symp- 
toms develop from five to twenty years after the initial lesion. At one time it 
was thought that it resulted from an infection long since past, but recent investi- 



DEMENTIA PARALYTICA 817 

gations have shown that in many instances the spirocheta pallida exist in large 
numbers in the perivascular spaces. These discoveries are of the greatest impor- 
tance in early cases since the use of salvarsan or neosalvarsan may arrest the malady, 
particularly if the antibodies engendered in the blood can be injected into the cere- 
brospinal canal and so get at the spirochetal hidden in the nervous system into 
which the specific remedy cannot enter, when given intravenously, because its mole- 
cule is too large to pass through the cells lining the arachnoid. Alcoholism, exces- 
sive sexual indulgence, and, indeed, excesses of every kind, are also without doubt 
predisposing factors of importance. The disease is a common one among roues. 
It affects males more frequently than females 10 to 1. Like locomotor ataxia 
its age incidence is between thirty and fifty years of age. 

The disease is one of the middle period of life, between thirty and fifty years, 
but a number of cases have been recorded as occurring in children who have usually 
had hereditary syphilis. 

Pathology and Morbid Anatomy. — The brain changes consist in a chronic parenchy- 
matous encephalitis produced by the invading spirochetes. The primary change 
in cases of this disease takes place in an increased blood supply to the pia mater 
and in the smaller vessels of the cerebral cortex, associated with degenerative 
changes in the bloodvessel walls. The progress of these degenerative changes 
results in the development of fusiform dilatations of the bloodvessels and the filling 
of the lymph spaces with serum. Ultimately the quantity of lymph present in 
the perivascular spaces is so great that a true cerebral edema is produced. There 
is an overgrowth of the neuroglia about the vessels, and this newly formed con- 
nective tissue sends fibrils down between the cells of the cortex, with the result 
that true sclerosis develops. Associated with these connective-tissue changes 
there are degenerative changes in the cerebral neurones. The body of the neurone 
undergoes hyaline and then fatty degeneration, pigmentation, and finally atrophy. 
Mantles of lymphoid and plasma cells are seen about the vessels in the cortex. 
When the disease has been present for a long time, autopsy reveals the presence 
of small cysts in the white and gray matter, and so marked a decrease in the size 
of the convolutions and of the entire brain that it is found to be much smaller 
than is normal. Its surface is harder than is natural, pigmented, and adherent 
to the pia mater, which is also found to be the site of overgrowth of connective 
tissue. The ventricles contain an excess of fluid, and their lining membrane, the 
ependyma, is thickened. It is noteworthy that the left hemisphere is usually 
more affected than the right, and that the changes already described affect the 
frontal lobes and the areas of the motor cortex before the rest of the brain is involved. 

In most cases of paresis degeneration is found in the spinal cord, so that spinal 
symptoms are added to the cerebral signs and form part of the clinical picture of 
the disease. The lateral and posterior tracts are usually affected, producing 
symptoms of ataxic paraplegia. Sometimes the posterior columns alone are 
degenerated, presenting symptoms of locomotor ataxia. Rarely, disseminated 
sclerosis is found; and recently the spinal cord in a case of paresis is found to be suf- 
fering from syringomyelia. In a few cases of locomotor ataxia (tabes dorsalis), fully 
developed and typical, the cerebral signs of paresis came on, as if the disease had 
finally "risen" to the brain. These cases constitute the "ascending type" of paresis. 

Some authorities believe that paresis is identical in nature with tabes — that 
it is a "tabes of the brain." A clinical picture of paretic dementia with tabes is, 
therefore, met with. Rarely the spinal symptoms precede the cerebral symptoms 
in the development of the disease. So, too, symptoms of spastic paraplegia may 
develop. Sometimes autopsy reveals the fact that pachymeningitis and hematoma 
have occurred as the result of the aneurysmal dilatations of the cerebral and pial 
vessels, already described, leaving behind them an organized membrane beneath 
the dura, or a mass of encysted blood clot. 
52 



818 DISEASES OF THE NERVOUS SYSTEM 

Symptoms. — When the symptoms of dementia paralytica are well developed, 
they are so characteristic and obtrusive that there can be little difficulty in reaching 
a correct diagnosis in regard to the condition from which the patient is suffering. 
It is only when the disease is in its stage of onset, or in an atypical form, that any 
doubt can be present. 

As a rule, the early symptoms are recognized in retrospect rather than at the 
time at which they occur, unless, perchance, these symptoms are very strongly 
developed. It is noticed that the patient seems to be nervously fatigued or mentally 
fagged, and often this condition is ascribed to the excesses which have been com- 
mitted in connection with venery, wine, and other forms of nervous stress. The 
temper is usually irritable, and the friends notice that the patient takes offense at 
remarks which ordinarily he would not notice. At times he is remarkably forgetful. 
Naturally tidy as to his habits and dress, he becomes careless and slovenly. Occa- 
sionally sleeplessness will be complained of. 

Although, before the onset of the symptoms, he may be apparently kind and 
faithful to his family, he begins to be brutal in his conduct toward his wife and 
children, and perhaps returns to the alcoholic and sexual excess which laid the 
foundation for his disease many years before. The speech becomes indistinct, 
hesitating, and if the tongue is protruded a very fine tremor may be seen in it. 
There is also a very marked tremor of the hands. Ataxia of station (Romberg's 
sign) is a common symptom. The pupils are generally unequal and irregular, 
and the pupillary light reflex may be lost, while reaction to accommodation is 
maintained. In other words, the Argyll-Robertson pupil is present, for the same 
reason that it is present in cases of locomotor ataxia, because Meynert's decussation, 
or other fibreis, involved in the light reflex arc are affected by the degenerative 
process already described. The loss of consensual reflex is also frequently 
observed. 

The symptoms of onset are often prolonged over the period of many months, 
and sometimes for several years, depending upon the rapidity with which the 
pathological changes in the brain develop. The disease is progressive and ulti- 
mately the symptoms of the later stages are developed. These symptoms may 
consist in delusions, which are usually composed of extravagant ideas. Thus, the 
patient may, on the one hand, believe that he is some great historical character, 
or that he is a ruling potentate, or, again, that he is possessed of fabulous riches. 
In one instance, for example, within the writer's knowledge, the patient took a room 
at a prominent hotel, after having provided himself with large sums of money, 
and from the balcony outside of the room showered the crowd beneath with coins 
of different values, with the idea that his wealth was limitless. In another instance, 
the manager of a small plant for making steel became imbued with the idea that 
his company had obtained and could fill contracts for the delivery of manufactured 
steel on a scale far beyond those ever attempted by any corporation, although as a 
matter of fact the business of the concern was at its last ebb, and his delusions aided 
in causing its final financial collapse, through its inability to carry out the agree- 
ments which he made with other concerns. In this instance the stress of business 
worry combined with previous excess was an active factor in producing the disease. 

As the degenerative process in the brain continues, the patient's judgment 
becomes profoundly impaired. He rarely is capable of continuous thought, and 
no longer adheres for hours at a time to his delusions. He frequently becomes 
exceedingly emotional, and laughs and cries without adequate cause. At times 
he is excessively depressed; at other times exalted, and he may occasionally become 
frenzied with rage, during which time he may commit some crime. 

The handwriting is often characteristic. It may become illegible, either because 
the letters are badly formed or because important words are dropped out. Still 
later, loss of power occurs in the limbs until total paralysis may be present. Sensa- 



DEMENTIA PARALYTICA 819 

tion is not so markedly disturbed, but areas of anesthesia and analgesia may be 
found. The reflexes may be markedly increased or entirely lost. 

Naturally, there is an impairment of the general health with the progress of 
the disease. Epileptiform attacks or sudden periods of unconsciousness (apoplecti- 
form attacks) develop, accompanied by paralysis of one limb, or by hemiplegia. 
Death usually ends the case by the end of the third to the sixth year, the patient 
dying of exhaustion or of some intercurrent disease, such as pneumonia, obstruction 
of the bowels, or of one of the epileptiform or apoplectiform attacks. 

Cases of paresis in which the delusion of grandeur is prominent are the earliest 
recognized, and constitute the classic form of the disease. There are many, how- 
ever, in which depression simulating melancholia is present throughout; that is, 
the depressed form of paresis. But in a large proportion of all cases the mental 
symptoms are mainly those of progressive mental loss, without distinct delusions 
(the simple or demented form of paresis). An alternation of excitement and 
depression (circular form of paresis) is observed rarely; delusions similar to those 
of paranoia or of alcoholic insanity may mask the underlying condition. 

Diagnosis. — Dementia paralytica must be separated in its early stages from 
neurasthenia. The patient suffering from nervous exhaustion usually studies 
his own symptoms in the greatest detail, and usually considers that he is an ill 
man, while the paretic has a very much more optimistic view and often insists 
that he is more than usually well, when it is manifest that his ill health is extreme. 
So, too, the neurasthenic rarely has complete lapses of memory and defects of 
speech. From cerebral syphilis paresis is separated by the fact that the former 
usually manifests severe pain in the head and true aphasia due to a syphilitic 
arteritis in the neighborhood of the speech centre. The fine tremor of the tongue 
and of the hand in paresis is absent in cerebral syphilis. Optic neuritis is usually 
present in cerebral syphilis, but not very common in paresis. So, too, the mental 
state is one of constant depression in syphilis, and not that of excitation. From 
multiple sclerosis paresis is separated by the presence in sclerosis of nystagmus and 
intention tremor and by the absence of delusions. 

While the blood may give a negative Wassermann reaction the spinal fluid 
often gives a positive reaction. An examination of the cerebrospinal fluid shows 
an enormous increase in the number of small lymphocytes, ranging from 30 to 
300 to the cubic millimetre. This is also true, however, of tuberculous meningitis. 
The fluid also contains a great excess of globulin. 

Prognosis. — This is very unfavorable. Cases rarely if ever recover, although 
temporary, and it may be prolonged; remissions, which cause encouragement on 
the part of the friends, may occur, particularly if salvarsanized serum is injected 
intraspinally. 

Treatment. — It must be evident, from the pathological condition already 
described, that treatment can do little. But it must be remembered that this 
disease is directly due to syphilis, and therefore antisyphilitic remedies should 
be employed. Their general tendency is favorable, and they may perhaps arrest 
for the time being the progress of the vascular changes, but they cannot cure 
those in existence. Salvarsan may be given intravenously, or better, the more 
recent method of Swift and Ellis of injecting salvarsanized blood serum intraspinally 
should be tried. This method of treatment is still "on trial" and while it is as 
yet too early to know its real value, certainly marked improvement has in many 
instances followed its use. That the improvement observed in a given case will 
eventually prove to be but a more or less prolonged remission, is however, probable. 
Mercury and the iodides should also be used freely in connection with hot baths. 
If the patient is difficult to control, it is far better both for himself and his friends 
that he should be committed to an asylum where he can be properly cared for, not 
only in the sense of being properly controlled, but of being well fed, as the main- 



820 DISEASES OF THE NERVOUS SYSTEM 

tenance of health and general nutrition is, of course, of importance. Sleeplessness 
may be treated by any one of the good hypnotics, of which chloral, trional, and 
veronal are the best. Occasionally, hyoscine may be used. Care must be 
taken that the carelessness of the patient in regard to his bowels does not result in 
obstinate constipation, which may be difficult to relieve. For this reason, active 
purgatives are often necessary. If outbreaks of excitement come on, y^-q of a 
grain of hyoscine may be given hypodermically. 

DISSEMINATED SCLEROSIS. 

Denfiition. — Disseminated sclerosis is characterized by the development of 
irregularly distributed patches of sclerosis in different parts of the brain and spinal 
cord. Similar changes also take place in the cranial nerves. It is sometimes 
called "insular sclerosis" or "multiple sclerosis." By the French it is called 
sclerose en plaques disseminees. It has only been recognized as a distinct disease 
for a little more than fifty years. 

Etiology. — The essential cause of multiple sclerosis is not known. It affects 
both sexes equally, and occurs chiefly in young adults, appearing infrequently 
in childhood and rarely after forty-five years of age. Its most common period 
of existence is from the twenty-fifth to the thirty-fifth year. Occasionally it 
has been known to follow one of the acute infectious diseases, and has been regarded 
as a consequence of disseminated myelitis of infectious origin (Marie) ; but it is 
doubtful whether this malady has any direct productive effect in the case. Syphilis, 
that great cause of organic nervous disease, does not seem to be frequently present 
as an etiological factor. The disease has been known to follow shock, trauma, 
and severe exposure, but in the majority of cases no causal factor can be traced. 

Pathology and Morbid Anatomy. — The lesions of disseminated sclerosis consist, 
as already stated, in irregularly distributed patches in which the nervous tissues 
have undergone sclerotic change. These patches are found chiefly in the white 
matter of the brain, being comparatively rare in the gray substance of the cortex. 
They are irregular in outline and in distribution and vary in size. In appearance 
they are reddish-gray and translucent. The surface of a patch is usually even 
with the surrounding brain tissue, but it may be slightly depressed. A sharp line 
of demarcation separates the diseased area from the healthy tissues. When touched, 
the patches seem harder than normal gray matter, but they are not usually met with 
until section of the brain or cord is made, when they appear in strong contrast 
to the surrounding white tissue. They may be found in considerable number in 
the lateral ventricle, in the corpus collosum, crura, and pons. The patches in the 
spinal cord are not so reddish in hue as in the brain, but are more gray in color and 
extend vertically rather than transversely; but this rule is not absolute, and at 
times the transverse extension of a patch may embrace the entire thickness of the 
cord. When one of the cranial nerves is involved; it is found to be gray in color 
and sclerotic for a certain portion of its length. In some instances the entire 
thickness of the nerve is involved. The olfactory, optic, oculomotor, trifacial, 
and facial nerves are the ones which are most commonly affected, and in the case 
of the optic nerve the favorite seat is the chiasm. 

The sclerotic process in this disease does not differ very materially from that 
met with in sclerotic processes occurring in other organs of the body; there is an 
overgrowth of the true neuroglia or connective tissue, and side by side with this 
overgrowth a corresponding atrophy or disappearance of the nerve cells and fibres 
themselves takes place. When the degenerative process is well advanced, we find 
scattered through the connective-tissue fatty granules and nerve cells which show 
evidence of degenerative change. In the nerve fibres the chief change takes place 
in the myelin, but after the disease is far advanced the axis cylinder also becomes 



DISSEMINATED SCLEROSIS 821 

affected and finally is completely destroyed. In the central nervous system it is 
usually found that secondary degeneration in the nerve fibres above or below the 
seat of the original sclerotic patch is only met with when the disease has been 
sufficiently severe to destroy the axis cylinders. On this account secondary 
degenerations are not common in disseminated sclerosis, the axis cylinders surviving 
in the midst of fully developed sclerotic patches. 

Symptoms. — The symptoms of disseminated sclerosis depend almost entirely 
upon the areas of the nervous system which are chiefly affected by the pathological 
changes just described. Among the earliest symptoms in many cases is a loss 
of power in the extremities. In the legs the symptoms may be ataxic, but usually 
simulate those of spastic paraplegia in a striking degree. When spastic paraplegia 
is present, this indicates that the sclerotic process has involved the pyramidal 
tracts; the knee-jerks are found to be exaggerated, and Babinski's sign is present. 
In other instances inco-ordination of the hands, or of one hand, may be the first 
manifestation of the malady, and in still others sensory disturbances in the legs 
or arms are first complained of by the patient. The inco-ordination of the muscles 
of the arms is often very marked indeed. Often it is impossible for a patient to 
carry a glass of water to his lips without spilling it (intention tremor) . The co-ordi- 
nated movements which are necessary in writing are impossible because of the 
quick or spasmodic contractions of the muscles employed for this purpose. The 
cause of these irregular movements is not known. According to some it is depen- 
dent upon the fact that certain fibres are affected, and impulses going along certain 
channels, particularly the motor, are delayed in passing through sclerotic areas, 
or that those which pass along fibres still unaffected are made inadequate and, 
as it were, embarrassed. By others it is thought that the sclerotic patches have 
involved afferent fibres of the cerebellar system which are concerned with muscular 
sense. 

If sensory fibres in the dorsal columns are involved, areas of anesthesia or hemi- 
anesthesia, also ataxia of the extremities, will develop, the severity of these symptoms 
depending, of course, upon the area involved in the sclerotic process. The eye 
symptoms are usually well marked. One of the earliest and most constant of 
these is nystagmus. Eyesight fails through involvement of the optic nerve or 
because of a sclerotic patch at the optic chiasm. As the disease advances pallor 
of the optic disk, particularly its temporal half, and sometimes optic atrophy can 
be recognized on ophthalmoscopic examination. One eye is often much more 
affected than the other, and loss of accommodation may occur. In other instances 
the pupillary reflex may be lost, yet the pupil will' react to accommodation. In 
other words, the Argyll- Robertson pupil is present. The affection of the external 
ocular muscles, aside from the production of nystagmus, consists most frequently 
in a failure in convergence and in conjugate deviation. More rarely a single 
muscle is affected and squint is produced. When the facial nerve is affected, the 
symptoms in the early stages may consist in clonic spasm of the muscles of the face, 
followed eventually by paralysis. The lesions of the cranial nerves, which produce 
these results, may, as already pointed out, occur in the nerves themselves or involve 
their nuclei. 

Of all the symptoms of disseminated sclerosis perhaps the most characteristic 
and most frequent is the peculiar disorder of speech in which syllables are enunciated 
in a measured manner. To this mode of speech the term staccato or scanning is 
applied. The exact cause of this is not clear. It does not seem to be dependent 
entirely upon paralysis involving the tongue or the lips. 

The mental condition of the patient is usually not materially altered. The 
memory may be slightly impaired and the patient seems somewhat emotional. 
Uncontrolled laughter, as first shown by Oppenheim, is an occasional symptom. 
Very occasionally actual insanity develops. Paroxysmal attacks of vertigo and 



822 DISEASES OF THE NERVOUS SYSTEM 

vomiting are occasionally met with, and in some cases the patient is seized with 
attacks which closely resemble an ordinary apoplexy. These attacks, it will be 
remembered, sometimes develop in patients who suffer from general paralysis of 
the insane, and they appear either as ordinary coma, as Jacksonian epilepsy, or as a 
hemiplegia which is fleeting in character. All these symptoms of an apoplectiform 
type may recur frequently, and are usually recovered from, but occasionally death 
comes on during coma. It is a fact worthy of note that, notwithstanding the 
profound changes which take place in different portions of the nervous system, 
trophic changes in the muscles are rarely met with, even in advanced cases. 

Diagnosis. — The most characteristic symptoms of disseminated sclerosis, as 
just stated, consist in the intention tremor, the staccato speech, the nystagmus, 
the peculiar jerking, inco-ordinated movements of the muscles of the arms and 
sometimes of the legs, weakness of the legs, and the gradual involvement of the 
cranial nerves, especially the optic. 

The disease is to be separated from locomotor ataxia by the jerking character 
of the inco-ordinated movements; and by the exaggeration of the reflexes, which 
are in contrast to the absent reflexes of ataxia. From paralysis agitans it is sepa- 
rated by the fact that in the latter disease there is a finer tremor of the hand, or 
of the parts of the body which may be affected (the tremor is passive), by the 
peculiar attitude of the patient in paralysis agitans, and by the absence, as the 
disease progresses, of the characteristic symptoms just spoken of as peculiar to 
multiple sclerosis. General paralysis of the insane is distinguished by the presence, 
in the classic type of this disease, of delusions of grandeur, by the twitching of the 
muscles of the lips and tongue, which are more constant and severe than they are 
in multiple sclerosis, and by the other evidences of mental change. In a case of 
disseminated sclerosis, in which the lateral columns of the spinal cord are involved, 
it may be difficult to differentiate multiple sclerosis from spastic paraplegia, but 
as the disease progresses the development of the other symptoms of disseminated 
sclerosis makes the diagnosis easy. From hysteria disseminated sclerosis is to be 
separated by the fact that nystagmus, optic atrophy and Babinski's sign do not 
appear in this functional nervous disorder, and by the inconstancy of the symptoms 
in many cases of hysteria. The other characteristic stigmata of hysteria may also 
be found. (See article on Hysteria.) 

Prognosis. — The prognosis in a case of disseminated sclerosis is absolutely unfavor- 
able as to ultimate recovery. The disease is characterized by various remissions 
or periods of arrest, so that death is sometimes postponed for a considerable period 
of time. The prognosis as to duration of life is worse in those cases in which the 
lesions involve nervous tissues closely associated with vital functions, as when 
sclerotic changes take place in the pons, or, above all, when they occur in the 
medulla. It is noteworthy that pregnancy or trauma increases the rapidity with 
which the disease progresses. 

Treatment. — Everywhere in this book, when we have considered the treatment 
of diseases depending upon sclerotic changes or overgrowth of connective tissue 
it has been pointed out that our therapeutic resources are inadequate. We do 
not know the causes of this connective-tissue overgrowth, and so are unable to 
combat it, nor do we know why the cells degenerate. Neither have we any reason 
to believe that. in the future we will discover any remedy which will cause the 
absorption of connective tissue when it is once formed, and it is certain that fibres 
which have once degenerated and have been destroyed cannot be regenerated by 
the action of any medicine. 



PLATE XII 




XIII 



The Cervical and Sacral Enlargements of the Spinal Cord in 
Cross-section, showing the various neurones in the gray matter, 
the direction of their axones, and the varieties of fibres in the 
different columns of the cord (Starr). Blue, motor-; red, sensory-; 
purple, association-neurones and axones. 

I. Ant. median column. II. Anterolateral column. III. Gowers' anterolateral ascending 
column. IV. Marginal column. V. Lateral pyramidal column. VI. Direct cerebellar column. 
VII. Lissauer's tract. VIII. Ext. portion of column of Burdach. IX. Root zone of the column 
of Burdach. X. Descending comma-shaped bundle of Schultze. XI. Post, commissural tract. 
XII. Column of Goll. XIII. Septomarginal tract. 



LOCOMOTOR ATAXIA 823 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE 

SPINAL CORD. 

LOCOMOTOR ATAXIA. 

Definition. — Locomotor ataxia is a disease characterized chiefly by inco-ordination 
of gait and station, loss of muscle and joint sense, and loss of the deep reflexes. 
It is often accompanied by pain. The most noteworthy loss of reflexes is in the 
patellar tendon and iris. Pathologically, it is characterized by slow progressive 
degeneration which affects chiefly the sensory nerve roots and the posterior or 
dorsal columns of the spinal cord. It is sometimes called tabes dorsalis, or pos- 
terior spinal sclerosis. 

History. — Cases of locomotor ataxia were recorded as a form of paralysis many 
years ago, but it was not till 1847 that Todd clearly separated this malady from 
other states of paralysis. In 1840 Stanley had recognized that the affection was 
associated with changes in the posterior columns of the spinal cord. In 1855 
Reynolds first showed that the disease was essentially a state in which the symptoms 
were due to a loss of muscle sense, and not to loss of power in the motor nerves 
or muscles — a view confirmed by Tiirck, who made a microscopic demonstration 
of the site of the lesions. 

Etiology. — Males suffer more than females in the proportion of 10 to 1. In a 
large general hospital experience of more than thirty years I have seen but one 
case in a woman. Half the cases develop in the decade of life between thirty and 
forty years, and 80 per cent, between thirty and fifty years. Gowers states that 
it rarely develops after fifty years. 

By far the most common cause of the disease is acquired syphilis. Rarely 
the syphilis is hereditary. Some writers have gone so far as to state that locomotor 
ataxia is due to this cause in over 90 per cent, of the cases (Sachs). Gowers gives 
the rather moderate proportion of 77 per cent.; Starr 70 per cent. The more 
acute methods of diagnosticating syphilis seem to indicate that it is the cause in 
100 per cent. C. J. White has recorded a patient twenty-one years old who 
developed tabes three months after infection. Rarely the ataxic symptoms develop 
within five years of the primary sore. In 226 tabetics he found the disease developed 
in 11 per cent, in the first five years, 25 per cent, in the first ten years, and 61 
per cent, in the first fifteen years; 76 per cent, developed the disease between 
thirty and fifty years of age. In many instances the ataxic symptoms develop 
so many years after syphilitic infection that the patient cannot believe that the 
two maladies have any relationship of cause and effect, the more so as ataxia 
is more frequently met with in patients who have presented very mild secondary 
symptoms than in those who have had severe symptoms in the early stages. 

Severe falls, or blows upon the spine, have been followed, months or years later, 
by tabes dorsalis, but it is impossible to tell just what relation the trauma has to 
the malady. 

Pathology and Morbid Anatomy. — In studying the morbid anatomy and pathology 
of locomotor ataxia it is important for the student to recall the fact that the primary 
lesion of the disease is in the posterior ganglia and posterior roots of the spinal 
cord, and in the ganglia of the cranial nerves, and not in the posterior columns of 
the spinal cord, as was thought at one time. The sensory cells in the posterior 
ganglia, outside of the cord, are flask-shaped bodies, each of which has a process 
which divides into two axones. One of these goes by the posterior nerve root to 
the spinal cord, and the other goes to the afferent nerve, which extends to the 
peripheral portions of the body. (See Plate XII.) Degenerative changes take 
place in the proximal axone as well as in the peripheral portion of the distal axone. 



824 DISEASES OF THE NERVOUS SYSTEM 

These changes are sclerotic and are carried into the cord, so to speak, by the proximal 
axone. Therefore, locomotor ataxia consists primarily in disease of the proximal 
axone, secondarily in disease of the distal axone, and finally in disease of those 
fibres in the posterior portion of the spinal cord which have their origin in the 
proximal axone just described. While it is true that the primary lesion is not in 
the cord, it is nevertheless a fact that the chief manifestations of the pathological 
process are to be found in this portion of the nervous system. Indeed, the changes 
in the spinal cord are so well developed in typical cases that the macroscopic 
examination suffices for the diagnosis at the autopsy. 

The affected portions of the cord are smaller than normal and more grayish 
in appearance. The distribution of those areas varies greatly. In some instances 
the disease is so moderate in degree and in distribution as to be difficult of recogni- 
tion, except by the microscope. In others, if the malady is far advanced, the whole 
length of the posterior columns may be affected. There are certain parts of the 
cord which are particularly prone to the development of the disease. Thus, the 
lesions are usually well developed in the posterior columns in the lumbar regions 
particularly in the neighborhood of the posterior root zones, and this accounts 
for the fact that the legs show the earliest and most severe symptoms. As we 
ascend the cord, however, the lesions are chiefly found in the posteromedian 
columns. 

In instances in which the disease affects the arms as well as the legs and is well 
developed, the postero-external co umns are affected even in the cervical region 
(Fig- 134). 

Under the microscope it is found that the connective tissue in the posterior 
columns of the cord has undergone hyperplasia or overgrowth. The fibrous 
sheath of the bloodvessels is particularly affected and is seen to be thickened and 
to project connective-tissue fibrils into nearby parts. The nerve fibres may have 
disappeared entirely or be represented by atrophied or wasted fibres. In some 
cases the vessels of the pia mater are also thickened, particularly in the part covering 
the posterior columns, and these vessels may also give off fibrils of connective 
tissue which add to the connective-tissue overgrowth in the superficial part of 
the cord. 

The changes which are found in the posterior nerve roots vary greatly in their 
degree. In some instances they are so slight that they can be recognized only 
by carefu microscopic examination; in other instances they are so well marked 
that the naked eye can detect them. Under these circumstances they appear 
atrophied and the connective-tissue elements may be somewhat increased. The 
root fibres in the cord are more affected than those outside of the cord The ganglia 
are also affected by an overgrowth of connective tissue, and by an atrophy of their 
nerve cells. Beyond the ganglia pathological changes in the mixed nerve are 
rarely seen as a continuation of the process found in the nerve roots, but it is a 
well-recognized fact that marked primary changes are to be found in the peripheral 
nerves, and especially in the cutaneous branches. These changes consist in an 
atrophy of the myelin sheath followed by degeneration and segmentation of the 
axis cylinder and they occur at the distal extremity of the nerve in greater degree 
than higher up. The main nerve trunks are rarely affected. It is largely because 
of these neural Lesions that sensation in the skin and in the joints and the muscular 
sense are lost. 

In certain cases the changes of locomotor ataxia may be well marked in the cord 
and slight in the nerve roots, and in others the nerves are chiefly involved. It is 
important that this fact be remembered because it serves to fix in the mind of the 
student the fact that locomotor ataxia is not solely a disease of the posterior columns 
of the cord. 

While locomotor ataxia chiefly affects the spinal cord and its nerve roots, it also 



LOCOMOTOR ATAXIA 



825 



Fig. 136 



attacks quite frequently the cranial nerves, and of these the optic nerve suffers 
most severely and most frequently. Its nerve fibres atrophy and its connective 
tissue undergoes proliferation. 

By no means rarely marked degenerative changes are found in the joints. The 
articulating cartilages are eroded, the joint may become filled with fluid, and for 
these reasons dislocations may occur. Trophic 
changes also occur elsewhere. (See Symptoms.) 

Symptoms. — In a case of locomotor ataxia 
which is typical in its course the following 
symptoms are present, and if they are well de- 
veloped it is not difficult to make a diag- 
nosis: 

The patient often states that his feet feel 
"muffled" that is, as if he had on several pairs of 
thick socks. In other cases he notices that on 
arising at night he has difficulty in getting a 
proper "purchase" with his feet on the floor, or 
the floor may feel as if its plane is at a different 
angle from that pictured in his mind. These 
awkward sensations are due to the interference 
with the sensory nerve fibres, that is, with con- 
duction of sensation to the spinal cord. He also 
has difficulty in walking in the dark, not only 
because his tactile sense is disturbed, but because 
his muscle sense is also impaired, with the result 
that he is in doubt as to the position of his limbs 
and as to the relative tonicity of opposing 
muscles. This loss of muscle sense depends upon 
the fact that the sensory nerves supplying the 
joints, tendons, and fasciae are impaired in func- 
tion and the tracts in the spinal cord which 
carry these impulses which reflexly co-ordinate 
movement are also involved. If the impulse 
passes this area of damage and reaches the cord 
it passes up the posteromedian columns without 
decussation, and probably goes directly to the 
cerebellum, which presides over balance. These 
columns are always diseased if the ataxia is 

marked, but cutaneous sensibility is often preserved, proving that the muscular 
and cutaneous sensations are carried by different tracts. 

Closely related to the disorder of muscle sense is inco-ordination, which produces 
the peculiar gait. In the ataxic gait the foot is raised awkwardly and then thrown 
down in front of the other foot with a characteristic uncertain movement, the whole 
under surface of the foot striking the ground at once. This uncertainty of move- 
ment becomes still more marked if the surface over which the patient has to walk 
is uneven, or if a rug upon the floor requires that the feet shall be lifted slightly 
to clear it. In other cases the edge of the foot rests on the floor instead of the 
plantar surface, and in the effort to correct this position another clumsy movement 
is made. If the light is poor or if the patient closes his eyes, the difficulty in muscu- 
lar co-ordination may be so great that he staggers and falls. As the involvement 
of the sensory pathways becomes more marked, support by means of a cane, nearby 
objects, or another person, is needful for locomotion, and finally all attempts at 
walking have to be given up. In cases in which the upper portions of the cord 
suffer, there is a similar inco-ordination of the arms, so that the patient cannot 




Sclerosis of the lateral and (in the 
anterior cervical region) pyramidal 
tracts, with slight degeneration of the 
anterior cornua. A, cervical; B, dorsal; 
C, lumbar sections. (After Gowers.) 



826 DISEASES OF THE NERVOUS SYSTEM 

carry food to his mouth if the eyes are closed. In other instances, however, even 
when the legs are practically useless, the arms entirely escape. If either the arms 
or the legs are extended the muscles do not remain steady, but alternately contract 
and relax, as the patient vainly endeavors to maintain his balance. There is no 
actual loss of muscle strength until the disease has lasted so long that the muscles 
waste from disuse. 

The same cause that produces the difficulty in gait also causes a disturbance of 
"station." That is to say, the patient cannot stand steadily, but sways in the 
endeavor to keep his balance. If his eyes are closed or if he is blindfolded he sways 
so widely that there is danger of his falling, and he may actually fall if he cannot 
co-ordinate his muscles by the use of his eyes, which will give him a conception of 
the relative position of surrounding objects. This instability is often very marked 
when the patient attempts to suddenly assume the erect posture after sitting in a 
chair for some time. As Romberg first called attention to this loss of station, the 
term " Romberg's symptom" is applied to this manifestation of the malady. 

Still another indication of the disease in the sensory pathways in locomotor 
ataxia is the diminution and final total loss of the knee-jerks when the patellar tendon 
is tapped. This is called "WestphaVs symptom" 

The diminished tonicity of the muscles and ligaments in tabes causes them to 
relax. This "hypotonia" can easily be demonstrated by having the patient lie 
on his back on a flat surface, the examiner pressing the knee down and elevating 
the heel. It will be found that in tabes the point to which the heel can be raised 
will be much higher than can be reached when the test is applied to a normal 
individual. 

So far only those disorders of motion which result from the loss of muscle sense 
have been discussed. There yet remain to be considered the characteristic sensory 
symptoms themselves. These consist in pain and loss of sensibility. Pain is a 
very frequent and often a very early symptom, occurring in about 90 per cent, of 
all cases, and it may be very severe. It occurs chiefly in the legs as sharp dartings 
called " lightning pains." Unlike the motor symptoms, these pains are not confined 
to the legs and arms, but are often present in the body and even in the head, where 
other symptoms of this disease are rare, except in the eyes. The pains are often 
agonizing and occur chiefly at night. In most instances they occur in periodic 
attacks, then ceasing for weeks or even months. They may develop in different 
parts of the body at each attack. They rarely have their seat in large nerve trunks, 
but exist in the more minute fibres of the nerves. When they attack the stomach 
they are called "gastric crises," a term also applied to severe attacks of vomiting 
in this disease. So, too, attacks of intense pain may suddenly develop in the 
bladder, "vesical crises ," and in the rectum, "rectal crises." There may be marked 
"girdle sensations" in the trunk. 

The pains are described as darting, rending, or burning, and the patient may speak 
of "burning toes" as his most troublesome symptom. Intense hyperesthesia of the 
skin in the painful areas may also be present. These pains are to some extent 
affected by atmospheric states. I have more than once known them to be produced 
or exaggerated by constipation, probably because of the absorption of intestinal 
toxins. 

It is important to bear in mind the fact that pain may be one of the earliest 
signs of this malady, and may vary from tingling to an agony without any of the 
disorders of the gait being as yet present. On the other hand, very severe ataxia 
may be present without any pain. In addition to these painful disorders various 
other disturbances of sensation also develop, such as formication, tickling, pricking, 
creeping, sensations of heat and cold, or hyperesthesia. When the disease is well 
advanced, diminution of sensation in the skin or even complete anesthesia may 
appear. The sense of pain and of touch may both be impaired. The pain sense 



LOCOMOTOR ATAXIA 827 

may be lost and the heat sense retained, or, again, the tactile sense may be inter- 
preted by the patient as pain or heat. A very interesting perversion of the function 
of sensation is the delay in the transmission of the sensory impulses, so that a very 
appreciable interval occurs between the moment at which the foot is pricked 
and the moment at which the patient appreciates the fact that the injury has been 
sustained. Obersteiner has recorded a case in which the interval was twenty -five 
seconds. So, too, the patient is unable to readily indicate the part touched. He 
may even assert that it is the left foot when it is really the right one that is irritated. 
To this symptom the term allochiria is applied. All these tests must be made, 
of course, with the patient blindfolded. The deeper portions of the body may be 
as anesthetic as the skin, and injury to a testicle, pleurisy, and severe muscular 
inflammation, as after a deep injection of mercury, may be painless. Biernacki 
has shown that the ulnar nerve is often insensitive to pressure at the elbow. Sexual 
power may or may not be lost. 

The changes which take place in the eyes in locomotor ataxia are so constantly 
met with and are so valuable to us from a diagnostic standpoint, that they are 
worth remembering. In about 80 per cent, of the cases the Argyll- Robertson 
pupil is present, that is, the pupil reacts to accommodation, but not to light. This 
state depends upon a lesion, somewhere in the path of the light reflex, which includes 
the optic nerve on the one hand and the oculomotor nerve and nucleus on the 
other, with a connection between these two nerves which is not known. Some have 
taught that Meynert's decussation, between the primary optic centres in which the 
optic nerve ends and the third nerve nucleus, forms this connection and is the seat 
of lesion determining the Argyll-Robertson pupil. Recent studies indicate that 
the fibres concerned pass from the optic tract to the third nerve nucleus before 
the former has reached the primary optic centres. 

There may be loss of accommodation in some cases. The pupils are usually 
myotic; they may be unequal and uneven, especially during contraction; they may 
also be irregular in shape. 

The' second important ocular symptoms are those which depend upon the nerve 
supply of the extrinsic muscles of the eye. Diplopia may develop as a fleeting 
or permanent symptom due to insufficiency of one cf the ocular muscles, the external 
rectus muscle being the one most commonly affected, although there is diversity 
of opinion as to this point. So, too, single or double ptosis may develop and be 
transient or permanent. In some cases all the extraocular muscles become par- 
alyzed so that a complete ophthalmoplegia may be present. The third ocular sign of 
importance is atrophy of the optic nerve, which takes place in about 10 per cent, of 
all cases. It is often present before any difficulty of the gait develops, and for this 
reason the presence of the disease may be first recognized by the ophthalmologist 
rather than by the general practitioner. It is thought by some writers that this 
manifestation of locomotor ataxia is more prone to develop in the instances in 
which the arms are involved than in those cases in which the lower portions of the 
cord are affected. Not rarely the presence of optic nerve atrophy seems to be 
accompanied by an arrest of the sclerotic process elsewhere. The field of vision 
is primarily diminished, there may be loss of color vision, but sometimes the failure 
is marked, even from the onset, in the neighborhood of the macula. The impair- 
ment of vision which ensues may progress to total blindness or become arrested 
and consist in more or less severe impairment. Usually the process is slow, but 
occasionally it is so rapid that even a few days produce great changes in the visual 
acuity. As is easily understood, when we consider the nature of the lesions which 
are characteristic of the disease the loss of vision is not always unilateral. 

When the optic nerve is examined by the ophthalmoscope in such cases the disk 
is seen to be pale and shrunken, but at times the degree of blindness is in excess 
of the changes in the disk. Finally, the disk becomes a pale gray. 



828 



DISEASES OF THE NERVOUS SYSTEM 



Fig. 137 



Occasionally deafness gradually or suddenly develops. It may be transient or 
fleeting. 

The bladder in locomotor ataxia is often greatly impaired in its functions. The 
urine is often imperfectly expelled and as a result residual urine produces cystitis. 
More rarely retention of urine ensues. The sphincter ani is also weakened, and 
so control of the feces is diminished, 

There still remain to be considered two results of the disease which are of interest 
and diagnostic importance. The first of these is the so-called "Charcot joint," 
to which reference has already been made. Owing to the changes in the elbow, 
shoulder, hip, and knees the landmarks of these parts may be completely obliterated, 
and great swelling often is present. The second of these trophic changes is the 
so-called perforating ulcer of the foot, which may or may not be accompanied by 
ulcerations about the toe-nails. In addition to these trophic symptoms the bones 
are sometimes abnormally brittle, so that fractures result spontaneously or from 
trivial causes. 

Diagnosis. — As already intimated, the most valuable diagnostic symptoms and 
signs of locomotor ataxia are the loss of the knee-jerk, the swaying station, the 

Argyll-Robertson pupil, the optic atrophy, and the 
lightning pains. No one of these, however, enables 
us to make a diagnosis because of its presence. The 
disease must be differentiated from peripheral neuritis 
due to alcohol, lead, and arsenic, and from that due 
to typhoid fever and diphtheria. In these conditions 
there is loss of knee-jerk, swaying station, and often 
severe pains or anesthesia, but the Argyll-Robertson 
pupil is absent and the history of the patient as to 
exposure to alcohol, lead, or arsenic aids us greatly in 
the differentiation. To these states the term pseudo- 
tabes has been well applied. A positive Wassermann 
reaction, given by the cerebrospinal fluid which con- 
tains an excess of lymphocytes of from 10 to 100 to the 
cubic millimetre, an excess of globulin, and which reduces 
Fehling's solution, practically decides the diagnosis. 

Locomotor ataxia is separated from the various 
forms of paraplegia by the loss of the knee-jerk, which 
is usually exaggerated in other spinal states, and by 
the actual loss of power in paraplegia. From the 
spastic paraplegia due to lateral sclerosis true loco- 
motor ataxia is separated by the spastic state of the muscles and the greatly 
increased knee-jerk. 

From general paralysis of the insane locomotor ataxia may be difficult of separa- 
tion, for in this disease the Argyll-Robertson pupil and other physical signs of 
locomotor ataxia may be present. As the case advances the predominance of the 
cerebral symptoms over the spinal symptoms becomes marked and so renders the 
diagnosis possible. (See Paretic Dementia.) 

The fact that in rare cases of locomotor ataxia severe pains are felt in the trunk 
should never be forgotten, for it has happened not infrequently that they have 
misled the physician into a belief that caries of the vertebra? was present. 

The staggering gait of cerebellar tumor can scarcely be mistaken for locomotor 
ataxia. If there is doubt as to its cause it can be dispelled by the absence of shooting 
pains, by the presence of headache and of nystagmus. 

Prognosis. — The prognosis of locomotor ataxia may be best considered in two 
]>arts. So far as complete recovery is concerned, this is out of the question. So 
far as rapidity of progress is concerned, we must always be guarded in expressing 




Perforating ulcer of the foot 
in locomotor ataxia. (Ober- 
steiner.) 



LOCOMOTOR ATAXIA 829 

an opinion. In the great majority of cases the disease lasts for years and is char- 
acterized not only by periods of arrest, but of actual improvement of a very marked 
character in some cases. In cases not too far advanced, with proper care and 
treatment, a useful life may be had for twenty years. The use of the proper 
specific remedies may arrest the malady, but they cannot cure the damage already 
done. Cases which attack those young in years and progress rapidly are most 
unfavorable, but even these cases make remarkable "stops" in the advance of 
the affection. 

Treatment. — There is probably no grave disease of the nervous system of an 
organic nature which, in some instances at least, yields such good results from 
treatment as does this one. 

As may be gathered from the discussion of the pathology of locomotor ataxia, 
it must be evident that the physician can only palliate the symptoms of this disease, 
and that a complete cure is practically impossible. The most that we can do is 
to prevent further progress of the malady. Nevertheless, in a large proportion 
of cases, benefit is obtained by the pursuance of a plan of treatment which consists 
largely in the administration of mercury and salvarsan (see Syphilis), and possibly 
iodide of potassium. If the specific infection is of comparatively recent date, 
the salvarsan should be used, but in many instances this is not the case, and mercury 
is the remedy of choice. In almost all cases salvarsan first and mercury afterwards 
should be the plan, and under their conjoint use the specific manifestations, already 
described, in the cerebrospinal fluid disappear and the symptoms moderate unless 
the morbid change in the nerve roots and cord, be so far gone as to be permanent. 
Usually four doses of salvarsanized serum are given within the first four weeks. 
The repeated use of salvarsan depends upon the findings in the cerebrospinal fluid. 
If they clear up it may be stopped and repeated if they return. The mercury is 
best used intramuscularly in the form of the salicylate or the gray oil. The 
Swift-Ellis method of injecting salvarsanized blood serum intraspinally is of 
recent introduction and seems to be of distinct value, especially in relieving the 
lightning pains and visceral crises. Very often the best results are obtained if in 
addition inunctions with mercurial ointment are practised twice or thrice a week. 

While, on the one hand, it should be our endeavor to use these two specific 
remedies very freely, it must also be remembered that the patient's vitality must 
be kept at the highest possible level by every means in our power. Poor health 
and digestive disturbance produced by the unwise employment of mercury probably 
does the patient more harm than the drugs do him good. Starr asserts that the 
use of mercury hastens the process of optic nerve atrophy, and in those cases in 
which this symptom is present mercurial treatment should not be resorted to. 
In those cases in which there is no syphilitic history, or in which the mercurials 
are badly borne, arsenic may be given as a nerve tonic particularly in the form of 
cacodylate of sodium. Nitrate of silver was at one time thought to be advantage- 
ous, but there is nothing in our knowledge of this drug or of the disease which makes 
its employment in any way specific. 

For the relief of the pains in the peripheral nerves, the coal-tar products are 
our best remedies, acetanilid, phenacetin, and antipyrin being commonly employed. 
In other instances the salicylates are useful. If the pain is excessive, morphine 
must be used. 

For the twitching of the limbs, the bromides, which quiet the sensory portions 
of the cord, may be employed in sufficiently large doses to produce sedation. 

A method of treating these cases which is of some value is that introduced by 
Fraenkel, of Berlin. This method is not curative in the sense that it is supposed to 
influence the lesions in the cord, but is employed with the object of training other 
nerve fibres than those originally used, so that the patient may to some extent 
regain his muscle sense. This plan consists in making him take certain exercises 



830 DISEASES OF THE NERVOUS SYSTEM 

which require co-ordination. A chalk line is drawn upon the floor and he is required 
to follow it as closely as possible; or, a series of cup-like depressions are made in a 
plank, which is placed across the foot of the patient's bed. These depressions are 
numbered from one to ten, and he is instructed by the nurse to raise his leg and 
then rest his heel in the cup which she names. In this way the patient in some 
instances is able to speedily respond to the order, and so is trained to carry out 
well co-ordinated movements. Still another method consists in supplying him 
with a small double flight of steps provided with railings so that he cannot fall. 
The patient is then required to mount a few steps on one side and then descend a 
few on the other, using his legs to lift himself up on each step, and not pulling himself 
up by his hands, which rest upon the rails. In other instances still, definite spaces 
are marked out on the floor, and he is directed to take a stride which will bring 
his heel on each mark. It can be readily seen that a large number of such exercises 
can easily be devised if a little ingenuity is used. Care should be taken that 
the exercises are not continued so long that the patient becomes in the slightest 
degree exhausted. For this reason they should rarely be continued more than 
five minutes at a time, although they may be resorted to several times a day. 
Additional methods of treatment consist in the employment of massage, which is 
designed to maintain the nutrition of the limbs and to keep in health the blood- 
vessels and lymphatic system, thereby to a certain extent compensating for the 
lack of exercise from which the patient inevitably suffers. 

The various forms of baths at home, or at health resorts, may be employed rather 
for the mental effect which they will exercise upon the patient than with any hope 
that they would be in any way curative. The great advantage in resorting to 
the various health resorts where baths can be obtained is that the patient goes 
away for the purpose of getting well and leaves his business cares behind him. 
The great difficulty with cool baths is that the patient usually has not sufficient 
power of reaction to stand them, and tepid and hot baths often seem to exercise 
an enervating effect. Where baths can be used with the object of aiding in the 
absorption of mercury and the iodides, and where they do not produce depression, 
they are valuable. 

So far as exercise is concerned, this should be governed entirely by the strength 
of the patient. Under no circumstances whatever should he be permitted to 
become exhausted. Not infrequently severe attacks of pains in the limbs are 
precipitated by exercise which is sufficiently severe or prolonged to diminish the 
nervous vitality of the patient or to tire the nerves themselves. 

Electricity may be used in the form of the galvanic current, the positive pole 
of the galvanic battery being placed at the nape of the neck and the negative pole 
at the sacrum and at the soles of the feet. The electrodes should be large so that 
the current will be well diffused. As a matter of fact the condition of the spinal 
cord and the nerve trunks is such that little real benefit can be expected from 
this plan of treatment except for its sedative influence. 



FRIEDREICH'S ATAXIA. 

Definition. — Under this name a disease of the nervous system is rarely met with 
which is hereditary and which depends for its clinical manifestations upon lesions 
in the posterior and lateral columns of the spinal cord. It is, therefore, an ataxic 
paraplegia which is peculiar in that it develops in early life. Friedreich's ataxia 
is also called "hereditary ataxic paraplegia," "hereditary ataxia," "Friedreich's 
disease," and "family ataxia." 

History. — The malady was first described by Friedreich in 1861 and again in 
187G. In the United States the most noteworthy study is that of Everett Smith 



FRIEDREICH'S ATAXIA 831 

in 1885. Schultze showed in 1877 that the disease was due to a congenital defect 
in the cord. 

Etiology. — The exact cause is unknown. Occasionally there is a distinct family 
history of the disease, but often no more than one child in a family is affected. 
Sometimes the symptoms develop after one of the acute infectious diseases of 
childhood, and it is then supposed to be due to development of the evidences of 
imperfect growth or to damage to poorly vitalized cells which have never become 
well developed. In some cases the parents have an alcoholic history; in others 
there is a history of syphilis. Neither of these facts are, however, of real etiological 
importance. The influence of age is uncertain. Rarely the malady manifests 
itself in infancy; more commonly it develops about the sixth or eighth year; if 
not at this period, then at puberty, and if not at puberty, then at about twenty-one 
years of age. The two sexes suffer about equally. It has been shown that defective 
development of the cerebellum may be a part of the pathological findings in this 
disease. Marie, however, believes that spinal cord atrophy in these areas, when 
due to cerebellar disease, is a separate malady, and the symptoms due to agencies 
of the cerebellum are sufficiently distinctive to constitute a separate type of 
hereditary ataxia. 

Fig. 138 



.,-fi- ":~ ^P*' 




The lesion of Friedreich's hereditary ataxia. Maldevelopment and sclerosis of the lateral and 

posterior columns. (Schultze.) 

Pathology and Morbid Anatomy. — As already stated, the lesions of Friedreich's 
ataxia are chiefly found in the posterior and lateral tracts of the spinal cord, and 
the disease may therefore be considered as a combination of two maladies so far as 
the lesions and symptoms are concerned. 

When the spinal cord is removed from such a case at autopsy it is usually seen 
to be smaller than normal, and the pia mater is commonly thickened, particularly 
over its posterior surface. 

If the cord is examined under the microscope with suitable staining (Fig. 138), 
it is found that the posterior dorsal columns, particularly those of Goll, the lateral 
pyramidal tracts, and the direct cerebellar tracts all show degenerative changes. 
These changes are not chiefly limited to one portion of the cord, as they are in 
most cases of locomotor ataxia, but extend up into the cervical region as well as 
in the lumbar region. The lesions are not only posterior and lateral, but anterior 
as well, for the direct pyramidal tract on either side of the anterior median fissure 
is affected. There is also atrophy of the cells in the anterior and posterior horns 
of the gray matter. The anterior and posterior nerve roots are also atrophied. 



832 DISEASES OF THE NERVOUS SYSTEM 

The cells in the column of Clarke are markedly degenerated, and round-cell infiltra- 
tion is present about the central canal of the cord. In this disease, as in other 
maladies, the loss of nervous tissue is followed by overgrowth of the neuroglia 
in the affected parts. 

Symptoms. — Friedreich's ataxia consists, pathologically, in lesions in the posterior 
and lateral columns of the cord, it necessarily follows that the symptoms are closely 
allied to locomotor ataxia and lateral sclerosis. The onset of the disease is char- 
acterized by gradual loss of co-ordination, affecting the legs before it affects the arms, 
which causes unsteadiness in station, so that the feet, when the patient is standing, 
are placed far apart to maintain the balance of the body. In some instances the 
first symptom is that the child falls over objects which hitherto have not been 
obstacles in its path. When the child walks its gait is tottering, and if it closes 
its eyes the lack of co-ordination and consequent instability is so great that it 
may fall. The muscles of the legs are often strongly contracted in an endeavor 
to maintain the upright posture, and this condition of muscular rigidity is increased 
by the disease in the lateral tracts. The child if stripped and left standing is 
seen to be continually writhing in an endeavor to adjust opposing muscles in order 
to maintain its equilibrium. The knee-jerks are lost, but cases are occasionally 
met with in which the reflexes are exaggerated. These cases closely approximate 
the group called hereditary cerebellar ataxia. (See below.) 

Loss of power is not as early a symptom as is inco-ordination. It affects the 
legs far more severely than the arms. The extensors suffer less than the flexors, 
and this may place the feet in a posture like that of talipes equinus or varus. This 
deformity may also be caused not only by one group of muscles overcoming others 
by reason of their loss of power, but by the fact that if the lesions in the lateral 
columns of the cord predominate, a spastic pareplegia develops which may result 
in contractures as in ordinary ataxic paraplegia. Marked hyperextension of the 
toes, especially of the great toe is a frequent and characteristic symptom. In 
those instances in which the muscles of the trunk become affected curvature of 
the spine may develop. 

The mind is not affected by the disease, but nevertheless the patient rarely 
develops mentally as does the normal child. 

When the disease is well advanced, the movements of the lower and upper 
limbs become not only irregular from inco-ordination, but jerking in character, 
and this jerking movement may extend to the head and be accompanied by tremor. 
Speech becomes impaired, the words are blurred because of imperfect articulation, 
and the utterance may be sudden or explosive. The disorder of speech is a late 
symptom of the malady, and may not appear for some years after the ataxic mani- 
festations appear. When the eyes are moved laterally or upward nystagmus may 
be present, and it is peculiar in that it is absent when the eyeballs are at rest. 
The extraocular muscles are rarely paralyzed, and the optic nerves always escape. 
In these respects, therefore, the disease differs very distinctly from locomotor 
ataxia, in which malady these parts are commonly involved. Occasionally, cases 
are met with in which the pupillary reflex is lost. In these cases, however, syphilis 
is the cause, and the case is probably one of tabes with Argyll-Robertson pupils. 

The disease is usually characterized by an absence of all disturbances of sensation 
save that cramp-like contractions of the muscles in the early stages may cause the 
patient some suffering. In rare instances severe darting pains have been met with, 
or the patient has experienced numbness in the limbs. The symptoms of ataxia 
are usually made worse by prolonged rest. 

Diagnosis. — The development of the characteristic symptoms just enumerated 
during the period of childhood renders the diagnosis easy, for the maladies which 
resemble Friedreich's ataxia are all of them affections of adult life, save multiple 
neuritis, which may cause, of course, pseudotabes and a disturbance of station and 



CHRONIC ANTERIOR POLIOMYELITIS 833 

gait. From Marie's cerebellar hereditary ataxia Friedreich's ataxia can be sepa- 
rated by a study of the symptoms of that affection described below. 

It must be recalled, however, that cases of Friedreich's ataxia develop which 
present symptoms which do not follow characteristic lines. Thus, in some cases 
great muscular atrophy has occurred. Nystagmus may not appear. Diplopia 
may be present. 

Prognosis. — The prognosis is, of course, hopeless. The only thing favorable 
which can be said is that the disease often develops very slowly and has long periods 
of arrest. The child, if attacked early in life, rarely reaches adult years. 

Treatment. — Treatment, aside from that devoted to the maintenance of good 
nutrition, is of little avail, for obvious reasons. 

Marie's Cerebellar Hereditary Ataxia. — Under this name a form of hereditary 
ataxia has been described by Marie in which he has shown that a congenital defect 
exists in the cerebellum. The condition is characterized by ataxia, difficulty 
in speech, and nystagmus, and in these points resembles Friedreich's ataxia. 
It differs, however, in the presence of defective pupillary reaction and various 
ocular palsies with optic atrophy and exaggeration of the knee-jerks. Further, 
it develops in the third decade of life, whereas Friedreich's ataxia nearly always 
appears before the fourteenth year. 

L. F. Barker has recently put the matter thus: The direct cerebellar tracts of 
the cord which are degenerated in Friedreich's disease end in the middle lobe of the 
cerebellum, which is defective in Marie's type. The ataxia of both these diseases 
therefore results from lesions of different parts of one system. In Barker's nomen- 
clature the spinal part of the posterior spinocerebellar system is affected in Fried- 
reich's ataxia, while the cerebellar part of it is involved in Marie's type. An 
analysis of the symptoms in all the reported cases of Marie's disease has led IT. T. 
Patrick to say that increase of knee-jerk is its sole distinguishing feature from 
Friedreich's ataxia. Probably the most advanced view is that the two conditions 
are phases of one disease. 

CHRONIC ANTERIOR POLIOMYELITIS. 

Definition. — It is evident from its name that this disease closely resembles acute 
anterior poliomyelitis. A very important difference lies in the fact that in the 
acute form the damage takes place suddenly, and then ceases to progress, some 
improvement occurring in most instances, whereas in the chronic form the atrophic 
process is slow in onset and progressive and so the symptoms get worse rather than 
better. When the symptoms develop during a period of from two weeks to a month 
the term subacute is applied, and when they come on even more slowly, so that 
several months are consumed in their advance, the term chronic is used. The 
dominant symptoms are muscular wasting with paralysis. Chronic anterior 
poliomyelitis is sometimes called "chronic atrophic spinal paralysis" or "progressive 
muscular atrophy." 

Etiology. — This is unknown. Exposure to cold and wet has been thought to be 
a cause in some cases. Among other possible causal factors mentioned are spinal 
concussion and general infections including syphilis. 

Pathology and Morbid Anatomy. — The lesions of chronic anterior poliomyelitis 
consist in atrophy of the nervous tissues of the anterior horns of the gray matter 
of the cord. Not only the cell bodies but their axones and dendrites all undergo 
degenerative change. There is no acute inflammatory process present as in the 
acute form of the disease, and no hemorrhages into the tissues about the vessels. 
The dominant change is a simple atrophy or wasting. The anterior nerve roots 
also suffer atrophic changes, and the so-called association fibres of the cord and 
the cells which give rise to them also atrophy. As these association fibres pass to 
53 



834 DISEASES OF THE NERVOUS SYSTEM 

the anterior lateral columns of the cord the degenerative process extends to them 
as well, and this, combined with the wasting of the anterior nerve roots, produces 
a shrinkage in the size of these columns, which is, however, not great enough to be 
recognized by the unaided eye. The atrophic process extends down these tracts 
and involves the motor nerve fibres all the way to the nerve plates in the muscles, 
which in turn undergo atrophy, the muscular fibres losing their striaB and showing 
fatty globules inside the sarcolemma. It is the rule, in a case of poliomyelitis of 
long duration, for the lateral tracts of the cord also to become affected, the condition 
then becoming an amyotrophic lateral sclerosis. 

Symptoms. — The symptoms of this malady vary somewhat with the portion of 
the spinal cord which is chiefly affected. Most commonly the earliest manifesta- 
tions of the disease appear in the upper extremities, and this is usually called the 
"Aran-Duchenne type of the disease." It generally first manifests itself in the 
adductor muscles of one thumb. From these it extends to all the small muscles 
of the hand, which rapidly become wasted. Flexion of the fingers upon the hand 
is impossible, and as the interossei which flex the first phalanges are paralyzed, the 
long flexor and extensor muscles of the forearms are unopposed. As a result we find 
that the long flexors flex the second and third phalanges and the long extensors 
extend the first phalanges, giving the so-called "claw-hand" deformity. This 
effect is increased by the prominence of the extensor tendons, caused in part by 
the wasting of the smaller muscles of the hand. The hand or the shoulder on the 
opposite side soon suffers. In a considerable number of cases the wasting appears 
first in the muscles of one or both shoulder girdles. Finally, all the upper arm and 
shoulder muscles atrophy, and later those of the upper thorax as well. Still later 
the lower extremities become involved. Often portions of the latissimus dorsi, 
the trapezius, the triceps, the pectoralis major, or other muscles escape. When the 
cervical muscles fail the head cannot be held erect, and when the costal muscles 
are atrophied the act of respiration may be solely diaphragmatic. Finally, symp- 
toms of bulbar paralysis may ensue. 

In that type in which the disease first affects the lumbosacral portion of the cord 
the peroneal muscles in one leg undergo paralysis and wasting. This condition 
then develops in the muscles of the other leg. A little later the anterior tibial 
muscles are affected, first on one side and then on the other. At this time there is 
"drop-foot" and the patient has to use his thigh muscles to raise the leg so that 
the toes will not strike obstructions and cause stumbling. As the pathological 
process in the cord advances the adductor muscles in the thighs and the gluteal 
muscles are paralyzed. 

In still another type, sometimes called "Duchenne's type of ascending paralysis," 
the paralysis and wasting extend upward from the legs and speedily affect the 
muscles of the trunk, the arms, the forearms, and the hands so that an almost total 
paralysis ensues and death comes from involvement of the centres in the medulla 
or by reason of some intercurrent disease such as pneumonia. Sensation is not 
disturbed, but in a few cases a sense of discomfort may be complained of in the 
legs. The reaction of degeneration develops quite early in the affected parts and 
finally response to electrical stimulation is completely lost. The muscles present 
fibrillary contractions both spontaneously and if irritated, but the bladder and 
rectum are not paralyzed and sexual power is preserved. The paralysis is due to 
the wasting. The reflexes are diminished or lost in the affected muscles. 

Diagnosis. — It is important to remember that chronic muscular atrophy may 
arise from other diseases than chronic anterior poliomyelitis, such as amyotrophic 
Lateral sclerosis, the muscular dystrophies, peripheral neuritis, and syringomyelia. 

From amyotrophic lateral sclerosis (which see) it is distinguished by the absence 
of spastic symptoms and lack of the exaggerated knee-jerk and of Babinski's reflex. 

From muscular dystrophy by the absence of fibrillary tremor and of the reaction 



BULBAR PARALYSIS 835 

of degeneration in the latter condition, and by the fact that the spinal form is a 
disease of adult life. From syringomyelia this condition is separated by the absence 
of the dissociated anesthesia and of trophic lesions in the skin. 

In neuritis the distribution of the paralysis is usually symmetrical; whereas, 
in chronic poliomyelitis the paralyzed parts are irregularly distributed. Unless 
the neuritis be purely motor in character there are sensory disturbances and tender- 
ness on pressure over the nerve trunks and in the bellies of the muscles. Moreover, 
in neuritis there is commonly a toxic or infection cause recognizable. 

The Charcot-Marie-Tooth type of muscular atrophy may be confused with 
certain forms of progressive muscular atrophy. The first of these, however, is a 
disease of early life, and the paralysis in the legs does not extend above the knees 
or above the elbows, as a rule. Further, sensation is usually disturbed or impaired 
in the Charcot-Marie-Tooth type and preserved in this chronic muscular atrophy. 

Prognosis. — The prognosis is grave. The future of the case can be determined 
somewhat by the rapidity of the development of the symptoms, for in the rapidly 
advancing cases the outlook is of course worse than in others. When the symptoms 
follow injury to the spine the prognosis is better than in the idiopathic cases. 

Treatment. — The rapid type of cases should be treated as we treat acute polio- 
myelitis. The chronic forms should be cared for in a manner practically identical 
with that of the advanced stages of acute poliomyelitis. The treatment, therefore, 
consists in hygienic surroundings, nutritious food, and an abundance of fresh air 
and sunshine. Care should be taken that the paralyzed muscles are not exhausted 
by too much rubbing or exercise. Strychnine may be given in moderate doses 
three times a day for several weeks at a time. Fowler's solution, in moderate 
dose, is also useful as a tonic. Therapeutic measures, however, cannot promise 
much in this disease. 

BULBAR PARALYSIS. 

Bulbar paralysis is a term applied to a group of symptoms referable to lesions 
of cranial nerve nuclei in the medulla oblongata or "bulb," which affect the tongue, 
lips, and larynx in peculiar association, so that the condition is called "glosso- 
labio-laryngeal paralysis." The lesions may implicate the cranial nerve nuclei 
in the pons and cms, and the gray matter of the spinal cord, but atrophy of the 
tongue and lips is the main feature of the disease which is centred in the medulla. 

Etiology. — The cause of this rare disease is unknown. It occurs most frequently 
between the thirtieth and fiftieth years. 

Pathology and Morbid Anatomy. — The lesions of this malady consist in degenera- 
tive changes in the nuclei of the motor nerves which supply the tongue, lips, larynx, 
and pharynx. As the disease advances, additional nuclei of the cranial nerves 
become involved so that the pneumogastric, the facial, the motor fibres of the 
trifacial, and more rarely the abducens and oculomotor nerves are affected. Occa- 
sionally, it occurs as part of amyotrophic lateral sclerosis. If the reader has a 
clear conception of the pathology of chronic anterior poliomyelitis he will understand 
the pathology of this affection as well. 

Symptoms. — The symptoms of chronic bulbar paralysis usually begin with 
difficulty in moving the tongue in speech so that the patient is unable to use easily 
letters like v, n, r, f, and I. The speech becomes nasal, swallowing becomes difficult, 
and when the muscles of the lips become affected labial sounds become imperfect, 
letters like b and p being difficult to pronounce. When the laryngeal muscles 
become paralyzed speech is lost completely. Chewing becomes difficult, owing to 
the paralysis of the tongue and lips. There is difficulty in swalloiving, and the food 
not infrequently finds its way into the larynx, from which it may descend and cause 
septic pneumonia. Owing to the paralysis of the facial nerves, the expression of 
the lower portion of the face becomes altered, the lips sag, and saliva may flow over 



836 DISEASES OF THE NERVOUS SYSTEM 

the chin. Fibrillary contractions of the affected muscles also occur, and the tongue 
lies relaxed and powerless in the floor of the mouth. 

Diagnosis. — True bulbar paralysis must be separated from that still more rare 
affection known as myasthenia gravis. In this condition the general muscular 
system also suffers from feebleness, but degeneration does not take place in the 
affected muscles, and they do not undergo material wasting. Furthermore, the 
condition in myasthenia gravis is often characterized by periods of remission or 
partial recovery. Autopsy in those cases of myasthenia gravis which have come to 
a fatal termination has always failed to reveal the lesions which have been described 
as characteristic of true bulbar paralysis. 

Prognosis. — This form of paralysis is invariably fatal. 

Treatment. — The treatment of bulbar paralysis consists in the administration 
of tonics, and in an endeavor to maintain the patient's general health at the best 
possible level. Do what we will, the disease cannot be affected by any plan of 
treatment yet devised. 

LATERAL SCLEROSIS. 

Definition. — Lateral sclerosis, also called "spastic paraplegia," is a condition 
in which the patient suffers from stiffness or spasticity of the muscles of the lower 
extremities, with loss of power which ultimately amounts to distinct paralysis. 
The condition is characterized by great reflex irritability. There are no sensory 
disturbances nor sphincteric symptoms. 

History. — Ttirck described sclerosis of the lateral columns of the cord in 1856, 
and Charcot made further contributions as to the symptoms in 1865. Seguin 
described it still further in 1873 as "tetanoid paraplegia," an excellent term, but 
it remained for Erb in 1875 and 1877 to make a full exposition of the disease. 

Etiology. — In many cases the cause of lateral sclerosis cannot be discovered. 
Syphilis may be a cause, or, to speak more correctly, the malady may be a sequel 
of syphilis. In some instances injuries to the back are followed by these symptoms. 
In one case in my experience a horse reared and fell backward on his rider, who at 
once found his legs paraplegic. This passed away in a few moments, but after a 
few months lateral sclerosis gradually developed. In another case under my care 
a man stood in very cold water washing sheep, and dated the beginning of his 
malady to that exposure. In both of these cases, however, it is quite probable 
that a pachymeningitis or a hemorrhage into the cord or a myelitis wa^ the cause 
of the symptoms rather than a true primary lateral sclerosis. In other cases 
prolonged marches have seemed to produce it. It is a disease of the third and fourth 
decades of life. In some instances the disease seems to depend upon an hereditary 
defect in the lateral columns of the cord (Strumpell's family type of lateral sclerosis) . 

Pathology and Morbid Anatomy. — The lesions of lateral sclerosis are clear and 
definite. As the name of the disease implies, they are situated in the lateral or 
crossed pyramidal tracts of the spinal cord, and they develop chiefly in their lower 
portions in the early stages of the disease. The axones progressively atrophy 
from below upward, and this is associated with disappearance of the myelin and an 
overgrowth of the connective tissue. 

When the disease invades the cervical region the anteromedian columns of the 
cord may he affected as well. 

Symptoms. — In studying the symptoms of primary lateral sclerosis it must not 
be forgotten that they may be simulated by secondary lateral sclerosis following 
lesions higher up in the cerebrospinal system. Thus, it is a well-known fact that a 
large number of lesions in the brain or cord may result in degenerative changes in 
these motor pathways, and so cause spastic paraplegia. Those in the brain are 
hemorrhage, abscess, tumor, and softening, which, affecting the motor cortex 
or the motor pathways, induce a descending degeneration in the pyramidal tracts. 



LATERAL SCLEROSIS 837 

In these cases the symptoms are usually limited to one side, but in the cerebral 
palsies of childhood the lesions are often bilateral. (See Infantile Cerebral Palsy.) 
Any lesion in the spinal cord which cuts off the fibres in the lateral tracts from 
their trophic cells in the brain, also results in lateral sclerosis. Thus, a transverse 
myelitis, disseminated sclerosis, hemorrhage into the cord, and syringomyelia may 
so result. Lateral sclerosis is not rarely a part of the pathology of paresis. Lesions 
outside the cord, such as tumors, disease of the spinal column, or thickening of the 
membranes may sometimes cause these symptoms. 

The symptoms upon which we base the diagnosis of lateral sclerosis are the 
peculiar spastic contractions of the muscles of the legs, so that they are in a state of 
extension as soon as the patient attempts to move them. The attitude of the legs 
is that of a person with ankylosis of both knees, and the foot is apt to be extended. 
When the patient walks he has difficulty in bending the knees and the ankles, and 
still greater difficulty in raising the toes as the foot is brought forward for another 
step. For this reason he is prone to trip over small obstructions and to have bad 
falls, because his muscles are so stiff that he cannot catch himself as he loses his 
balance. The stress and strain of walking are therefore very great, and the muscles 
may become so fatigued that they ache, but this is the only sensory symptom. 
Crossing the legs when sitting becomes impossible, and if the patient is recumbent 
the knees may be approximated owing to the greater -strength of the adductor 
muscles. This adduction of the knees also interferes with walking. If the patient's 
muscles are grasped they are found to be hard and tense. On further physical 
examination it will be found that the reflexes are all increased. Ankle clonus is 
marked, and the Babinski reflex is soon manifested. The reactions of degeneration 
do not appear and the muscles do not atrophy until the disease has lasted several 
years, when they may waste from disuse. 

Finally, when the malady has continued for a very great length of time the 
position of the lower extremities in stiff extension may be changed to that of con- 
tracture so that they are sharply flexed at the knees and fixed in this position. 

The upper extremities nearly always escape, but in the rare instances in which 
they are involved the extensor muscles suffer first and suffer most. 

Diagnosis. — As already pointed out, the diagnosis of this disease should not be 
made till the causes capable of producing secondary lateral sclerosis are excluded. 
Occasionally hysteria may produce symptoms very like it. A typical picture of 
such a case will be found in my book on Diagnosis in the Office and at the Bedside. 
In such an instance the sex of the patient and the other signs of hysteria should be 
carefully considered before a diagnosis of lateral sclerosis is made. When spastic 
paraplegia is combined with muscular atrophy the condition is one of amyotrophic 
lateral sclerosis (which see). 

Prognosis. — This is bad as to recovery, but its unfavorable character is modified 
by the fact that the progress is usually very slow. Often the disease lasts twenty- 
five years or more. I have a case now under my care which I have observed for 
thirty years. 

Treatment. — Unfortunately the results which may be obtained from the treat- 
ment of lateral sclerosis are not brilliant. The suggestion that mix vomica or 
strychnine be employed does not seem to be based on very rational views of the 
physiological action of this drug. Excitation of the motor tracts of the spinal 
cord is already present, and strychnine rather tends to increase this condition 
and to exaggerate the spastic condition of the lower extremities. In some instances 
full doses of the extract of conium are advantageous. In others large doses of 
chloral or one of the bromides may be employed. The gentle forms of massage 
may also relieve the sensation of tension and aching in the limbs. Care should 
be taken that the patient does not walk far enough to exhaust himself. In some 
instances a hot pack will give relief, particularly if it is taken at bedtime, although 



838 DISEASES OF THE NERVOUS SYSTEM 

of course it exercises no curative influence upon the progress of the disease. Elec- 
tricity is useless. 

Syphilitic Spastic Spinal Paralysis. — Under the name of syphilitic spastic spinal 
paralysis Erb has described a form of lateral sclerosis developing within five years 
of the primary sore, but differing from ordinary lateral sclerosis by the presence of 
some lack of rectal and vesical control and mild disorders of sensation. This 
so-called syphilitic spinal spastic paralysis of Erb is due to a specific endarteritis, 
which produces embolism or thrombosis of the vessels of the spinal cord and a true 
myelomalacia, although some clinicians have considered it a meningomyelitis. 

AMYOTROPHIC LATERAL SCLEROSIS. 

Definition. — Amyotrophic lateral sclerosis is a progressive form of chronic spinal 
paralysis characterized by advancing musuclar atrophy associated with spastic 
paraplegia, or, in other words, the symptoms of lateral sclerosis are present. 
Although the symptoms are largely spinal, modern research has shown that the 
motor pathway is affected throughout in advanced cases, from the beginning of its 
upper segment in the motor cortex to the endings of the lower segment in the 
peripheral nerves. The cardinal symptoms depend, however, upon degeneration 
of the contiguous parts of these segments, namely, the pyramidal tracts and the 
anterior horns of the gray matter; and the disease may be regarded as a combination 
of lateral sclerosis with chronic poliomyelitis. Not rarely the disease invades the 
medulla, and symptoms of progressive bulbar paralysis are added to the clinical 
picture. 

Etiology. — Amyotrophic lateral sclerosis is usually met with in persons between 
thirty and fifty years of age. In some instances there is a history of exposure to 
cold or of violent exertion. In still others, it is found that the patient has been an 
artisan employed in the handling of such metallic poisons as mercury, lead, or 
arsenic, or that he has been addicted to the excessive use of alcohol. In some 
instances, too, the disease has apparently followed severe injuries, but in no instance 
has it been proved that there is actual relationship between any of these causes 
and the development of the disease. In all probability, these factors only become 
active in those cases in which there is a defective development in the central nervous 
system, which renders its motor elements peculiarly susceptible to damage or 
disease. 

Pathology. — The pathological conditions in amyotrophic lateral sclerosis may 
be considered in three parts. The first and most important is the advancing 
atrophy which involves the motor neurones in the anterior horns of the gray matter 
of the spinal cord. Indeed, the condition is very similar to that which occurs in 
chronic anterior poliomyelitis or even identical with it. As a rule, the alterations 
take place chiefly in the cervical portions of the cord, but in some instances, par- 
ticularly if the disease lasts a long time, the anterior portion of the gray matter 
in the lumbar region is also affected. Similar atrophic changes take place in the 
motor nuclei of the cranial nerves in the pons and medulla. Next in importance 
to these alterations in the trophic portions of the spinal cord is the atrophy and 
degeneration of the fibres in the lateral columns and the anterior median columns. 
These changes extend to the motor cells of the brain and are not limited to the 
lateral columns, the cortex being involved secondarily by "retrograde" degeneration 
from the cord and medulla upward through the pons, crura, capsule, and corona 
radiata. In other words, the degeneration does not begin in the motor cortex, 
but in the spinal cord. Following the wasting of the nervous elements of the spinal 
cord, there is an overgrowth of connective tissue which not only involves the lateral 
columns and the anterior median columns, but also the association fibres which are 
closely connected with the anterior horns of the gray matter. 



AMYOTROPHIC LATERAL SCLEROSIS 839 

Symptoms. — The symptoms of amyotrophic lateral sclerosis are quite character- 
istic, and depend in their development to some extent upon the portion of the 
nervous system which is first affected by the disease. In those instances in which the 
, lesion first affects the cervical portion of the cord and the anterior horns of the gray 
matter the arms are first affected. These extremities manifest some stiffness in 
the muscles, and their reflex excitability is increased. Almost simultaneously with 
these symptoms there is wasting of the muscles of one or both hands, with associated 
loss of power. From the hand the paralysis extends to the forearms, or it passes 
directly to the muscles of the shoulder and affects those of the forearms afterward. 
Fibrillary contractions develop very early, occur spontaneously, and may be pro- 
duced by tapping the muscles or by exposing them to cold. The fingers are often 
in semi-flexion, and if the physician endeavors to straighten them, it is found that 
the muscles are rigid and resistant, even though the patient has lost power in 
them. 

When the disease develops chiefly in the pyramidal tracts of the motor columns 
of the cord, the evidences of spastic paralysis are the first things to impress them- 
selves upon the observer, and it may be impossible in the early stages of the disease 
to separate the malady from ordinary lateral sclerosis, since the legs are stiff and 
move with difficulty, the knee-jerks are exaggerated, and ankle clonus and the Babin- 
ski reflex are usually present. When the patient walks the toe is dragged along 
the ground, the whole leg is stiff, and one foot is often placed awkwardly in front 
of the other, through the contraction of the adductor muscles. By far the most 
common clinical picture is for the wasting to be confined to the upper extremities, 
and the spasticity to be manifest chiefly in the lower extremities. 

Whether the disease first begins in the arms or in the legs, it is worthy of remem- 
brance that it is often very much more marked upon one side than upon the other. 

As the disease advances it sometimes happens that evidences of bulbar paralysis 
develop, the speech becoming affected, as in ordinary bulbar paralysis. Swallowing 
may also become difficult. Owing to paralysis of the uvula and palate, choking 
often takes place, and fluids when taken into the mouth escape through the nose. 
Indeed, all the symptoms of bulbar paralysis may be present, and inequality of the 
pupils may be noted. When contractures occur the hands may become greatly 
deformed, and the feet may be distorted into any of the forms of talipes. 

In the advanced forms of the disease the muscles of the trunk and neck become 
atrophied, so that it is impossible for the patient to sit up, and the head falls to 
either side or forward. The muscles develop the reactions of degeneration and lose 
their electrical excitability. There is no loss of intelligence, but sometimes in 
advanced cases a mild dementia appears. When the bulbar symptoms are marked, 
palpitation of the heart is often present. 

Diagnosis. — From bulbar paralysis amyotrophic lateral sclerosis is separated 
by the fact that lateral sclerosis presents marked spinal symptoms with paralysis 
of the upper extremities and spastic paraplegia of the lower extremities. If in a 
case of supposed bulbar paralysis these symptoms develop later it proves that the 
bulbar palsy has been due to the oncoming of amyotrophic lateral sclerosis. If the 
symptoms are due to the presence of a meningitis in the cervical portion of the cord, 
there is stiffness and loss of power in the arms, and there will also be pain of a 
severe character. So, too, injury or pressure upon the spinal cord in the dorsal 
and lumbar regions, producing a spastic paraplegia, will also produce sensory 
disturbances and involve the functions of the bladder and rectum. 

From syringomyelia amyotrophic lateral sclerosis is separated by the presence 
in the former of analgesia and the rapid trophic changes which take place not 
only in the muscles, but in the bones, the skin, and its appendanges. In many 
instances it is almost impossible to differentiate between amyotrophic lateral 
sclerosis and ordinary lateral sclerosis, and it is only by the development of the 



840 DISEASES OF THE NERVOUS SYSTEM 

symptoms which arise from involvement of the gray matter of the cervical portion 
of the spinal cord and the medulla that the separation can be made. 

Prognosis. — The prognosis in a case of amyotrophic lateral sclerosis is absolutely 
unfavorable so far as recovery is concerned. The duration of life depends upon 
the rapidity with which the vital centres in the medulla become involved. In 
some instances death comes within two years after the onset of the malady, whereas 
in others it lasts for a decade or even longer. The prolonged cases are usually 
those in which the involvement of the lateral columns seems to be the first stage 
of the disease. As a rule, death does not occur as the direct result of the disease, 
but from complications which are produced by it; as, for example, the inhalation 
of partciles of food into the respiratory passages because of the bulbar paralysis. 
Rarely there is heart failure due to involvement of the cardiac centres. 

Treatment. — There is no form of treatment which can be considered curative. 
Gentle massage and the use of electricity, with the hope that the wasting of the 
muscles may be diminished, has been tried by some clinicians, but it is manifest 
that this plan of treatment must be used with great caution, since if the trophic 
centres are destroyed, the muscles must necessarily undergo wasting more rapidly 
if they are exercised than if they are not used. If bulbar symptoms are present 
the patient should be fed by means of a stomach-tube. The employment of 
nervous stimulants, such as strychnine, is inadvisable, because it exaggerates the 
spastic condition of the lower extremities. 

MYELITIS. 

Definition. — Myelitis is a term which at one time was loosely applied to all 
inflammatory processes in the spinal cord. Its application is becoming limited as 
our conception of the diseases in this part of the body becomes more definite, but 
it is still used to describe an inflammatory process in the cord, which is general 
or widely diffused or disseminated. A myelitis may be acute, subacute, or chronic. 
If it extends across a given segment of the cord it is called a "transverse myelitis ;" 
if it is distributed in several foci through the cord, it is called " disseminated mye- 
litis," and if it extends upward or downward, it is called an " ascending or descending 
myelitis." 

The term "acute myelitis" is applied to those cases of sudden onset taking but 
a fortnight to develop. The term subacute is applied to those which consume from 
two to six weeks in onset, and the term chronic to those which develop so slowly 
that a longer time elapses before the disease is marked. 

When the gray matter of the spinal cord is affected, it is called "poliomyelitis," 
from the Greek word tto^oc, meaning gray. 

When the brain and cord are involved it is called "encephalomyelitis," and 
when the gray matter about the central canal in the cord is affected it is called 
a "central myelitis." 

Acute and Subacute Myelitis. — Etiology. — The chief cause of this condition 
is without doubt an intoxication, due to the action of toxins developed during the 
course of acute infectious diseases. At one time it was thought that exposure, 
sexual excess, and severe toil were causes, but we now know that at the most they 
are but predisposing factors in that they diminish vital resistance. In addition 
to the ordinary infectious fevers, myelitis may be caused by gonorrhea and malaria. 
Occasionally severe vesical infection produces acute myelitis. Myelitis has also 
been said to follow concussion of the spine and other injuries, but they probably 
act solely as predisposing agencies. 

Pathology and Morbid Anatomy. — If we take transverse myelitis as a type of 
the various forms of this disease, we will find on opening the spinal cord that the 
pia mater at the level of the lesion is hyperemic and reddened. The cord is also 



MYELITIS 841 

reddened and somewhat swollen, and its bloodvessels engorged. On section of 
the cord the lines of demarcation between the white and gray matter are to a great 
degree obliterated. The cord is softened and its texture may be actually diffluent, 
this very soft state being, however, at least in part a postmortem change. If this 
part of the cord is placed under the microscope it is seen to be filled with granular 
cells, the bloodvessels are surrounded by extravasated leukocytes, and bacteria 
may be found. Small extravasations of blood into the tissue of the cord may be 
present from rupture of the vessels. The nerve cells are found to have undergone 
granular degeneration, and their axones and dendrites have also been destroyed. 
The axis cylinder of the nerve fibres is greatly swollen and has evidently undergone 
segmentation. Fatty degeneration of the myelin is found. The connective-tissue 
cells are swollen, and if any time has elapsed, an overgrowth of the neuroglia is 
present. 

For a clear understanding of the cause of the symptoms met with in acute myelitis, 
myelomalacia, and chronic myelitis it must be remembered that the presence of a 
lesion in the spinal cord in the motor tracts produces a descending degeneration 
in that tract, because the nerve fibre is cut off from its nerve cell or neurone. If 
the lesion be in the sensory tracts the degeneration is ascending. The ultimate 
symptoms, therefore, consist not only in those which arise from the primary focus 
or lesion, but in those which develop as the result of those secondary changes. 
These changes are demonstrable within a few days after the injury, and rapidly 
progress so that at the end of three weeks the degeneration of the affected fibres 
is at its height. The overgrowth of the connective tissue is not marked until a 
later period. Thus, we find that the chief degenerative change below the lesion 
is in the anterior and lateral pyramidal tracts, and above the lesion in the dorsal 
columns of Goll and Burdach, in the direct cerebellar tracts, and in the columns of 
Gow^ers. In addition to these chief secondary changes, there is also, for a short 
distance below the primary lesion, descending degeneration in the anterior and 
anterolateral columns, and in certain small "fields" of the dorsal columns (oval 
field of Flechsig, etc.), which contain the so-called association fibres. 

The ascending degeneration which takes place after a transverse lesion affects 
chiefly Goll's and Gowers' columns, and the higher the primary lesion the greater 
the degree of the degenerative process. The column of Burdach, on the other 
hand, while markedly degenerated near the site of the lesion, is less and less affected 
higher up in the cord. 

Symptoms. — The symptoms of myelitis vary somewhat with the portion of the 
cord which is affected and with the extent of the pathological process. 

When there is a transverse myelitis of the dorsal portion of the spinal cord the 
symptoms on the stage of onset consist in wretchedness and moderate fever. There 
may be pain in the back and numbness and tingling in the lower extremities. Tivitch- 
ings or cramp-like contractions of the muscles in the legs may occur, and, very rarely 
in adults, a convulsion may develop. Sometimes, however, these prodromata 
are absent, and the first symptom complained of is loss of power in the lower limbs, 
which speedily develops into a complete paraplegia. Paraplegia may become 
complete in a few minutes or a few hours. In other instances of the subacute 
type the onset is so slow that days and even weeks may elapse before the loss of 
power is complete. 

The paraplegia arising from a transverse myelitis in the dorsal region is usually 
spastic, and the deep reflexes are increased. The legs are outstretched, as in ordinary 
paraplegia, unless degenerative or irritative lesions arise in the lateral pyramidal 
tracts below the site of the transverse lesion, when they may become flexed by the 
spastic state of the muscles of the thighs. In other instances these muscles suffer 
from twitchings and temporary contractions, which may be strong enough to prevent 
the examiner from eliciting any signs of exaggeration of the deep reflexes. There 



842 DISEASES OF THE NERVOUS SYSTEM 

is always paralysis of the bladder and rectum in transverse myelitis, and retention 
or incontinence of urine and feces may be present. Partly because of pressure and 
unavoidable uncleanliness, but chiefly because of trophic disorders and abnormal 
blood supply, bed-sores are prone to develop on the sacrum and buttocks. The 
muscles in the legs do not rapidly atrophy, because they receive trophic impulses 
from the cells in the anterior cornua of a lower level of the cord than that of the 
lesions. The skin of the legs and of the body below the level of the lesion is anesthetic 
to all forms of irritation, and at the upper margin of this anesthetic area there is a 
girdle sensation, and, it may be, a band of hyperesthesia. 

When the myelitis affects the lumbar cord the paraplegia is not only absolute 
as to voluntary movement, but as to reflex action as well, all reflexes being lost. 
A similar condition also occurs in some cases when the injury is at a higher level, 
provided that the cord is completely severed or the injury so severe that severance 
is practically complete. 

If the lesion is in the cervical cord the arms are not only paralyzed, but undergo 
atrophy and are flaccid, the legs suffer from a spastic paraplegia, and the arms, 
legs, and body are anesthetic. There may also be dilatation or contraction of the 
pupils. If the lesion is high up in the cervical area, then the paralysis of the arms 
may be spastic instead of flaccid, and they do not undergo atrophy. In such a 
case respiration is very difficult, because of the loss of power in the diaphragm and 
in the other respiratory muscles. 

Prognosis. — While it is a fact that the prognosis in transverse myelitis is always 
grave, it is also a fact that partial recovery sometimes takes place. Thus, 
Oppenheim states that that form following gonorrhea always gets better under good 
treatment, and that that form due to the acute infectious fevers has good chances 
for recovery. On the other hand the outlook in syphilitic cases is not good, and 
in septicemia, tuberculosis, or puerperal sepsis it is bad. Again, the prognosis 
varies with the severity of the symptoms and the lesion, for manifestly it must be 
worse in complete transverse myelitis than in that form in which the destruction 
of the cord is not so complete. The cause of death is usually bed-sores, with 
exhaustion and septic cystitis. 

Treatment. — An understanding of the lesions of this disease makes it evident 
that treatment of a curative nature is useless. Careful feeding with easily digested 
food, the maintenance of perfect cleanliness in the parts pressed upon in the dorsal 
position, and the cautious use of the catheter should be resorted to. Hyoscine 
may be given to stop the annoying twitchings of the muscles. 

Chronic Myelitis. — Definition and Etiology. — Chronic myelitis is, as its name 
implies, a chronic form of inflammatory process in the cord which develops as a 
result of a large number of causes. Not only may the causes of acute myelitis 
set up a process which may become slow and chronic in its progression, but other 
factors may produce it, of which the most important are impairment of its blood 
supply resulting from degenerative changes in the bloodvessels from atheroma or 
syphilitic arteritis. Chronic myelitis may also arise as a result of pernicious anemia. 
In some cases, too, the primary cause lies in a meningitis of the membrane surround- 
ing the cord, whether this meningitis be due to an infection or to injury followed 
by infection. When syphilis is the cause, it not rarely happens that the inflam- 
matory process is limited to one or more parts of the spinal cord, so that the symp- 
toms of spastic paraplegia due to disease of the lateral pyramidal tracts develops, 
or in other instances the symptoms of locomotor ataxia are present, because the 
posterior tracts in the cord are affected. Rarely but one side of the cord may be 
affected, producing a crossed paralysis of motion and sensation (Brown-Sequard 
syndrome). 

Finally, the physician must recall the fact that most of the forms of chronic 
disease of the spinal cord, such as disseminated sclerosis, amyotrophic lateral 



MYELITIS 843 

sclerosis, and the various forms of poliomyelitis, may, in their advanced stages, 
resemble what has been called chronic myelitis. Indeed, it is so rare to meet 
with a case of chronic myelitis which cannot be placed under one of these headings 
that many neurologists are inclined to deny the existence of chronic myelitis as a 
separate malady. (See below.) 

Pathology and Morbid Anatomy. — The changes in the spinal cord which are found 
in cases of so-called chronic myelitis are not so manifest as in the acute form when 
the cord is studied by the naked eye. In one class of cases the appearance is 
quite like that of disseminated sclerosis in that areas of overgrowth of connective 
tissue are found in both the white and gray matter of the cord. This overgrowth 
of the neuroglia is situated chiefly around the bloodvessels, the walls of which are 
also thickened and their lumen narrowed. When as a result of the degenerative 
process an axis cylinder has become distended or swollen, a small cavity is formed, 
and if many of these are present they may give the section of the cord a cribriform 
appearance. The pia mater is often found adherent to the cord. 

In the other type of case a microscopic study of the cord reveals changes which 
are evidently the result of the several diseases of the cord already named, and 
which are really the cause of the symptoms presented by the patient rather than 
that a true primary chronic myelitis has been present. Thus, it is found that as a 
result of a lesion in the pyramidal tracts, a descending degeneration of the fibres 
in that tract takes place, or if the lesion has been in the posterior columns, an 
ascending degeneration ensues. 

Symptoms. — When the condition of chronic myelitis follows acute myelitis, 
symptoms of that state persist with gradually increasing severity until death by 
exhaustion or some intercurrent malady ensues. If, however, the process is of the 
slow or chronic type from the time of onset, the primary feeling of weariness and 
weakness on exertion passes gradually into a state of paralysis, more or less complete. 
Owing to the degenerative changes in the lateral tracts, the paralysis is usually 
spastic. There is often an exaggeration of the deep reflexes, with ankle clonus and 
Babinski's sign. In other instances the character of the response to reflex stimula- 
tion is entirely dependent upon the portion of the cord which is involved. The 
muscles may gradually waste and give the reactions of degeneration. Not rarely 
the loss of power extends gradually to the trunk and arms. Sensory disturbances 
are common. There may be patches of anesthesia and paresthesia, and occasionally 
moderately severe pains may be felt in the nerves in the extremities. Vasomotor 
disorders in localized areas of the skin may be present, one part being very pallid 
and another hyperemic. Bed-sores finally develop, as in the acute form of the 
disease. 

Diagnosis. — Chronic myelitis as a separate disease is so rare that a diagnosis 
of its presence should be made only after a most careful study of a case. From 
disseminated sclerosis it is separated by the absence of evidence of lesions in the 
brain and lower cephalic centres, such as nystagmus, intention tremor, optic 
atrophy, and scanning speech. From lateral sclerosis it is separated by the absence 
of vesical and rectal paralysis in that disease. Then, too, lateral sclerosis is not 
characterized by loss of sensation. Paralysis due to poliomyelitis is separated 
also by the absence of anesthesia, and the fact that the paralysis of the muscles 
is not, as a rule, so general. 

Prognosis. — Recovery does not occur. Life may be prolonged for years if the 
process is not progressive and no intercurrent disease attacks the enfeebled sufferer. 

Treatment. — This is, of course, concerned entirely with the maintenance of 
good health, with the hope that a terminal infection may not occur. If there is a 
clear history of syphilis, salvarsan, the iodides and mercury may be used, but 
they are rarely of much value in this state. 



844 DISEASES OF THE NERVOUS SYSTEM 

SENILE PARAPLEGIA. 

Under this unsatisfactory clinical title may be described a condition occasionally 
met with in old persons, and probably depending upon impaired blood supply to 
the cord, resulting from degenerative changes in the vessels which are not severe 
enough to result in myelomalacia. 

Symptoms. — The symptoms consist in a moderate degree of loss of power in the 
lower limbs so that it is difficult for the patient to move about. The legs may be 
shuffled along the floor instead of lifted clear of it. There is sometimes an associated 
weakness of the sphincters, especially of the bladder, and minor sensory changes 
have sometimes been noted. When the malady develops rapidly and is severe it 
may be impossible for a time to separate it from true myelitis. 

Treatment. — The treatment consists in rest in bed, massage, and hydrotherapy. 
Internally, the iodides and circulatory stimulants, such as strychnine and digitalis, 
should be used. 

MYELOMALACIA. 

This term is applied to a state of the spinal cord in which it undergoes softening 
because of embolism or thrombosis of its bloodvessels, with the result that its 
blood supply is impaired. The degenerative changes consist in those which we 
would expect to find when necrosis of these parts occurs, namely, extravasated 
red and white blood cells, fat-globules, and broken axones. When the patient 
lives for a considerable length of time after this accident to the circulation occurs, 
a microscopic examination of the cord will reveal an overgrowth of connective 
tissue. The essential difference between this state and one of acute myelitis is 
that in this condition the process is necrotic; whereas, in the latter it is primarily 
inflammatory, and diapedesis of white and red cells takes place as a part of a vital 
process. 

SYRINGOMYELIA. 

Definition. — Syringomyelia is a condition of the spinal cord characterized by the 
formation of a cavity or cavities in its substance; by loss of pain sense and tempera- 
ture sense, with preservation of tactile sense; by the development of progressive 
muscular atrophy and paralysis, and by nutritional changes in the skin, muscles, 
bones, and joints. 

History. — Although a very rare disease, it was described before many other 
very common maladies, the state of the spinal cord having been first noted in 
1546 by Etienne and given its name by Ollivier in 1824. We are, however, able 
to diagnosticate the affection by reason of researches of Schultze and other later 
investigators. 

Etiology. — This is unknown. In some cases it is probably dependent upon a 
congenital defect. In other instances it has been thought to be due to disease of 
the spinal arteries, and in some cases Van Gieson has shown that it has developed 
from a perforating hemorrhage into the cord itself. Westphal, Oppenheim and 
others, believe that trauma plays an important role in the development of syringo- 
myelia. 

Pathology and Morbid Anatomy. — When the spinal cord in a case of syringomyelia 
is examined maeroscopicaliy, the membranes are found to be normal, but the 
surface of the cord may be irregular and portions of it protrude, while at other 
places retraction of its surface seems to be present. A closer examination of the 
areas of bulging may reveal fluctuation, and from such areas, if they be punctured, 
a clear serous fluid may run quite freely. This cystic state may extend very 
considerable distances up and down the cord, and may extend so far transversely 
as almost to cut the cord in two. The cavity is usually largest in the cervical and 



SYRINGOMYELIA 845 

upper dorsal regions of the cord, but it may be confined to the lower part of the 
cord. On the other hand, as just stated, it may extend from the end of the cord 
even to the pons. The cavity may have large dimensions as to length and be so 
wide as to convert the cord into a thin-walled tube. 

It is because of these extraordinary changes that the Greek words syrinx, a 
tube, and myelon, marrow of the spine, are applied to it. So complete may be the 
excavating process that when the cord is severed from the medulla the fluid may 
escape and the cord flatten out like a ribbon. In some cases there are several 
cavities superimposed. On cross-section the cavity is usually found to be just 
back of the central canal in the gray commissure and in the posterior cornua, or 
it may be present where the central canal should be. Occasionally it affects the 
anterior horns or the lateral or posterior white columns. 

The wall of the cavity consists in a well-developed mass of neuroglia (gliomatosis), 
which in its growth encroaches upon surrounding tissues and may cause definite 
symptoms before its centre becomes broken down. Some neurologists, on that 
account, prefer to call this disease, at least in its earliest stages, spinal gliomatosis, 
or gliosis. 

The loss of pain sense and temperature sense which is so characteristic has been 
ascribed to pressure by the neuroglia mass upon the fibres conducting these sensa- 
tions as they cross in the central gray matter on their way to the lateral region of 
the cord. This is at least a good working hypothesis. 

Around the margin of the connective-tissue boundary just described there is 
usually an abnormal development of bloodvessels which are numerous, distorted, 
and larger than normal. 

Dilatation of the central canal by serous fluid is called hydromyelia, and is 
ordinarily associated with hydrocephalus. 

Symptoms. — The symptoms of syringomyelia consist in loss of pain sense and 
of temperature sense, so that the patient may be cut or burnt without feeling pain, 
although his sense of touch in the affected part is still preserved. In some cases 
the temperature sense may be preserved, or the sense of heat is lost and that of 
cold preserved, or vice versa. The areas in which the loss of pain sense exists are 
not symmetrical, but are irregularly distributed over the body. The fact that 
the lesion usually affects the cervical portion of the cord explains why it is that the 
areas of analgesia are usually found in the upper extremities. Associated with 
this impairment of pain sense there develop, as the disease advances, nutritional 
changes in the bones, muscles, and skin, and a progressive paralysis due to the 
muscle changes. 

The outward evidences of trophic disturbance are usually first noticed in connec- 
tion with some injury which fails to heal and, becoming infected, forces a recognition 
of its presence upon the patient, not by pain, but by his observation with his eyes 
that healing does not take place. In some instances, however, nutritional changes 
occur without any history of injury. Felons may develop. When they are accom- 
panied by severe necrosis the condition is usually called "Morvan's disease/' 
In still other cases the finger-nails become deformed, or superficial gangrene of the 
skin develops. The shoulder-, elbow-, and wrist-joints become swollen, filled with 
fluid, and absorption of the articulating surfaces takes place, the condition in the 
upper extremities in this disease being practically identical with that seen in the 
joints of the lower extremities in certain cases of locomotor ataxia. 

The shafts of the long bones often suffer fracture, but these fractures are painless 
and only enforce attention because of the incapacity produced. Painless disloca- 
tions may be caused by insignificant traumata. Curvature of the spine may also 
occur, due to muscular atrophy, and perhaps to changes in the vertebrae. Secondary 
contractures may take place and produce great deformity of the hands, which, added 
to the progressive muscular atrophy and the paralysis, impairs the use of the upper 



846 DISEASES OF THE NERVOUS SYSTEM 

extremities very much. In addition to these symptoms several special symptoms, 
dependent upon the site of the lesion, must be considered. Thus, if the lower 
part of the spinal cord is affected there may be vesical or rectal paralysis; whereas, 
if the upper cervical cord is affected there may be unilateral retraction of the eyeball, 
narrowing of the palpebral opening, and a slow pupillary reaction because of involve- 
ment of the spinal centre of the cervical sympathetic. When anesthesia is found 
on the face it is ascribed to implication of the spinal root of the fifth nerve in the 
cervical region. 

Diagnosis. — As already stated, the loss of pain sense with preservation of tactile 
sense, the trophic changes, and the muscular atrophy all form a picture which 
reveals syringomyelia. Before all these symptoms develop the presence of a 
slowly increasing muscular atrophy may mislead the physician into the diagnosis 
of chronic poliomyelitis or progressive muscular atrophy. Indeed, in its commonest 
type, syringomyelia presents the picture of progressive muscular atrophy when 
it is advanced, including the "claw-hand." Less frequently the white columns 
of the cord are pressed upon by the central mass and symptoms of locomotor 
ataxia or of lateral sclerosis are found. The true condition is recognized by the 
dissociated anesthesia already described. Tumor in the cord usually produces 
so much pressure that the symptoms of paraplegia are more marked than in syringo- 
myelia, and a tumor is usually associated with severe pain. The dactylitis of 
syringomyelia bears a resemblance to leprosy, which, however, does not reveal the 
more general signs of disease in the cord. 

Prognosis. — The chance of recovery is of course nil, but as the disease progresses 
very slowly indeed, life may be prolonged for years. 

Treatment. — There is no treatment for syringomyelia. The affected extremities 
should be carefully protected from injury. 

HEMORRHAGE INTO THE SPINAL CORD. 

Definition and Etiology. — Spontaneous hemorrhage into the spinal cord is a very 
rare accident, so rare that some writers have denied its existence except when it 
has arisen from a direct traumatism. Minute hemorrhages, of course, occur in 
severe forms of acute myelitis. The most common period of life for this accident 
to occur is between the twentieth and fortieth years, but it may occur in infants. 
Hemorrhage due to injury may, of course, develop at any time. Gowers cites a 
case of hemorrhage occurring apparently as the result of repeated sexual intercourse. 
Occasionally hemorrhage into the cord ensues in cases of asphyxia, as in coal-gas 
poisoning, and cases have been reported in which hemophilia produced this lesion. 
The clot is usually found in these cases chiefly in the gray matter of the cord. 
Sometimes it is single; in other instances there are multiple clots. If the escape 
of blood has been copious the blood may perforate the white matter and find its 
way to the pia. 

When the clot is of any size and the cord is examined shortly after the accident, 
changes resembling those due to hemorrhage into the brain are present. The cord 
is softened and infiltrated with small round cells and with red and white corpuscles 
which are seen to be undergoing granular change. The tissues are also stained by 
blood-coloring matter. If the patient lives for some weeks and then at death 
the cord is studied, there is found fatty degeneration of the neighboring tissues or a 
cicatrix of connective tissue which occupies the site of the hemorrhage. Secondary 
descending and ascending degenerations may ensue as in myelitis. 

Symptoms. — The symptoms of hemorrhage into the spinal cord vary, of course, 
with the level at which the lesion takes place. The general symptoms are para- 
plegia with loss of sensation in the paralyzed limbs, and loss of control of the bladder 
and rectum. These symptoms are those of acute myelitis as well. In addition 



HEMORRHAGE INTO THE SPINAL MEMBRANES 847 

quite severe pain may be felt in the spine or be referred to the front of the thorax 
or to the epigastric region, and even to the legs. 

When the hemorrhage is in the cervical cord there is paralysis of the arms as 
well as the legs. The reflexes are usually lost at first because of shock, but soon 
reappear and are usually exaggerated unless the cervical or the lumbar enlargemen 
of the cord is affected, when they are permanently absent in the arms or in the 
legs. Spastic contractions may develop later from descending changes in the crossed 
pyramidal tracts, as in myelitis. The muscles may undergo degenerative changes 
very rapidly because of damage to the cells in the anterior horns of the gray matter 
at the level of the lesion. 

Not rarely, if the hemorrhage has been at all large, a stage of secondary irritation 
and inflammation develops as a result of the extravasation of blood, and this may 
not only greatly increase the gravity of the symptoms, but destroy life. On the 
other hand, it not infrequently happens that the hemorrhage in the gray matter 
may not only destroy this part of the cord, but by pressure abrogate the function 
of the white matter. 

After the acute process is over, the paraplegia is greatly decreased as the pressure 
is decreased, but complete recovery does not ensue because the cord is permanently 
damaged, and so atrophy of the muscles, governed by that part of the gray matter 
which has been damaged, ultimately develops as in acute poliomyelitis. Some 
degree of spasticity persists through loss of fibres in the pyramidal tracts, and 
various sensory defects if the dorsal columns have not completely recovered. 

Diagnosis. — The diagnosis of hemorrhage in the cord is not to be made until the 
symptoms are so well defined that there can be little doubt as to their cause. The 
onset of the symptoms must be sudden, that is, almost instantaneous. If several 
hours are passed in their development it is probably a case of acute myelitis. Pain 
is also an important symptom, for, if it is present, it points to hemorrhage. 

Prognosis. — This depends upon the severity of the symptoms and upon the site 
of the lesion. If it is in the cervical or lumbar enlargements, the prognosis is 
more grave than if it is in the dorsal cord. If bed-sores speedily develop the 
outlook is correspondingly bad not only because their presence shows grave lesions 
in the cord, but also because their existence is a menace to the patient's life. 

Treatment. — Absolute rest in bed is essential. An ice-bag should be kept over 
the spine, and small doses of aconite and the bromides used to allay circulatory 
excitement. The use of ergot in such cases, as commended by Gowers, does not 
seem to be based upon a correct conception of the physiological action of this drug. 
Some time after the hemorrhage the iodides may be used to aid in clearing up the 
inflammatory exudate. 

HEMORRHAGE INTO THE SPINAL MEMBRANES. 

Definition and Etiology. — A hemorrhage about the spinal cord may be outside 
the dura mater (extrameningeal or extradural), or inside the dura mater (intra- 
meningeal). If it is between the dura mater and the arachnoid it is called subdural, 
and if it is between the arachnoid and pia mater it is called subarachnoid. 

Rupture of a vessel in the spinal meninges occurs usually in adult life, and more 
frequently in males than females. Its most common cause is injury to the spine. 
It has been known to follow violent convulsions and as a sequel to those infections 
which result in purpura. In newborn infants the blood found between the spinal 
membranes has its origin in the meninges of the brain, and follows the cord down- 
ward. Sometimes, in cases of very severe inflammation of the spinal meninges, 
small extravasations of blood take place. 

In extradural hemorrhage the blood comes from the veins which lie between the 
dura and the bony canal. The quantity of blood which is poured out varies greatly. 



848 DISEASES OF THE NERVOUS SYSTEM 

In some instances it reaches the full length of the cord. In other instances but a 
small area is covered by a clot. The most common seat for the hemorrhage is the 
cervical portion of the cord. The cord may or may not be compressed. 

Subdural hemorrhage, that is, the escape of blood between the dura and the 
arachnoid, also varies greatly in quantity. In subarachnoid hemorrhage the blood 
comes from the vessels of the pia mater, and the clot may surround the cord for a 
few inches or extend throughout the whole subarachnoid space. In very rare 
instances it may actually force its way into the cerebral ventricles. 

In all cases of hemorrhage into the spinal membranes, save the extradural type, 
the cerebrospinal fluid is blood-stained. This may be a valuable diagnostic point, 
since lumbar puncture may reveal the presence of blood in this fluid. 

Symptoms. — No symptoms may be present unless the hemorrhage is extensive 
enough to cause compression, or unless a secondary meningeal inflammation 
develops. When the effusion of blood is considerable there is sudden severe pain 
in the back, usually about the level of the hemorrhage, which extends into the loins, 
and it may be to the anterior surface of the body. There may also be some muscu- 
lar spasm in the parts involved by those nerves, the roots of which are pressed upon 
after leaving the spinal cord. These spasms may be severe enough to produce a 
convulsion, localized or general. Immediately after these symptoms evidences of 
loss of power develop and the symptoms resemble the early stages of acute myelitis, 
or of hemorrhage into the cord itself, save that it is rare for the paralysis of either 
sensation or motion to be as complete as it is in those conditions. 

If the hemorrhage is in the cervical region, the pain is felt in the neck and arms. 
There is difficulty of swallowing and of breathing, and, it may be, dilatation of the 
pupils. When it is in the dorsal region the pain is in the chest and abdomen, and 
when in the lumbar region it is chiefly felt in the legs. Consciousness is preserved 
unless it be lost through shock. Some hours or days after the hemorrhage a 
secondary reaction with febrile movement may develop. In fatal cases death 
usually comes on within a few hours. 

From a medicolegal standpoint it is interesting to note that at least one case of 
meningeal hemorrhage in the spine very closely resembled strychnine poisoning. 
If the symptoms are severe, death is very likely to occur within a few hours. If 
the patient survives the first few days, partial recovery from the paralysis may occur. 

Prognosis. — The prognosis as to life is worse when the hemorrhage is high up 
in the meninges than when it is low down. 

Treatment. — The treatment of this condition consists in absolute rest, the employ- 
ment of small doses of the bromides and aconite as nervous and circulatory sedatives, 
and counter-irritation over the back in the shape of dry cups or leeches. The 
patient should be made to lie on his side or on his face rather than on his back, 
in order to prevent the accumulation of extravasated blood at the posterior portion 
of the cord. Where the quantity of blood which is poured out is very large, and 
the symptoms so severe that death is threatened, it may be advisable to call upon 
a skilful surgeon to relieve pressure by operation. 

COMPRESSION OF THE SPINAL CORD. 

Definition and Etiology. — Compression of the spinal cord occurs as the result 
of disease of the vertebras, of growths in the vertebrae or the meninges; of growths 
occurring within the spinal canal, inside or outside of the dura mater; of aneurysm 
of the aorta, which, by pressure on the vertebra?, cause their absorption; as the 
result of syphilitic inflammatory processes in the spinal canal, or by the develop- 
ment of a pachymeningitis, which may involve the cervical or lumbar portions of 
the cord, and which is characterized by a thickening of the parts involved. The 
result of pressure exercised by any of these causes interferes with the nutrition of 



COMPRESSION OF THE SPINAL CORD 849 

the spinal cord and with the transmission of impulses along its tracts, and the 
symptoms which arise vary in their character and severity with the degree of 
pressure and the alterations caused by it. 

Disease of the vertebra is most commonly the result of tuberculous infection, 
particularly in children. As a result of this process, the bones become softened, 
give way under the pressure which is exerted upon them, and as they do so pressure 
upon the cord results. In other instances a suppurative process results in the 
development of so much pus that pressure is produced by it, and not uncommonly 
a carious process in the vertebras is associated with an inflammation of the dura 
mater, with consequent thickening of this membrane, so that pressure is produced. 
Again, the caseous masses which are formed, or the overgrowth of connective 
tissue which takes place, may cause pressure. In some instances the dura mater 
suffers from tuberculous infection, and tubercles are found upon its inner surface, 
and both the arachnoid and pia mater may be involved. As a result the nutrition 
of the spinal cord at this point is impaired through interference with the circulation 
in its bloodvessels and probably also because of the obstruction to the circulation 
of lymph as well. The cord, in the majority of instances, is involved. If, however, 
the pressure is severe, there is apt to be an overgrowth of connective tissue whereby 
a sclerotic process is developed. The axis cylinders become swollen, and fatty 
globules can be found in the myelin sheaths. If the pressure is severe and is 
long continued, the cord may be markedly atrophied and the overgrowth of con- 
nective tissue be very great. In some instances there may be nothing left of the 
cord but a band of connective tissue. If the damage done to the cord is of a more 
severe type, ascending and descending degenerative changes occur. 

The symptoms produced by these lesions consist in pain in the spine and in the 
distribution of the nerves supplying the trunk and limbs. Not infrequently pain 
will be felt in the abdominal wall or in the neighborhood of the sternum because 
of the irritation of the nerve trunks as they make their exit from the spinal cord, 
according to the well-known law that pain is frequently referred to the peripheral 
ends of the nerve affected. Any jarring of the body by a misstep or a sudden 
movement or even a gentle blow upon the spinal column may cause the patient 
suffering. The muscles of the back are usually fixed, in order to protect the spinal 
column as much as possible. This fixation is partly voluntary and partly involun- 
tary. In some instances a girdle sensation is felt in the nerves which make their 
exit from the area which is diseased. 

When the lesions are high in the cord there may be painful sensations in the arms, 
and if the lateral tracts are compressed there is an exaggeration of the reflexes, with 
a tendency to spasticity of the muscles. In other instances the patient may present 
all the symptoms of transverse myelitis and develop bed-sores. The rapidity 
with which these symptoms develop in different cases varies very much, depending 
entirely upon the activity of the pathological process in the spinal column. In 
some instances years are consumed in the development of the advanced stage of 
the malady. In others paralysis of the lower extremities may be produced in a 
few months. 

The diagnosis of these cases is not difficult if the physician will carefully examine 
the spine. 

The prognosis is, of course, not very favorable, but it is a noteworthy fact that 
in those stages in which the process in the spinal column becomes arrested a very 
marked degree of recovery may take place. On the other hand, it sometimes 
happens that spinal disease in infancy results in later life in the development of 
lateral sclerosis or other diseases of the spinal cord. Much depends in the way of 
prognosis upon what the surgeon is able to do for the spinal disease. The nervous 
symptoms are to be considered purely secondary, and every effort made to modify 
the pathological process in the spine. 
54 



850 DISEASES OF THE NERVOUS SYSTEM 

The treatment of compression of the spinal cord due to disease of the vertebra? 
is entirely in the hands of the orthopedic surgeon, who, by means of proper appara- 
tus, can often do much good. The medicinal plan of treatment consists in the 
use of cod-liver oil, iron, and arsenic, the following of a perfectly healthy mode of 
life, and the use of good food. Pain is to be relieved, if necessary, by opiates, 
and the nervous twitchings by sedatives, like bromide and chloral. In some cases 
hydrotherapeutic measures are advantageous. 

Malignant growths of the vertebrae, such as carcinoma and sarcoma, are rare. 
They are usually rapid in their growth and produce symptoms of spinal compression 
as soon as they invade the spinal canal. These malignant growths soon penetrate 
the dura, the arachnoid, and the pia, and speedily infiltrate the spinal cord itself, 
although the dura mater is usually capable of protecting the spinal cord from 
direct infection when the disease is tuberculous. 

When a tumor of the spinal cord develops it is in the great majority of instances 
due to sarcoma. Tumor of the spinal cord is, however, exceedingly rare. Schle- 
singer found only 147 spinal tumors in 35,000 autopsies, and Starr states that the 
ratio of tumors of the spinal cord to tumors of the brain is 1 to 13. 

Here, again, the symptoms consist, as a rule, in intense neuralgic pain of a 
shooting or stabbing character caused by pressure upon the nerves as they leave 
the spinal canal. These pains are more severe than those produced by any other 
form of spinal disease, and they are felt in different portions of the body, according 
to the portion of the spinal cord which is involved. If the lower cervical portion 
of the cord is affected, the pain may be felt in one or both hands and forearms. 
If the growth is in the upper cervical region, they are felt in the shoulder or neck; 
if it occurs as low as the sixth dorsal segment the pain is felt in the chest, near the 
nipple; in the tenth dorsal segment it is felt in the abdomen and groin. When a 
tumor compresses the cord in its entire thickness degenerations ensue, descending 
in the lateral columns, ascending in the dorsal and other sensory columns, just as 
they arise in cases of marked caries of the vertebra?. Under these conditions the 
symptoms are those of a transverse myelitis. The level at which the tumor is 
growing can largely be determined by localizing the symptoms, and the fact that 
tumor is present may be pointed to by the presence of growths elsewhere in the 
body. If the tumor is of the malignant type its growth is usually exceedingly 
rapid. 

Spinal symptoms due to new growth differ from those due to caries of the spine 
by the fact that the stiffness of the muscles of the back and tendons on jarring 
the spine is not so marked in growths as it is in tuberculous disease. In the latter 
case, also, there may be found a primary tuberculous focus. 

When compression is due to tumor the treatment is operative. In many instances 
it is possible to give the patient some relief ^by this means. Starr has collected 
58 cases of tumor of the spinal cord in which an operation was attempted. In all 
his cases the tumor was found, and in 16 of them the patients recovered. If the 
growth is malignant the possibility of doing much good by operation is, of course, 
remote. Pain may, however, be temporarily relieved by the removal of the 
pressure. 

The compression of the spinal cord produced by gummatous growth or by 
syphilitic exudations about the spinal cord present symptoms which also depend 
upon the area which is involved, particularly upon the level of the lesion. The 
condition may arise either in acquired or in hereditary syphilis, and the diagnosis 
is made by the history of the patient and the presence of pressure symptoms. The 
treatment is antisyphilitic. 

When an aneurysm of the aorta grows in such a manner that it erodes the ver- 
tebra?, it may produce symptoms of compression of the spinal cord. Thus, para- 
plegia may be developed, or severe pain may be felt in those parts of the body which 



SPINAL MENINGITIS 851 

are supplied by the nerve trunks which have their origin in that portion of the 
spinal cord which is affected. If the physical signs of the presence of aneurysm 
are demonstrable the diagnosis is not difficult, but if the growth is in a backward 
direction it may present no symptoms which indicate its presence. An examination 
of the patient's back may not only reveal signs of vertebral disease, but a bruit or 
a transmitted pulsation and a history of syphilis and of trauma, if added to a dis- 
covery that the bloodvessels are sclerotic, will aid in discovering this cause of the 
symptoms. 

A sixth cause of compression of the spinal cord is hypertrophic cervical pachy- 
meningitis, the pachymeningitis cervicalis hypertrophica of Charcot. This disease 
consists in thickening of the dura mater to such a degree that the spinal cord and 
the spinal nerves as they pass through the dura are pressed upon. As a result 
the spinal cord suffers from meningomyelitis, and the dura mater becomes adherent 
to the pia mater. Sometimes hemorrhagic extravasations occur under the dura, 
and there is usually an overgrowth of connective tissue about the bloodvessels, 
both in and about the cord. 

The symptoms of this form of meningomyelitis are identical with those already 
described as occurring in cases in which the cord is compressed by other causes in 
the cervical region, but they have certain peculiarities which may aid in the diagnosis 
of the condition. There is pain in the back of the head and neck, with a certain degree 
of stiffness and difficulty in movement. The pain radiates down into the bands and 
arms, and is often exceedingly severe and neuralgic in type. Patches of anesthesia 
or paresthesia may be present and localized muscular spasms may occur, followed 
by loss of power and the development of reactions of degeneration, when the disease 
has lasted long enough to interfere with the transmission of trophic impulses from 
the cord to the muscles affected. Finally, if the pressure becomes great enough 
to seriously impair the nutrition of the spinal cord, there will develop symptoms 
of spastic paraplegia due to descending degenerative changes in the lateral tracts. 
If the muscles supplied by the ulnar and median nerves are chiefly affected, the 
disease is present in the lower part of the enlargement; but if those muscles supplied 
by the musculospiral nerve lose power, the upper part of the cervical enlargement 
is involved. Loss of power in the triceps, anconeus, supinator longus, extensor 
carpi radialis longior, and the brachialis anticus, therefore indicate disease of the 
upper segment; whereas, a loss of power in the flexor carpi ulnaris and flexor pro- 
fundus digitorum (ulnar nerve) and all the muscles of the front part of the forearm 
and thumb (median nerve) indicates disease in the lower segment. In some cases 
myosis from paralysis of the cervical sympathetic may be present. 

Treatment of cervical pachymeningitis promises more than would be supposed 
from the character of the lesions, probably because the condition is so often due to 
syphilis. Active counter-irritation of the back of the neck by the electrocautery 
and the administration of salvarsan, combined with the free use of the protiodide 
of mercury, alternating with large doses of iodide of potassium, should always be 
resorted to. Pain is to be relieved by the use of acetanilid or phenacetin, and if 
these drugs fail to give relief they must be combined with morphine. 

SPINAL MENINGITIS. 

Definition and Etiology. — A condition of inflammation of the membranes covering 
the spinal cord is practically always secondary to some lesion at another part of 
the body. In some instances the specific micro-organisms of croupous pneumonia, 
of enteric fever, of acute articular rheumatism, or septicemia finds its way to these 
parts and causes the pathological process. In other instances tuberculosis is the 
cause, whether it be primarily present in distant parts of the body or in the vertebral 
column. In some instances an injury affords a means of entrance to the body 



852 DISEASES OF THE NERVOUS SYSTEM 

for micro-organisms, which attack the spinal meninges, particularly if the vital 
resistance has been lowered by an accident. Spinal meningitis may also arise from 
cerebral meningitis by direct extension of an infection. 

Pathology and Morbid Anatomy. — Following the stage of acute hyperemia present 
in all acute inflammatory processes, there is an excess of serous fluid poured out 
between the dura mater and the pia, which fluid may, at autopsy, be found to be 
purulent. Patches of fibrinous exudate are found on the surface of the pia mater, 
the bloodvessels of which are engorged with blood and often suffer from small 
hemorrhagic extravasations. The spinal cord, the pia and the dura mater are 
often adherent. After the inflammatory process has been present for some time, 
the pia mater becomes much thickened by the development of connective tissue. 
The secondary changes which ensue consist in an inflammatory process which 
affects the superficial parts of the spinal cord and causes degenerative changes 
in the spinal nerve roots, the axis cylinders of which become swollen. Fatty 
globules appear in the myelin sheath. The changes in the spinal cord are most 
marked in the posterior and lateral columns, and in subacute or chronic cases these 
are affected by an overgrowth of connective tissue, which ultimately produces 
sclerotic patches. 

Symptoms. — The onset of acute spinal meningitis develops, as do most acute 
inflammations of serous membranes, with pain, chill, and general wretchedness. 
The pain is felt in the back and limbs, and is greatly increased by movements. 
There is also a state of hyperesthesia of all the spinal nerves, so that touching the 
patient may cause great suffering. It is soon noticed that the patient is stiff and 
more or less fixed by muscular rigidity, which is, in part, due to the pain produced 
by movement and to the irritation of the nerves as they pass from the spinal cord. 
The stiffness of the muscles of the back and of the neck is the most marked. At 
this time " Kernig's sign" is developed, which consists in an inability of the physician 
to straighten the patient's leg at the knee after the thigh has been flexed to a right 
angle with the trunk. This state is due to spasm of the flexor muscles induced by 
the irritation at the point of exit of the nerve trunks. There is often soon developed 
an increase in the reflexes, chiefly in the legs, and this in turn is succeeded by 
paralysis and final loss of reflexes if the process is severe and prolonged. Along 
with these symptoms there speedily develops a paralysis of the bladder and rectum, 
so that there is retention or incontinence of urine and incontinence of feces. There 
may also be paralytic incontinence. Because of the lesions produced in the nerve 
roots and in the spinal nerves as they pierce the meninges, trophic changes in the 
skin may develop, as shown by localized areas of pallor and congestion and the 
speedy development of bed-sores. 

If the disease is severe and the inflammatory process spreads until the upper 
portions of the cord are involved, death may ensue by reason of the inflammation 
reaching the level of the medulla and causing fatal disturbance of the function of 
respiration or of the heart. In such cases Cheyne-Stokes breathing and irregularity 
of the pulse may be the symptoms of impending dissolution. Not rarely the 
development of paralysis of the cranial nerves with convulsions and coma precede 
death. Death may come within a few days of onset or after several weeks. In 
the severe cases which recover the patient often permanently suffers from localized 
palsies, anesthesias, and atrophic lesions in the skin and muscles. 

Diagnosis.— Aside from the character of the symptoms just described, which 
points strongly to spinal meningitis, we may resort to lumbar puncture for the pur- 
pose of making the diagnosis more certain. A strong, hollow needle attached to a 
syringe, so that it may be easily handled, or a small trocar and cannula are passed 
into the spinal canal between the third and fourth lumbar vertebrae, on a line 
drawn between the crests of the ilia. The direction of the needle should be slightly 
to one side and upward. (For further details as to this method see Meningococcic 



SPINAL MENINGITIS 853 

Meningitis.) As soon as it enters the spinal canal the cerebrospinal fluid will 'escape, 
drop by drop, or with a squirt, if the pressure is great. This fluid should be examined 
for bacteria to determine the nature of the infection. If the fluid contains disin- 
tegrated blood, the cause of the affection is a pachymeningitis or an injury. If 
fresh blood is present, the blood is probably due to the puncture. If the fluid is 
clear there is probably no true meningitis present. In cases of tuberculosis of the 
meninges it is usually quite cloudy. If it contains pus a purulent meningitis is 
present. If inflammation of the meninges is present no sugar will be found in the 
fluid. A study of the leukocytes in the cerebrospinal fluid may throw light upon 
the case. They are much increased in number in acute inflammatory processes. 
In chronic conditions the mononuclear cells are particularly increased. 

Prognosis. — Tuberculous meningitis is, of course, a state giving a hopeless prog- 
nosis. Septic cases are also grave. Those types due to pneumonia and typhoid 
fever sometimes recover. (See Pneumonia and Typhoid Fever.) 

Treatment. — The treatment of spinal meningitis consists in absolute rest, the 
patient being placed upon a soft bed. In some instances if there is any sign of 
bed-sores it is essential that an air-bed or water-bed should be used. The applica- 
tion of blisters or the actual cautery has been recommended, but in view of the 
possibility of bed-sores developing, it is questionable whether their use is safe. 
The same objection holds in regard to such forms of counter-irritation as cupping 
and leeching. Twitchings or cramps of the muscles are to be relieved by the 
administration of sedatives to the spinal cord, such as bromide and chloral, and 
if the pain is very severe morphine must be used. At one time it was believed that 
full doses of calomel combined with opium were exceedingly valuable in the treat- 
ment of acute inflammation of all serous membranes, particularly those covering 
the brain and spinal cord. At the present time this method of treatment has almost 
entirely ceased, but in certain instances it would seem advisable to have recourse 
to it. The object is to give enough mercurial to exercise its so-called antiphlogistic 
influence, and to use the opium not only for the relief of pain, but for the purpose 
of preventing the calomel from purging the patient. The mercurial may be pushed 
until slight tenderness of the gums is manifested. 

Chronic Spinal Meningitis. — Etiology. — Chronic spinal meningitis is said to 
occasionally have its origin in an acute inflammation of the meninges of the 
spinal cord. In all probability, however, such an origin is exceedingly rare, 
and in the majority of instances it is the result of syphilitic infection, whereby 
there is a thickening of the dura and the formation of an abnormal quantity of 
serum and connective tissue under it. As the result of the chronic inflammatory 
process in the membrane, a somewhat similar one is set up in the spinal cord near 
its surface, producing a meningomyelitis, which is in its nature closely allied to 
the acute form of meningitis just considered. There is always present a thickening 
of the bloodvessels, a small-cell infiltration about their walls, and, if the process is 
severe, an obliterating endarteritis. Sometimes gummatous masses are formed. 
In most of these cases there is also present cerebral meningitis as well. 

Symptoms. — The symptoms of chronic spinal meningitis consist in stiffness 
of the back and extremities, with pains and cramps. There are also disturbances 
in sensibility, some portions of the skin being hyperesthetic, others anesthetic. 
Motor power is also impaired, and if the inflammation is in the lower portion of the 
spinal cord there may be interference with the function of the bladder or rectum. 

Diagnosis. — Chronic spinal meningitis is to be recognized by the presence of the 
symptoms just described and by the use of lumbar puncture, which, if meningitis 
is present, will show an increased quantity of cerebrospinal fluid, which is usually 
under pressure, and which will, therefore, escape from the needle with a spurt. 
Care must be taken that ordinary lumbago with spasm of the muscles of the back 
and fixation and pain is not confused with this condition. Myelitis is to be sepa- 



854 DISEASES OF THE NERVOUS SYSTEM 

rated by the absence of severe pain and of cramps in the extremities, and by the 
presence of paraplegia. 

Treatment. — The treatment of chronic meningitis consists, as must be evident 
from its cause, namely, late syphilis, in the free use of protiodide of mercury and 
the iodide of potassium, given until a full physiological effect is produced. In 
other words, it is not a question of grains administered, but effects obtained. These 
cases are usually much benefited by going to the various hot springs, because, in 
addition to the use of mercurials by the mouth, they permit the simultaneous 
use of hot baths and mercurial inunctions. While salvarsan has not proved to 
be of so much value in syphilis of the nervous system as in specific lesions elsewhere, 
still its use is often followed by marked improvement, and the remedy should be 
used in conjunction with our longer known drugs. Whether the use of salvarsan- 
ized serum is a safe procedure in these cases is unknown. It is certainly a doubt- 
ful method in view of the inflammation already present. Everything should be 
done to keep the general condition of the patient at the highest possible level 
approaching that of health. 



ACUTE ASCENDING PARALYSIS (LANDRY'S PARALYSIS). 

Definition. — This is an acute ascending flaccid paralysis beginning in the lower 
extremities and rapidly passing upward until it involves the muscles of the trunk 
and upper extremities, finally causing death by failure of respiration. The con- 
dition is a very rare one. It must be clearly separated from those forms of acute 
ascending paralysis due to an acute ascending myelitis, or to a hemorrhage into 
the spinal membranes, and from ascending peripheral neuritis. It is a symptom- 
complex which results from a lesion of the lower segment of the motor pathway, 
either in the cord and bulb or in the peripheral nerves. It is sometimes called 
acute progressive paralysis, or Landry's paralysis, having been first described by 
Landry in 1859. Rare cases have been recorded in which the disease has begun 
in the arms and passed to the legs. 

Etiology. — The exact etiological causes of this malady are not understood. The 
disease occurs more frequently in males than in females, and its most common period 
of occurrence is between twenty and forty years of age. In all probability every 
case is due to an infection of the peripheral nerves and spinal cord, for it sometimes 
follows an acute illness due to a micro-organism, as, for example, influenza, small- 
pox, erysipelas, typhoid fever, and pelvic peritonitis. The excessive use of alcohol 
has seemed in some cases to be a powerful predisposing cause, and cases have been 
recorded in which, in the presence of a history of syphilis, the malady has been 
arrested by the use of specific remedies. 

Pathology and Morbid Anatomy. — The lesions found at autopsy in a case of Lan- 
dry's paralysis are by no means constant in all cases. In some instances the chief 
lesions have been found in the spinal cord, in others in the peripheral nerves and 
nerve roots. In the spinal cord the lesions described in some cases have been 
practically identical with those of acute disseminated myelitis, and in others they 
have been identical with those met with in severe peripheral neuritis. In every 
case, however,, it is evident that the peripheral motor neurones are the portions 
of the nervous system most affected. 

Symptoms. — In some cases of acute ascending paralysis the onset of the paralytic 
symptoms is preceded for a few hours by a sense of general wretchedness, with tingling 
or pain in the limbs or back. This is followed by a rapidly increasing weakness 
in the lower limbs, which may amount to a complete loss of power in from a few 
hours to several days. The muscles of the lower part of the trunk are next involved, 
and finally the muscles of the arms and of the upper thorax fall victims to the 



CAISSON DISEASE 855 

rapidly spreading malady. The respiration becomes difficult, the speech indistinct, 
and dysphagia may be present. Sensation in the paralyzed parts may be impaired, 
but it is not lost. The reflexes are decreased, and perhaps lost, but they may be 
restored later on and ultimately become excessive. Muscular atrophy does not 
develop even when the patient survives for weeks, and the sphincters usually, 
but not always, retain their power. Bed-sores do not develop. The mind nearly 
always remains clear, and the temperature is usually not elevated. Very rare 
cases have been reported in which the paralysis has been of the acute descending 
type, the arms being the parts first affected. In such cases fatal bulbar paralysis 
may occur before the lower parts of the body are affected. 

Diagnosis. — Acute ascending paralysis is to be separated from acute poliomyelitis 
by the absence of rapid atrophy. From the paralysis due to an acute hemorrhage 
into the spinal meninges it is separated by the absence of pain and of spasm. From 
an acute ascending myelitis it is separated by the fact that there is no loss of sensa- 
tion, that the sphincters are unaffected, and that the paralysis progresses more 
rapidly. 

Prognosis. — The prognosis depends upon the state of the respiratory centre and 
the lungs, and upon the condition of the centres governing cardiac action. If 
these parts are involved, death, of course, speedily ends the case. Death may 
come in a few hours or days, or not for several weeks. Cerebral and bulbar symp- 
toms are always grave. A fatal ending usually occurs, but cases sometimes improve 
and recovery may occur. 

Treatment. — The treatment of a patient suffering from Landry's paralysis should 
be almost identical with that advised in cases of acute myelitis. A warm bath 
may be given to draw the blood to the surface, and moderate counter-irritation 
should be applied over the vertebrae. It is absolutely essential that perfect rest 
be obtained, and that the patient shall lie upon the side rather than upon his back 
since the dorsal position may increase the tendency to congestion of the cord. 
As the disease is probably dependent upon infection and toxemia, the skin should 
be kept active by mild diaphoretics, and the kidneys should be stimulated to activity 
by the use of the vegetable salts of potash or other mild diuretics. Some writers 
recommend the administration of salicylate of sodium, although they do not seem 
to be able to explain how it can do good. Gowers speaks highly of the use of 
ergo tin, and mentions the case of a man of fifty-seven who developed symptoms of 
Landry's paralysis after exposure to cold and wet. To this patient ergotin was 
given every hour till 20 grains had been taken, when the symptoms became markedly 
improved and the patient speedily recovered, so that by the end of a week he was 
well. One cannot help feeling that in all probability the ergotin had little to do 
with this remarkable recovery, as it is hard to see how this drug could be useful in 
combating an infection which was so severe in its nervous effects. When there is 
a history of syphilis the protiodide of mercury should be administered freely. 



CAISSON DISEASE. 

Caisson disease is a condition met with in persons who have been exposed to 
high atmospheric pressures for a number of hours, and is particularly prone to 
develop if severe toil has been maintained during the exposure. The disease is 
usually met with in artisans, or laborers, who are engaged in the building of piers 
or foundations many feet under water, where it is necessary to have a pressure of 
several atmosphers in order to keep the caisson dry. In some instances the 
pressure is as great as ninety pounds to the square inch. The atmosphere 
in the caisson often has a high proportion of humidity, and the temperature 
may also be quite high. The symptoms develop when the workman leaves the 



856 DISEASES OF THE NERVOUS SYSTEM 

caisson and is exposed to normal atmospheric pressure. In mild cases nothing 
more than a feeling of dizziness and vertigo develop, associated, it may be, 
with neuralgic pains in the head. In severe cases the neuralgic pains become 
excruciating, so that the patient feels as if his muscles were being stripped from 
his bones, and this pain is followed by a loss of both motion and sensation in 
the lower limbs, although the patient still complains of the pain. Often nausea 
and vomiting are present, accompanied by violent epigastric paroxysmal pain. 
Occasionally, there is loss of power in the sphincters. In some instances pain 
is absent, but paralysis is present, paralysis being the more constant symptom. 
In still more severe cases coma develops, in which case death invariably results. 
The prognosis is generally favorable unless the symptoms of paralysis and pain are 
unusually severe. The mildest cases rarely last over twelve hours, sometimes only 
three or four; but in severe cases, recovery may not take place for days or weeks. 

The pathology of this curious condition is not well understood. (A discussion 
of many of the views concerning it will be found in the author's Fiske Fund Prize 
Essay for 1886. x ) It would seem probable that the symptoms are largely dependent 
upon disorder of the circulation in the central nervous system. Air emboli have 
been found in the small arteries of the posterolateral tracts of the spinal cord. 
These vessels may rupture and allow blood and gas to pass into the tissues. Autopsy 
reveals congestion of the central nervous system and at the base of the lungs. 
Vacuolated areas in the cord indicate the presence of gas. In those who recover, 
secondary softening may follow severe lesions. A microscopic examination of the 
brain also reveals dilatation of the lymph spaces, irregularly distributed areas of 
edema, but no changes in the ganglion cells. Small hemorrhagic extravasations are 
also found in addition in the pons and medulla oblongata. Hemorrhages in the 
dorsal portion of the spinal cord are also present and in this area the ganglion cells 
are degenerated. Those who have had a large experience with the disease in this 
country are Jaminet, Bauer, and Woodward, who made many observations during 
the building of the St. Louis Bridge, and A. H. Smith, of New York, who studied 
it during the building of the Brooklyn Bridge. 

Treatment. — The treatment is both prophylactic and palliative. The prophy- 
laxis consists in having superimposed air chambers, each one having a different 
pressure so that the workmen may pass by degrees from the high-pressure caisson 
to the pressure of atmospheric air. It is also advisable to have the workmen 
brought to the surface with as little muscular effort as possible. In the building 
of the St. Louis Bridge, thirteen of the men who were employed in the building 
of the east pier, which was sunk 127 feet below high-water mark, died; but in 
building the east abutment, which was sunk five feet deeper, only one man died. 
In the latter case the workmen were lifted to the surface by an elevator instead of 
having to climb a ladder. 

When the symptoms come on, morphine should be given hypodermically in 
adequate dose. A. H. Smith considered that ergot is of value. Hot compresses 
should be wrung out and applied to the feet and spine. Jaminet recommends a 
draught of a strong alcoholic stimulant, with ginger. 

The whole object of the physician should be to re-establish and equalize the cir- 
culation. If the pulse is full and the heart laboring, venesection should be freely 
employed. Sometimes relief can be obtained by returning the patient to the 
caisson. In some instances a small caisson for the resuscitation of workmen has 
been built on the surface, with advantageous results. 

1 New and Altered Forms of Disease due to the Advance of Civilization in the Last Half Century. 



NEURITIS 857 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE 

NERVES. 

NEURITIS. 

Definition. — Neuritis is an inflammation of a nerve. When the inflammatory 
process chiefly involves the perineurium it is called " perineuritis;" if the tissue 
surrounding the nerve bundles and between the nerve fibres are affected, it is an 
"interstitial neuritis/' and if the nerve fibres themselves are primarily affected 
it is said to be a "parenchymatous neuritis." The latter condition is usually a 
subacute or chronic process and is characterized by degenerative changes in the 
nerve fibres. The distinction, however, between these different forms is theoretical 
rather than clinical, because it is not possible to draw a definite line between them 
in most cases. 

Etiology. — The causes of neuritis are very numerous. Any injury to a nerve 
trunk, as by a blow, stretching, or a wound, may give rise to the inflammatory 
process, as may also tumors, which by pressure cause irritation. Sometimes the 
use of a tool or a crutch may, by constant pressure on a nerve, produce neuritis. 
Various infectious diseases and the abuse of alcohol may produce it, as may also 
many of the metallic poisons. In those cases, however, in which the malady arises 
as the result of a poison, the neuritis is usually a multiple neuritis and does not 
affect one nerve alone. (See Multiple Neuritis.) Gout and lithemic states also 
cause it. 

Pathology and Morbid Anatomy. — The nerve, which is acutely inflamed, is found 
on examination to be red and swollen and lacking its usual lustre; the bloodvessels 
supplying it are hyperemic or congested. If the process has been present for some 
time the nerve may be marked by swellings due to overgrowth of connective tissue 
and its endoneurium may be infiltrated by small cells. At this time one of three 
processes develops. Either the results of the acute inflammatory process undergo 
resolution or the inflammation becomes so severe that the nerve is destroyed, or 
if the process is more moderate, but continued, there is an overgrowth of connective 
tissue and gradual atrophy and loss of function. Microscopically, the inflamed 
nerve presents additional changes which serve to separate the parenchymatous 
form of the disease from that in which the perineurium and interstitial tissues are 
chiefly affected. In the parenchymatous type the myelin is opaque and swollen 
and soon undergoes segmentation with granular material between the segments. 
The axis cylinder may be continuous or broken into segments corresponding to the 
breaks in the myelin. Finally, the myelin and cylinder entirely disappear and 
only the nerve sheath containing a little granular matter is left. This last state 
may also arise as a result of the interstitial form of neuritis, but in this form the 
nerve is, in the early stage of the inflammation, more swollen and congested and 
the sheath filled with serum or purulent exudate. 

Symptoms. — The symptoms of neuritis vary over a wide range in severity. When 
the inflammatory process is very mild so that the normal function is but slightly 
perverted, as from moderate pressure, a tingling sensation is felt or, in its place, 
a sense of numbness is experienced. This is called paresthesia and can scarcely 
be said to be due to any real change in the nutrition of the nerve. 

When the change in the nerve is more severe the symptoms are more definite. 
Tingling or pricking sensations may be present not only at the site of the lesion, 
but at the peripheral part of the nerve. If the damage is the result of pressure 
there is rarely any pain, and motor paralysis, more or less complete, is present 
instead. If, on the other hand, the lesion is associated with any wound, and an 
infection of the nerve has taken place, then pain is usually present and is often 



858 DISEASES OF THE NERVOUS SYSTEM 

severe. Pressure upon the inflamed nerve trunk by the finger-tips also increases 
the pain not only at the point of pressure, but at the end of the nerve as well. 
After the process in the nerve is so advanced that its function is greatly impaired, 
trophic changes occur in the muscles and skin, the former wasting and the skin 
becoming glossy. The muscles cease to respond to faradic electricity and later fail to 
respond to galvanic electricity, the reactions of degeneration being first developed. 
Injuries to parts supplied by the nerve affected may result in sloughing, but sores 
rarely develop unless an injury is suffered. 

When recovery begins the electrical contractility to galvanic stimulation first 
returns in part and later the power of voluntary movement. 

Diagnosis. — The diagnosis of neuritis involving a single nerve, or several nerves 
in nearly related parts, is not difficult, for the pain is limited to the area of the nerve, 
as is also the anesthesia or hyperesthesia and loss of power. The condition is 
also pointed to by the history of injury or of some diathetic state which produces 
the affection. Pressure on the nerve trunk will elicit pain. 

Prognosis. — The outlook for recovery in most cases of neuritis is quite good 
because of the extraordinary power of regeneration possessed by nerves. Even if 
the damage to the nerve has been so severe that its function is abolished by the 
division of all its conducting fibres, the function can be restored by the surgeon, 
who, by excising the destroyed portion and joining the distal and proximal ends 
together, may re-establish the pathway for both sensory and motor impulses. 
So rapid is the regeneration that if a nerve is severed by accident, and immediately 
sewed together, power may return in two weeks. When the damage has been 
done by pressure or inflammation the recovery rarely ensues in less than six weeks, 
and even eight months or a year may be consumed in the regenerative process. 
When recovery fails to occur and it is believed that only a small part of the nerve 
is diseased surgical procedures are necessary, but if there is reason to believe that 
permanent damage to a large part of a nerve has taken place, then the prognosis is 
hopeless. Sometimes the mere exposure of the nerve and the breaking up of 
adhesions or exudates that cause pressure is sufficient to produce recovery. 

Treatment. — The treatment of neuritis may be divided into two parts, that 
devoted to the relief of pain and that to the abatement of the inflammation and to 
the regeneration of normal function. For the relief of pain the part affected may be 
wrapped in lint, which is heavily smeared with equal parts of an ointment of ichthyol 
and lanolin, outside of which is placed some oil-silk to retain moisture. In some 
instances a hot poultice of flaxseed or hot compresses may be used in the earlier 
stages to diminish the activity of the inflammatory process. If the pain is so 
severe that sleep is interfered with, the various coal-tar products may be employed, 
of which the most valuable are phenacetin in the dose of 5 grains four or five times 
a day, if need be. Acetanilid may be given in similar dose, and antipyrin in slightly 
larger dose. On other cases better results accrue if to these products of the coal-tar 
group are added small doses of codeine or morphine. If the pain does not yield 
to these remedies, hypodermic injections of morphine may be necessary for a short 
time, but their continued use is dangerous, as the patient only too readily develops 
the morphine habit. If the neuritis affects the arm or some portion of the body 
which does not by its disability force the patient to lie in bed, it is essential that 
the part involved shall be placed at rest. Thus, if the arm is affected it should be 
carried in a sling, and it may be necessary to protect it by a splint. 

For the restoration of function no therapeutic measure should be instituted 
beyond those already named until the acute stage of the inflammatory process 
has ceased. When it is evident that the acute process is no longer present, strych- 
nine or nux vomica may be given internally in full doses. These may also be 
coml)ined with phosphorus and small quantities of quinine. The area of the skin 
which is supplied by the affected nerve should also be stimulated by the application 



NEURITIS 859 

of faradic electricity, care being taken that the current employed is not so strong 
as to damage the part. It is a good rule never to use a current so strong as to 
produce suffering. This method of treatment not only tends to rapidly restore 
sensation in the paralyzed part, but also to bring back faradic contractility in the 
muscle, and so ultimately restore motor power. If, however, the parts fail to 
respond, then galvanic electricity must be used, and the current interrupted so as 
to produce a stimulant effect. In some instances the muscle seems to respond 
better to the negative than to the positive pole, much depending of course upon 
the stage of degeneration which is present. Care should be taken that the applica- 
tions of electricity are not prolonged for more than a few minutes at a time, and 
that they are not made oftener than once a day. Additional measures for improving 
the nutrition of the part are massage and manipulation. None of these measures 
should, however, be employed if there is tenderness in the nerve trunk or if they 
produce exhaustion in the parts affected. Indeed, it is possible in some instances to 
produce injuries of the nerve by too active manipulation. It must be remembered 
that the electricity, the massage, and the Swedish movements only do good by 
increasing the circulation and modifying the nutritional processes in the parts 
affected. If anesthesia of an extremity exposes it to injury, by reason of the 
patient being unconscious of the presence of heat or cold, or of objects which are 
capable of doing damage, the part should be carefully protected by a splint or soft 
dressing. 

Special Forms of Neuritis. 

Cervicobrachial Neuritis. — Cervicobrachial neuritis follows injuries to the neck 
and shoulder, and is usually produced by falls or severe blows. Symptoms may 
also arise as the result of disease of the vertebrae or from an aneurysm. In other 
cases the acute infectious diseases or gouty or rheumatic conditions, associated with 
exposure to cold, seem to be responsible for the condition. The symptoms depend 
to a large extent upon the portion of the cervicobrachial plexus which is affected. 
If the four upper cervical nerves are involved, severe pain in the neighborhood of the 
occiput is felt, and the head is held in a fixed position because movement increases 
the suffering. When the fifth or sixth cervical nerves are involved, the pain is in 
the neck and the upper portion of the shoulder and axilla, and it may be felt down 
the back of the arm. Whereas, when the lower cervical nerves are affected, includ- 
ing the branches of the first dorsal, the pain is clavicular and axillary in the area 
of its distribution and extends down the front of the arm and forearm into the 
fingers. There is also loss of power in all the muscles which are supplied by the 
nerves making up the cervicobrachial plexus when their fibres are involved. Because 
of the fact that the cervical sympathetic nerve receives fibres from this part of 
the spinal cord it sometimes happens that ocular symptoms accompany manifesta- 
tions of the neuritis in the lower portions of the cervicobrachial plexus, with the 
result that there may be retraction of the eyeball and narrowing of the palpebral 
fissure, with a mild degree of myosis and some pallor of the side of the face affected. 
The skin on this side is dry and does not become flushed on exercise. Cases of 
neuritis of the cervicobrachial plexus show marked evidences of pain when pressure 
is made over the plexus or when the arm is moved away from the body. 

The same numbness and tingling as has been described under neuritis in general, 
followed by loss of sensation and of motor power, occurs in cervicobrachial neuritis. 
Trophic changes in the skin and muscles take place, and the reactions of degenera- 
tion develop. 

In some instances of cervicobrachial neuritis of very sudden onset actual hemor- 
rhage may occur into the sheath of the nerves, the so-called "apoplectic neuritis." 

Before making a positive diagnosis of cervicobrachial neuritis exclude cervical 
rib. 



860 DISEASES OF THE NERVOUS SYSTEM 

Prognosis. — The prognosis in cases of cervicobrachial neuritis, like that of neuritis 
in general, is good provided the injury has not been so severe as to sever the nerve 
fibres, and provided the condition has not lasted too long. 

Treatment. — The treatment consists in absolute rest, the employment of hot 
compresses if the condition is seen early in its course, and later on the constant 
use of counter-irritation. It is often advisable to carry the affected arm in a sling 
or to render it immoblie by placing it upon a right-angle splint. Rubbing the 
parts with some stimulating liniment like that of chloroform or ammonia is of 
value. Electricity, massage, and Swedish movements are to be resorted to after 
all evidence of acute inflammation is passed. The rest of the treatment is identical 
with that given for neuritis. 

Obstetrical or Birth Palsy. — A paralysis of brachial nerves is a frequent occur- 
rence in difficult and protracted labors, especially in cases of breech presentation. 
Pressure with the finger or tenaculum introduced into the axilla in order to facilitate 
delivery will injure the nerves and produce paralysis. In birth palsy the following 
muscles are affected; deltoid, biceps, supinator longus, and infraspinatus. This 
leads to inward rotation of the arm, extension of the forearm, and pronation of the 
hand. The paralysis is soon followed by atrophy of the muscles. The prognosis 
of birth palsy is, generally speaking, favorable, except when reaction of degeneration 
exists. As to treatment, massage and electricity are the only means, and should 
commence as early as possible. 

Sciatica. — Sciatica, or pain in the course and distribution of the sciatic nerve 
is usually unilateral and occurs as sciatic neuralgia and as the result of a true 
sciatic neuritis. The onset of the pain is generally sudden and it may vary in 
severity from a dull ache to agony. In some instances the pain is felt only near 
the sciatic notch; in others it extends all the way to the foot. In still ether cases 
pain is felt in the thigh and a sense of fullness or numbness in the leg. Sciatic 
neuritis is to be separated from neuralgia by the fact that in the latter state flexing 
the thigh on the trunk and extending the leg does not increase the pain and by 
the fact that the neuralgic pain is not so prone to be constant. Care must be 
taken before reaching a diagnosis of sciatica that sacro-iliac strain is excluded and 
that flat-foot is not responsible for the pain. In some instances sciatic pain is 
due to a growth in the spine or in the pelvis. Sometimes a sarcoma of the femur 
gives rise to a diagnosis of sciatica. 

Treatment. — The treatment of sciatic neuralgia consists in the use of coal-tar 
analgesics such as phenacetin, combined w T ith salicylates, and avoidance of cold 
and damp. / When neuritis is present these facts are also essential and in addition 
wet or dry cups may be used over the nerve, or the leg protected by cloth or news- 
paper and ironed with a hot laundry iron. Morphine or codeine may be needed 
if the pain is excessive. In obstinate cases the nerve should be exposed and any 
adhesions broken up. 

Multiple Neuritis. — Definition and Etiology. — Multiple neuritis, sometimes 
called "polyneuritis" or "peripheral neuritis," is a condition in which a large 
number of the peripheral nerves of the body suffer from subacute or chronic inflam- 
mation as a result of the action of some toxic agent. These toxic agents may be 
derived from external or internal sources. The external agents are alcohol, lead, 
arsenic, copper, mercury, anilin, carbon monoxide, and carbon bisulphide. The 
internal agents are the poisons developed in the various acute infectious fevers, 
as typhoid fever, smallpox, scarlet fever, influenza, erysipelas, pneumonia, diph- 
theria, dysentery, and other infectious maladies. Occasionally, too, a multiple 
neuritis develops as a complication of septic infection, either that following a 
wound or occurring during the puerperal period. Cases have also been recorded 
in which the toxic substance apparently has arisen from decomposition changes 
in the intestines. In some instances syphilis, tuberculosis, diabetes mellitus, and 



NEURITIS 861 

malarial fever have seemed to be provoking agents, but in all probability these 
affections act indirectly by rendering the nerve trunks susceptible to the action 
of the poison. A special form of multiple neuritis is that which is known as beriberi 
or "kakke." (See Beriberi.) In several instances small epidemics of multiple 
neuritis have been described. Multiple neuritis occurs most frequently between 
the twentieth and the fiftieth year of age, and is very rare in children, unless it is 
due to diphtheria. Whatever may be the cause of an attack of multiple neuritis, 
the pathological changes which are found in the affected nerves do not differ greatly 
from those already described as occurring in ordinary neuritis of a more limited 
extent. 

Symptoms. — The symptoms of multiple neuritis, be the cause what it may, are 
fairly constant, although slight variations in the character of the symptoms occur 
according to the peculiar influence exercised by the poison. As alcoholic neuritis 
is the type most frequently met with, a description of this disease may be used 
for all forms of multiple neuritis. At the beginning of the malady there may be 
some slight elevation of temperature, but in many cases this does not occur. The 
patient first complains of tingling or numbness in the feet and fingers. In other 
cases dull pain may be experienced. Rarely this pain may be severe. These 
disturbances of sensation are usually increased by moving the affected limb and 
by deep or superficial pressure over the nerve trunks, and especially by deep pressure 
upon the muscle bellies of the forearms and of the calves. 

Following these symptoms weakness develops, and it may become so severe 
that the patient is unable to move his hands or feet, and foot-drop or wrist-drop 
may develop. After the paralysis has lasted for some little time, some wasting of 
the muscles of the affected parts takes place. The reflexes are diminished or 
altogether arrested. 

A peculiarity of the paralysis of peripheral neuritis is that very often it does not 
involve all the nerves of a limb. Thus, it not infrequently happens that the pero- 
neal nerves suffer chiefly. In other instances the tibialis posticus is chiefly affected ; 
and it is only when the condition is unusually severe that a complete paraplegia 
is present. In the arms the musculospiral nerve is most commonly affected. It is 
a noteworthy fact that the paralysis is usually symmetrical. In some instances the 
symptoms are more sensory than motor, but this is rarely the case. Sensory 
symptoms are, however, very constant in alcoholic neuritis, and in most of the 
other forms. They may, however, be absent or be very slight, as in neuritis due 
to lead, and in such forms of infectious disease as diphtheria and influenza. These 
forms of neuritis are often spoken of as "motor neuritis" to indicate that the 
sensory functions escape. 

In addition to the numbness and tingling already mentioned, patches of anes- 
thesia and hyperesthesia are often found existing near one another or even coincid- 
ing. So, too, there may be a hypersensitiveness to pain and a loss of the sense 
of touch, or vice versa. 

Not infrequently the affection develops a train of symptoms which are so exactly 
like those met with in locomotor ataxia that even the most skilful neurologist 
may have difficulty in differentiating the two diseases. In other words, a so-called 
"pseudotabes" due to multiple neuritis is present. This resemblance depends upon 
the fact that the fibres for "muscle sense" which are affected in their spinal course 
(posterior columns) in tabes are implicated in cases of multiple neuritis in the 
joints and muscle fasciae. The presence of the Argyll-Robertson pupil in true 
ataxia, however, usually determines that the case is not one of peripheral neuritis. 
As an illustration of how closely multiple neuritis may resemble locomotor ataxia, 
cases have been reported in which perforating ulcer of the foot occurred due to 
neuritis. 

Aside from the trophic changes already spoken of as occurring in the muscles, 



862 DISEASES OF THE NERVOUS SYSTEM 

local disorders of blood supply and secretion are often present. There may be 
areas of skin which suffer from excessive sweating. In other cases localized patches 
of edema are found, and rarely the joints become swollen, so that the case resembles 
Charcot's joints in ataxia. Actual breaking down of the skin as the result of 
trophic changes, however, rarely occurs. The bladder and rectum are usually 
unaffected, and this aids materially in separating the paraplegia of severe neuritis 
from that due to myelitis. Rarely, however, this valuable aid to differentiation 
fails us, and retention or incontinence of urine or feces is present. 

Associated with these evidences of impairment in function in the peripheral 
nerves it is not infrequent for disturbances to occur in connection with intellection. 
Confusion of thought and impairment of memory are frequently present, occasion- 
ally in a peculiar form characterized by fabrication or "pseudoreminiscence," 
the patient relating imaginary recent experiences. This mental condition, com- 
bined with multiple neuritis, is sometimes called "Korsakoff's disease." 

The cranial nerves also share in the malady. Indeed, in some instances they 
suffer most. Nystagmus, or squint, may be present, but the optic nerve is not 
often affected, although occasionally it may suffer very slight atrophy. The 
paralysis of the cranial nerves may be symmetrical. Thus, Oppenheim has reported 
cases of double facial palsy due to this cause. 

Tachycardia and interference with the function of the diaphragm may be mani- 
fested from the infection involving the pneumogastric and phrenic nerves. Manna- 
berg asserts that the multiple neuritis may be confined entirely to the cranial nerves. 

When the multiple neuritis is due to lead, it is a noteworthy fact that the inflam- 
matory process is not, as a rule, very widely distributed, and that the sensory 
nerve fibres usually escape. In association with the symptoms of neuritis, already 
described, there may be a history of lead colic, which will aid in determining the 
cause of the paralysis. The presence of a blue line on the gums is also pathogno- 
monic. Anemia is often marked. Aside from the fact that sensation is usually 
not involved, the multiple neuritis caused by lead is noteworthy, in that it chiefly, 
and it may be exclusively, affects the extensor muscles of the hand and fingers. 
Indeed, the paralysis may be so localized in mild cases that only the extensor 
communis digitorum may be involved, so that the ring and little finger cannot be 
extended. When the paralysis is very marked, double drop-wrist is present. 
Another peculiarity of lead palsy is that the supinators, especially the supinator 
longus, and the triceps, escape. The deltoid, however, may be partially paralyzed, 
and the abductor pollicis longus and the interossei may be palsied. Occasionally, 
however, the supinators are affected, as is also the biceps. Muscular atrophy 
is nearly always marked in lead paralysis, and the reaction of degeneration usually 
speedily develops. Muscular tremor may also be present. The noteworthy 
fact that sensation is not disturbed in most cases may be well reiterated. Drop-foot 
is rarely seen in cases of lead paralysis. Paralysis of the cranial nerves due to lead 
is exceedingly uncommon. (See Lead Poisoning.) 

When the paralysis is due to arsenic, it is not infrequently associated with gastro- 
intestinal disturbances, and, unlike that due to lead, it is usually associated with 
marked disturbances of sensation in the affected parts. Wasting of the muscles 
supplied by the affected nerves usually develops quite early. Not only are the 
extensors affected, as they are in lead poisoning, but the flexors are also involved. 
Another point of difference between arsenical paralysis and that due to lead lies 
in the fad that the lower extremities are quite as frequently affected as the upper 
extremities, so that quadriplegia, that is, a paralysis of all four extremities, is 
present. Reactions of degeneration speedily develop. The pulse is apt to be 
rapid. Disturbances of the psychic functions are said to occur, which is rare in 
lead poisoning, unless encephalopathia saturnina is present. Symptoms of ataxia 
arc usually marked. The reflexes are lost, and these two factors may make the 



■ NEURITIS 863 

case more closely resemble true locomotor ataxia than any other form of multiple 
neuritis. Nutritional changes in the skin are quite frequent in arsenical neuritis. 
In some instances herpetic eruptions develop. In others the skin becomes glossy, 
and there may be falling out of the hair. It is exceedingly rare for the cranial 
nerves to be involved. 

Of all the forms of multiple neuritis due to toxic substances having their origin 
in the body, that due to the poison of diphtheria is most frequently met with . As 
diphtheria is essentially a disease of childhood, it is evident that diphtheritic multi- 
ple neuritis must be more commonly met with in young persons. The peculiarity 
of this form of neuritis is that it most frequently affects the muscles of the soft 
palate, changing the character of the speech and rendering swallowing difficult. 
This paralysis is both motor and sensory, and is often accompanied by wasting. 
Sometimes the external ocular muscles are paralyzed. In other instances the 
internal ocular muscles suffer chiefly, and accommodation may be paralyzed as 
the result of oculomotor involvement. The pupillary reflex is, however, usually 
preserved. In other instances the paralysis produced by diphtheria is almost 
universal. I have seen more than one instance in which the child was not only 
paralyzed in all its extremities, but was unable to exercise any control over the 
movements of its head, and could only swallow when put in such a position that 
the liquids could readily pass down the gullet. Such cases are usually characterized 
not only by loss of motor power, but by loss of sensation as well. The bladder 
and rectum usually escape the general paralysis, but they may be involved. It is 
a noteworthy fact that diphtheritic paralysis is not a concomitant symptom, but a 
sequel to an attack of diphtheria, and the full severity of the symptoms may not 
be present for several weeks after the diphtheria has ceased. In some instances 
the diaphragm is paralyzed, and if the nerve supply of the heart becomes affected 
sudden death may occur. (See Diphtheria.) 

Diagnosis. — The presence of numbness and tingling followed by more or less 
impairment of motion and sensation in certain nerve trunks, with complete or 
partial escape of other nerve trunks, of course, points to multiple neuritis as the 
cause of the malady, particularly if the history of the patient reveals the fact 
that he or she has been exposed to one of the provoking causes already named. 
In some instances more than one of these causes has been effective, and, therefore, 
the precise factor in determining the neuritis cannot be relied upon. Thus, I 
have known more than one instance in which the administration of very large 
quantities of alcohol as a stimulant during typhoid fever has produced a multiple 
neuritis, which was attributed to a typhoid toxin, when in reality the alcohol was 
the active agent. In those cases in which the paralysis comes on very rapidly 
and is severe, the differentiation must be made between this condition and Landry's 
paralysis (which see), and this is the more important because Eichhorst has described 
a neuritis acutissima progressiva. A so-called apoplectiform type has been described 
by other observers. The presence of the Argyll-Robertson pupil, optic nerve 
atrophy, and the laboratory examination of the blood and cerebrospinal fluid 
on the one hand, and the history of exposure to a poison on the other hand, aid 
us in differentiating between true locomotor ataxia and multiple neuritis. 

Prognosis. — The prognosis is favorable in nearly every case, unless the patient 
has been exposed to the evil influences of lead or arsenic or alcohol for so long a 
time that the nerves cannot undergo regenerative change. In cases of profound 
alcoholic intoxication sudden death may take place when the pneumogastric 
nerve becomes involved. In nearly all instances recovery is exceedingly slow. 
The first symptom of improvement is a diminution in the pain and a decrease in 
tenderness of the nerves on palpation. In other instances the power of motion 
returns before the sensory functions are restored to their normal condition, and 
inability to get about may be caused by the intense hypersensitiveness of the feet. 



864 DISEASES OF THE NERVOUS SYSTEM 

Even if the patient does not recover for eighteen months or two years, the condition 
is by no means hopeless. Care should be taken, however, that complete recovery 
should not be promised in cases which have been exposed to the poisons for very 
long periods of time. Not infrequently great disappointment is caused by periods 
in which no improvement takes place, or, indeed, in which a relapse seems to be 
threatened. 

The prognosis in multiple neuritis due to lead is good so far as the preservation 
of life is concerned. It is bad in direct proportion to the duration of the condition 
and of the exposure to the poison. The same facts hold true in regard to the 
peripheral neuritis due to arsenic. 

Occasionally secondary contractures occur as the result of the contraction of 
non-paralyzed muscles, whereby deformities are produced. 

After diphtheria, even in those cases in which the paralysis is most severe, the 
progress is not necessarily very grave. The immediate danger is that some nervous 
mechanism connected with a vital function may be involved. If this does not 
occur, partial or complete recovery of motion or sensation nearly always takes 
place, although twelve months may pass before recovery occurs. Usually, however, 
two or three months is sufficient. 

Treatment. — The treatment of multiple neuritis gives better results, than that 
devoted to the relief of any other form of paralysis. If the cause of the malady 
is one of the metallic poisons already named, the patient must be removed from 
further exposure to the poison. Thus, workers in lead and arsenic must cease 
following such occupations. For the purpose of aiding in the elimination of any 
of the poisons which may remain in the body, moderate doses, 20 to 30 grains, of 
iodide of potassium may be given twice or thrice a day. If the patient uses alcohol 
to excess, this agent must, of course, be withdrawn. While the nerves are hyper- 
sensitive to pressure and while pain is present, strychnine and faradic electricity 
should not be applied to them, since they tend to increase irritation; but when there 
is anesthesia and loss of power, full doses of strychnine and phosphorus are often 
useful, and the rapidly interrupted faradic current may be used to stimulate the 
affected nerve fibres. Muscles which are suffering from loss of power may be 
exercised by the use of the slowly interrupted faradic current. Massage may also 
be employed, but it is of vital importance that no form of exercise shall be used to 
the point of exhaustion of the affected parts. In other words, only healthy exercise 
designed to improve the nutrition of the parts affected should be resorted to. 

If it is thought that the neuritis is due to toxic materials arising inside the body, 
these should be removed, if possible. The administration of laxatives or purges 
is usually needful. If anemia is present, particularly if it is associated with septic 
conditions such as are met with in sepsis and puerperal fever, iron and arsenic are 
useful. If the patient is rheumatic or of gouty tendency, hot baths, or a visit to any 
of the well-known hot springs may be resorted to, and the various salicylates or 
iodides should be administered in sufficiently full doses to produce mild physiological 
effects. For the purpose of aiding in the elimination of toxic materials, pure water 
should be drunk freely to flush the kidneys, and Turkish baths may be taken to 
produce sweating: Pain is to be relieved by the use of such remedies as phenacetin 
or acetanilid, and by hot applications to those areas which suffer most. Sometimes 
the application of splints to provide perfect rest for the painful part is useful. 

In those forms of multiple neuritis which depend upon infection, such as diph- 
theria, smallpox, or typhoid fever, the heart should be carefully examined, and if 
any evidences of tachycardia, bradycardia, or arhythmia are present, the patient 
should be warned against sitting up in bed, and should be protected from all causes 
which may throw an increased strain upon the circulation. This is particularly 
important in diphtheritic multiple neuritis. Contractures should be prevented by 
massage and Swedish movements and remedied, if they occur, by tenotomy. 



DISEASES OF THE CRANIAL NERVES 865 

DISEASES OF THE CRANIAL NERVES. 

The Olfactory Nerve. — Disease of the olfactory nerve, of course, interferes 
with the special sense of smell, and if this sense is entirely lost the condition is 
called anosmia. Partial or complete loss of this sense results from lesions of the 
peripheral ending of the nerve in the nasal mucous membrane and from pathological 
states of the tissues beneath it, such as morbid growths or disease of the ethmoid 
bones. Similar loss of function results from meningitis, from injury of the bones 
forming the base of the skull, or morbid growths affecting these bones. Tumors 
of the brain may destroy the olfactory nerves or the olfactory bulbs. When com- 
plete loss of the sense of smell occurs and no local lesion in the nasal bones or mucous 
membranes is present, it is usually an evidence of a tumor or abscess in the anterior 
cranial fossa. 

The Optic Nerve. — The optic tract of either side arises by two roots from struct- 
ures in the midbrain called the primary optic centres. These structures are the 
external geniculate body, the posterior part (pulvinar) of the optic thalamus, and 
the anterior quadrigeminal body. 

It is important to remember that the fibres from the optic tract undergo partial 
decussation in the chiasm. The outer fibres do not decussate and they connect 
the outer half of the retina with the primary optic centres of the same side. The 
inner fibres, on the other hand, all cross to the opposite side, and they connect 
the inner half of the retina with the nuclei on the opposite side. It is evident, 
therefore, that the right optic tract contains fibres which carry impulses from the 
right halves of both retinae to the right side of the brain, and that the left optic 
tract contains fibres which convey impulses from the left halves of both retinae 
to the left side of the brain. It is essential to remember these facts in order to 
understand the condition known as hemianopsia, which will be described shortly. 

Optic neuritis, sometimes called papillitis, is an inflammatory condition which 
is manifest in the intra-ocular end of the nerve, and it may be due to several causes. 
In the great majority of cases it is due to brain tumor. Choked disk is an edematous 
state. The degree of neuritis has no direct relationship to the size of the tumor, 
nor to the area of the brain which it affects, although a tumor of the corpora quad- 
rigemina seems to cause the condition more commonly than do growths elsewhere. 
Tumor of the parieto-occipital region and of the cerebellum also produces papillitis 
in a large proportion of cases in which these growths occur, while a tumor of the 
frontal lobes of the cerebrum causes it less frequently. The condition is not 
materially affected as to frequency or severity by the character of the growth. 
Meningitis in any of its forms may cause papillitis, but tuberculous meningitis 
does so more commonly than any other form. Rarer causes are cerebral softening, 
inflammation, and atrophy, or any cause, such as aneurysm or hydrocephalus, 
which produces an increase in intracranial pressure. Very rarely, general paresis, 
or myelitis may cause papillitis, as may the various acute infectious diseases, or 
the excessive use of alcohol, or lead poisoning. 

Symptoms. — There are often no symptoms whatever which point to optic neuritis, 
at least in so far as the patient complains of impairment of vision. The diagnosis 
rests solely upon the use of the ophthalmoscope and upon a study of the fields of 
vision. The ophthalmoscope reveals an indefinite outline of the head of the nerve, 
with redness, followed by swelling of the papilla, which becomes grayish in hue. 
Finally, the disk protrudes, its outlines become lost and whitish patches may be seen 
upon its surface. The retinal arteries are contracted and the veins congested and 
tortuous. At the point of exit and entrance of the vessels this part may seem devoid 
of vessels, because they are hidden in the infiltrated mass. Small, narrow, flame- 
like hemorrhages may be seen along the vessel walls. The field of vision is concen- 
trically contracted, and the perception of red and green is lost before the other color 
55 



866 DISEASES OF THE NERVOUS SYSTEM 

senses are destroyed. Hemianopsia is present if the lesion is so situated as to cause 
this symptom. 

Another form of optic neuritis, called retrobulbar neuritis, exists in which the 
inflammatory process develops in the optic nerve in the orbit. In the acute form 
the symptoms consist in dimness of vision which always occurs in the centre of the 
field, and which may end in complete blindness in from one to eight days. With 
the ophthalmoscope, when the disease is well developed, the edges of the disk are 
seen to be indistinct, its surface hyperemic, and its main bloodvessels shrunken. 
The cause of the acute form is usually some one of the acute infections, such as 
influenza, scarlet fever, or one of the diathetic diseases, such as rheumatism, gout, 
and sometimes syphilis. 

The treatment of retrobulbar neuritis consists in the production of profuse 
sweating by pilocarpine, the use of large doses of the salicylates if gout or rheumatism 
is present, or the employment of mercury and the iodides if syphilis is suspected. 
Counter-irritation on the temple is also advisable. 

The chronic form of retrobulbar neuritis is usually a toxic condition produced, in 
the majority of instances, by tobacco, alcohol, arsenic, lead, or poisons made by 
infectious diseases. Its symptoms consist in diminution of vision and in color 
scotomata. The prognosis when the cause is tobacco and alcohol is good, if the 
patient will give up these drugs, and if he does so in the early stages of the disease; 
otherwise the prognosis is bad. 

The treatment consists in the elimination of the causes as far as possible, in the 
use of massive doses of strychnine, and the employment of the iodides and free 
sweating. 

Treatment. — This depends upon the cause. If it is due to brain tumor or abscess, 
operative treatment is required, unless a gummatous growth is present, when 
mercury and the iodides are needful. Trephining of the skull to relieve pressure 
may be resorted to as a palliative measure in cases where a growth cannot be 
removed, 

Optic Atrophy. — Atrophy of the optic nerve, as its name implies, is a condition 
in which a degenerative process affects its fibres. It is divided into five forms: 
the primary, secondary, consecutive, retinitic, and choroiditic atrophy. The last 
two forms are really of the consecutive class. 

Etiology. — Primary atrophy of the optic nerve has been thought to be due to 
impaired nutrition, sexual excesses, and to such diseases as chronic malarial infection, 
diabetes, syphilis, and to the overaction of certain drugs. The most important 
causes of primary optic atrophy are diseases of the spinal cord, notably locomotor 
ataxia. It is also seen in cases of general paresis and disseminated sclerosis. In 
many instances the optic atrophy may be one of the early symptoms of ataxia. 
It has also been met with in cases of lateral sclerosis, chronic myelitis, and bulbar 
palsy. 

Secondary atrophy arises from causes which produce pressure upon the optic 
tract and the optic fibres, as, for example, the growth of a tumor or an aneurysm, 
or meningitis. So, too, injuries to the head sometimes produce atrophy. Con- 
secutive atrophy follows the various forms of optic neuritis. 

Pathology. — The axones lose their medullary sheaths and are converted into 
fine fibrils, between which are interspersed numerous fatty granules. When the 
condition is far advanced, the nerve elements entirely disappear and there is a 
marked increase in connective-tissue formation. 

Symptoms. — The subjective symptom complained of by the patient is diminution 
in the am ity of vision. The other symptoms are developed by the use of the ophthal- 
moscope. When this instrument is used it is found that the optic disk is gray or 
greenish-gray, or actually white in color, although there may be patches of red 
throughout it. The centre of the disk is depressed in direct proportion to the degree 



DISEASES OF THE CRANIAL NERVES 867 

of atrophy which has taken place. The margin of the disk is distinct, and in some 
cases when the condition of the optic nerve is due to disease of the spinal cord, 
there is broadening of the normal scleral ring. The bloodvessels are narrowed, but 
in some cases only the arteries seem to be affected, the veins escaping. An examina- 
tion of the central vision shows that it is markedly impaired, or absolute blindness 
may be present. The field of vision is greatly narrowed and there may be a central 
scotoma or hemianopsia. The color fields are markedly diminished, the green 
being most affected; after it the red, and then the blue and yellow. Sometimes 
the field for red is first affected. The pupil usually manifests some degree of 
paralytic dilatation, and when the nerve is completely atrophied the pupil is dilated 
and the iris motionless. In secondary atrophy the disk is apt to be whiter than 
in the primary forms, when it is usually gray. In that form of optic nerve atrophy 
called retinitic and choroiditic atrophy, the disk is often slightly yellowish in hue, 
but its borders are not distinct. 

Diagnosis. — The mere discovery that the optic disk is grayer than normal and 
that its margins are sharply defined, does not justify the diagnosis of optic atrophy. 
If, however, any of the diseases so far named are also present, such a diagnosis is 
usually correct. 

Prognosis. — The prognosis as to complete recovery is bad. On the other hand, it 
must be remembered that the atrophic process is often a slow one which may last 
for years. Indeed, the prognosis in secondary cases depends largely upon the 
rapidity with which the underlying disease is advancing. 

Treatment. — The treatment consists in the administration of full doses of mercury 
and the iodides if there is any suspicion that a recent or ancient syphilitic infection 
has been present. Strychnine in large doses combined with nitroglycerin is also 
useful. 

Of the functional disorders of the optic nerve the most important are blindness 
due to uremia, that due to diabetes, malaria, profound anemia, and the abuse of 
drugs. When uremia is the cause the presence of the symptoms of that condition, 
in association with dimness of vision or blindness, make the diagnosis clear. The 
so-called albuminuric retinitis may be present, but the ophthalmoscope may, 
however, reveal no morbid changes. If the patient survives, vision usually returns. 

When the dimness of vision is due to diabetes, the prognosis is unfavorable 
because the disease is incurable. That form which is due to malarial infection 
has associated with it other symptoms of this disease. Recovery usually takes 
place if proper treatment is administered. So, too, in cases of dimness of vision, 
due to hemorrhage and profound anemia, the prognosis is good, unless the anemia 
is one of the so-called essential anemias which always go from bad to worse. The 
treatment in such a case consists, of course, in the use of drugs designed to combat 
anemia. 

Hemianopsia. — Hemianopsia, or blindness of one-half of the visual field, occurs 
in three forms: that known as bitemporal hemianopsia, binasal hemianopsia, 
and homonymous hemianopsia, each variety being named not from that part of 
the retina which is blind, but from the visual field which is affected. In the first 
there is loss of vision in both temporal fields, in the second in the nasal half of each 
field, and in the third form the same side of each eye is lacking in function — that 
is, for example, the outer half of the left eye and the inner half of the right eye. 
When the left half of each retina is inactive, the condition is called right homony- 
mous bilateral hemianopsia, and when the right half is functionless it is designated 
left homonymous bilateral hemianopsia. Homonymous hemianopsia is the most 
common. Binasal hemianopsia is very rare. Bitemporal hemianopsia is produced 
by a lesion, such as a tumor or an aneurysm, which presses upon the middle of the 
chiasm. Homonymous lateral hemianopsia is produced by a lesion of one optic 
path at any point back of the chiasm, either in the neighborhood of the calcarine 



868 



DISEASES OF THE NERVOUS SYSTEM 



fissure (occipital lobe), in the optic radiations, including the point where they pass 
just back of the internal capsule, in the primary optic centres, or in the optic tract. 
(See Fig. 139.) It is important to remember that the lesion in cases of hemianopsia 



Fig. 139 



£eft Eye 



VisualFjieltf 







Wtai 



Lobe 



The visual tract. The result of a lesion anywhere between the chiasm and the cuneus is to produce 
homonymous hemianopsia. H, lesion at chiasm causing bilateral temporal hemianopsia. N, lesion at 
chiasm causing unilateral nasal hemianopsia. T, lesion at chiasm causing unilateral temporal hemi- 
anopsia. N.Y, substantia nigra of cms. L, lemniscus in crus. RN, red nucelus. 777, third nerves. 
J', Q, R, S, U, lesions in the occipital lobe and in front of it, producing left homonymous lateral 
hemianopsia. 

is on the opposite side to that of the dark field. 1 (See Fig. 140.) de Schweinitz 
has condensed the following rules as to the significance of various forms of hemian- 
opsia from a series prepared by Dr. Seguin: 



jii ' For a complete study of the significance of this difficult subject see the author's Practical Diagnosis, 

fill h flit ion. 



DISEASES OF THE CRANIAL NERVES 



869 



(a) The lesion in hemianopsia is on the opposite side of the dark fields. 

(b) If the preserved fields are accompanied by concentric contraction, the 
smaller half -field will be in the eye opposite to the lesion; contraction of the pre- 
served half-field is most common with lesions of the cortex, but also may occur in 
lesions of the tractus. 

(c) If the hemianopsia is relative, the lesion is probably in the cortex; but cortical 
lesions are not excluded by absolute hemianopsia. 

(d) A lesion confined to the cuneus, or to it and the gray matter immediately 
surrounding it, on the mesial surface of the occipital lobe, produces homonymous 
lateral hemianopsia without motor or sensory symptoms, at least without these 
as a direct consequence of the lesion, although they may appear as indirect or, as 
they are sometimes called, distant symptoms. Slight motor symptoms such as 
deviation of one eye inward may, however, be added to the visual symptoms of a 
lesion in the occipital lobe (Mills) . 

Fig. 140 

LEFT VISUAL FIELD. RIGHT VISUAL FIELD > 

Fixation Point. Fixation Point. 

.nuuiimmnnnn,,,,,,,^ 

Lf Mrs0^?<^ portion 

>0l " 




Diagram illustrating why it is that the lesion is on the opposite side to the dark field. (Oliver.) 



(e) A lesion producing typical hemiplegia, aphasia, if the right side is paralyzed, 
little or no anesthesia, and lateral hemianopsia, is probably due to disease in the 
area supplied by the middle cerebral artery. 

(/) A lesion causing hemiplegia, hemianesthesia, and lateral hemianopsia is 
probably situated in the posterior portion of the internal capsule. 

(g) A lesion causing hemianesthesia, ataxic movements of one-half of the body, 
no distinct hemiplegia, and lateral hemianopsia, could be situated in the posterior 
lateral part of the optic thalamus. 

(h) A lesion causing the symptoms of disease of the base of the brain, associated 
at the same time with changes in the pupil, changes in the nerve head, and lateral 
hemianopsia, could be situated in one optic tract or in the primary optic centres 
on one side. 

(i) Incomplete hemianopsia, assuming usually a quadrant-shaped defect, may 
be present on account of a lesion confined to the lower half of the cuneus. It may 



870 



DISEASES OF THE NERVOUS SYSTEM 



Fig. 141 



also occur with less definite limitations in lesions of the subcortical substance of 
the occipital lobe, and then may be associated with other symptoms, as hemiplegia 
and hemianesthesia. Finally, it may occur from a lesion of the tract, but then 
will be accompanied by other symptoms indicating basal disease, or from a lesion 
of the external geniculate body. 

(j) A hemianopsia in which there is preservation of the light sense, but loss of 
either the color sense or the form sense, indicates that the lesion is in the visual 
centre of the cortex. 

The Third or Oculomotor Nerve. — The third nerve has its origin from groups 
of cells in the floor of the aqueduct of Sylvius. It then passes through the tegmen- 
tum of the crus cerebri, and makes its exit 
in a bundle on the inner side of the crus. 
(Fig. 141; see also Plate XIV.) It then 
passes from the crus to the sphenoidal 
fissure and so into the orbit, where its 
fibres divide and go to supply the ciliary 
muscle, the sphincter of the iris, the super- 
ior rectus, internal rectus, inferior rectus 
and inferior oblique muscle. (See Plate 
XIII.) It also sends fibres to the levator 
palpebral muscle. As it is a motor nerve, 
paralysis follows its injury. The causes 
of disturbance in its function are num- 
erous. They may exist at the base of the 
brain, where the nerve leaves the crus, 
in the sphenoidal fissure, in the orbit, and 
even in its peripheral filaments in the eye 
itself, although change in its functional 
activity in the latter area is usually due to 
the effect of drugs. Of the causes which 
produce disturbance of its function at its 
origin in the crus, we find tuberculous 
meningitis or that due to some acute in- 
fectious disease, abscess of the brain, and 
hemorrhage. For this reason meningitis 
of either form in infancy very frequently 
involves this nerve, and so produces symp- 
toms which call the attention of the phy- 
sician to the existence of the disease at the 
base of the brain. In adults, aside from 
tuberculous meningitis, there may be 
syphilitic exudation, or the nerve itself 
may be inflamed, owing to the presence of 
this same disease. Tumors or abscess at 
the base of the brain may press upon it. 
When the nerve is injured in its passage through the sphenoidal fissure, the cause 
is usually some traumatism which results in fracture of the bone, or very rarely a 
severe blow which damages the nerve by pressure against the bone. In a case 
which came to the writer's attention, a severe blow with the hilt of a sword upon 
the forehead caused paralysis of this nerve, probably in this manner. 

In the orbit a tumor may press upon the nerve fibres. Occasionally the nerve 

loses power through the action of the poison produced by diphtheria or typhoid fever. 

Symptoms. —The dominant symptoms of paralysis of the oculomotor nerve 

are ptosis, mydriasis, and consequent loss of pupillary reaction to light and accommo- 




Showing the nearness of origin of the oculo- 
motor (3), pathetic (4), and abducens (6). 
The roots of these nerves are shown by an 
incision which has divided the fons. 77/, the 
third nerve, arising from several roots. IV, 
the fourth nerve. VI, the sixth nerve, arising 
from three roots. (Modified from Arnold.) 



PLATE XIII 




Showing the Distribution of the Troehlearis, Oculomotor, and 
Trifacial Nerves. (Modified from Rudinger. ) 

1. The troehlearis nerve. 

2, 3, 4, 5, 6, 7. The oculomotor nerve fibres. 
8, 9, 10, 11. The trifacial fibres. 



DISEASES OF THE CRANIAL NERVES 871 

dation. As it supplies the internal rectus, external squint may be present. The 
paralysis of the ocular muscles also results in diplopia. If the patient is directed 
to look upward, downward, or inward he is unable to do so. The inability of the 
pupil to contract when light is thrown into the eye may be due to a lesion of the nerve 
before it enters the orbit, or, as already stated, to the action of a drug upon its 
peripheral filaments. It will be remembered that pupillary contraction, when 
produced by the entrance of light into the eye, is due to a reflex impulse which passes 
along the optic nerve to the neighborhood of the corpora quadrigemina, thence to the 
third nucleus and along the fibres of the third nerve to the ciliary ganglion, from 
which, by way of the ciliary nerves, it goes to the iris and causes contraction of 
its circular muscular fibres. A lesion in any portion of this reflex arc interferes with 
pupillary reaction. In addition to those injuries of the oculomotor nerve already 
mentioned which cause paralysis, a loss of pupillary reaction may occur in locomotor 
ataxia, in multiple sclerosis, in general paresis, in bulbar palsy, and in myelitis when 
that disease involves the fibres of the arc. When these diseases are responsible 
for the loss of pupillary reaction, the lesion is supposed to exist, in the majority 
of instances, in fibres which connect the optic tracts in front of the corpora quad- 
rigemina with the oculomotor nuclei. When drugs produce paralytic mydriasis, 
their action is usually exercised upon the peripheral ends of the nerve. 

Diagnosis. — The diagnosis of paralysis of the oculomotor nerve is readily made 
if the symptoms just described are kept in mind. • 

Prognosis. — The prognosis depends upon the underlying cause of the paralysis. 
In diphtheria and typhoid fever recovery usually takes place, and unless the damage 
produced by an injury is very great, the outlook is favorable. On the other hand, 
if the cause is tuberculous meningitis, tumor, or abscess, or any one of the progresive 
nerve diseases just named, recovery is, of course, impossible. 

The Fourth or Trochlearis Nerve. — This nerve supplies the superior oblique 
muscle of the eye (1, Plate XIII). Interference with the action of this nerve is 
not uncommon and is rarely recognized by the general practitioner. The symptoms 
are not developed until the eye is tested by means of placing a colored glass over 
one eye, when it will be found that the object which is placed before the patient 
stands in its normal position as seen by the normal eye, but is displayed outward 
and obliquely when seen by the eye supplied by the impaired pathetic nerve. 
As the nerve arises from an area almost identical with that of the third nerve, the 
centric causes of trochlearis paralysis are practically identical with the causes of 
oculomotor paralysis. It is important to remember that, should paralysis of the 
fourth nerve be present without involvement of the third or sixth nerve, it probably 
indicates a growth in the cerebellum or an inflammatory exudate upon the under 
surface of its middle lobe. 

The Fifth or Trifacial Nerve. — The trifacial nerve contains motor and sensory 
fibres, the sensory fibres being by far the more numerous. The motor fibres have 
their origin in the pons, a little above its middle, receiving also the root descending 
from the midbrain; they pass out in a bundle separate from the sensory fibres until, 
outside the cranial cavity, they take part in forming the inferior maxillary division 
of the nerve, through which they supply the muscles of mastication. 

The sensory fibres of the fifth nerve arise from a nucleus at about the middle 
of the pons, and, in addition, by the spinal root, from a chain of cells descending 
through the medulla as far as the first cervical segment of the cord; they emerge 
from the pons in a heavy trunk, which passes to the Gasserian ganglion (8, Plate 
XIII) and then, beyond the ganglion, divides into three branches: ophthalmic 
(9), superior (10), and inferior maxillary (11). In addition to providing sensation 
to the greater portion of the face, it also supplies the anterior two-thirds of the tongue. 

Symptoms. — When the fifth or trifacial nerve is paralyzed in its motor fibres, 
the patient is unable to contract his masseter muscles and there is dropping of the 



872 DISEASES OF THE NERVOUS SYSTEM 

lower jaw. Unless the paralysis is bilateral, however, it may not be easily dis- 
covered, since the muscles on the unaffected side may hold the jaw in position. 
And, moreover, if the lesion be in the brain the function of mastication is maintained 
from the other side by bilateral innervation. In some instances of paralysis of the 
fifth nerve, deafness arises as the result of interference with the function of the 
tensor tympani muscle, for a small branch from the motor fibres of the fifth nerve 
passes through the otic ganglion and supplies this muscle. When this muscle is 
paralyzed, the tympanic membrane is relaxed and this interferes with its function. 
Motor paralysis of the fifth nerve is rarely met with. Certain poisons like gelsem- 
ium may cause dropping of the jaw by paralyzing the muscles of both sides. When 
the sensory portion of the nerve is affected there is anesthesia of the skin of the face 
in the areas supplied by the particular branches affected. 

If the area be that of the forehead, the upper eyelid, the conjunctiva, and the 
nostril, the ophthalmic branch of the fifth nerve is at fault, and the lesion is probably 
at the sphenoidal fissure or within the orbit, reflex winking of the eye no longer takes 
place because the conjunctiva is anesthetic, and for the same reason a flow of tears 
does not occur upon irritating the conjunctiva, because the lachrymal reflex is 
abolished. 

If the skin of the upper part of the face is anesthetic, the superior maxillary 
branch is involved; and if the skin of the temporal region and that of the jaw and 
the under lip are anesthetic, the inferior maxillary branch is diseased. When 
both of these branches are paralyzed there is probably a tumor of the superior 
maxillary bone; and if the entire area of the three branches is anesthetic, the 
Gasserian ganglion may be the part affected, and this will be accompanied by trophic 
changes in the anesthetic parts. The most common cause of anesthesia of the 
trifacial is, however, neuritis. 

Romberg makes the following differential statement : 

(a) The more the anesthesia is confined to single filaments of the trigeminus, 
the more peripheral the seat of the cause will be found to be. 

(6) If the loss of sensation affects a portion of the facial surface, together with the 
corresponding f aucial membrane, the disease may be assumed to involve the sensory 
fibres of the fifth pair before they separate to be distributed to their respective 
destinations; in other words, a main division must be affected before or after its 
passage through the cranium. 

(c) When the entire sensory tract of the fifth nerve has lost its power, and there 
are at the same time derangements of the nutritive functions in the affected parts, 
the Gasserian ganglion, or the nerve in its immediate vicinity, is the seat of the 
disease. 

(d) If the anesthesia of the fifth nerve is complicated with disturbed functions 
of adjacent cerebral nerves, it may be assumed that the cause is seated at the base 
of the brain. 

When the fifth nerve is paralyzed the mucous membrane of the nose and mouth 
are also anesthetic and usually dry. The sense of taste is lost and trophic lesions may 
develop, although it is questionable as to whether these depend upon affection of 
the sensory fibres. These lesions consist in ulceration of the cornea, loosening of 
the teeth, atrophy of the gums, and the development of herpes zoster. As the sensation 
in the anterior two-thirds of the tongue is impaired, this organ is often damaged by 
the teeth. The dryness of the mucous membrane of the nose also interferes with the 
sense of smell, and irritating substances may be inhaled through the nostrils without 
pain, because of the lack of sensation in the nasal mucous membrane. Paralysis 
of this uerve is, however, very rarely met with. 

In the great majority of instances in which a physician is called on to treat a 
lesion of the trifacial nerve, the patient complains of severe neuralgic pain, which 
in most cases arises from the Gasserian ganglion (8, Plate XIII). When trophic 



PLATE XIV 




Base of Brain, showing the Superficial Origin of the Cranial 

Nerves. 



The Roman numerals refer to the twelve cranial nerves. 



DISEASES OF THE CRANIAL NERVES 873 

changes are very well marked, they result in hemiatrophy of the face. In those 
cases in which the motor fibres of the fifth nerve are irritated, there may be lockjaw 
as in true tetanus, and so-called masseter spasm may have a reflex origin because 
of the presence of dental irritation. 

Paralysis of the Sixth Abducens Nerve. — The sixth nerve has its origin from 
cells in the floor of the fourth ventricle, passes through the pons, and makes its 
exit in the groove between the pons and the medulla (Plate XIV), whence it passes 
through the sphenoidal fissure. It is subject to the same lesions at the base of the 
brain as is the oculomotor nerve, such as tuberculous meningitis and syphilitic 
exudation, tumor and fracture of the base of the skull. Injury may occur to it in 
the sphenoidal fissure. The sixth nerve supplies the external rectus and its paralysis 
thus causes internal squint, the patient being unable to rotate the eye outward. 

The exact lesion which produces paralysis of the sixth nerve can only be deter- 
mined by a study of the associated symptoms. In those cases in which there is 
facial palsy on the same side as the squint, and paralysis of the arm and leg upon 
the opposite side, in other words, "crossed hemiplegia," the lesion is in the pons 
or at the base of the brain in such a position that it produces pressure on the pons 
on one side and above its lower third. 

Disturbances of Motility in the Ocular Muscles Depending on the Third, Fourth, 
and Sixth Nerves. — The movements of the eyeballs depend, of course, upon the 
associated action of different muscles supplied by different nerves. When the 
axes of the eyeballs converge, they do so by the action of the internal recti muscles 
supplied by the third nerve, and when they diverge they move in these directions 
by the external recti supplied by the sixth nerve. If, however, there is conjugate 
deviation, then a much more complicated nervous mechanism is brought into play, 
for if the axis of each eyeball is turned to the right, for example, this motion is 
made by contraction of the external rectus of the right eye and the internal rectus 
of the left eye, each being supplied by different nerves, the right sixth and the left 
third, and yet it is essential that they shall act in accord. This is accomplished 
by the presence of association fibres which, by joining together the nuclei of the 
nerves, enable them to act in unison. If by disease these association fibres are 
destroyed (in the posterior longitudinal bundle), conjugate deviation of the eyes 
becomes impossible. When the eyeballs are deviated by reflex action, the pathway 
of the nervous impulse is through the optic nerve by connecting fibres to the motor 
nuclei of those nerves governing the ocular movements, which not only join the 
nuclei of the different nerves of one side, but connect them with the nuclei of the 
opposite side as well. When they are moved by voluntary action, the impulse 
leaves the motor centres in the anterior part of the motor area of the cortex, and 
thence passes down through the anterior part of the knee of the internal capsule, 
thence through the crus cerebri, and finally crosses in the raphe, passing to the 
nuclei of the oculomotor nerves and of the fourth and sixth nerves. When the 
impulse for conjugate deviation arises in the motor cortex, it passes first to the 
nucleus of the opposite sixth nerve, and thence is sent along the association fibres 
through the posterior longitudinal bundle to the nucleus of the third nerve on the 
opposite side, just as it is in reflex deviation. When a nervous explosion takes place 
in the motor cortex, as in cases of epilepsy, it often happens that there is conjugate 
deviation of the eyes away from the side on which the lesion exists, and, conversely, 
if the ocular centres in the cortex are destroyed, there is conjugate deviation of the 
eyes toward the side on which the lesion exists. This has given rise to the state- 
ment that in the coma of ordinary apoplexy the patient " looks toward his lesion" 
at least in those instances in which an apoplexy destroys these centres. (See 
Apoplexy.) 

There as two states which give rise to an erroneous diagnosis in connection with 
these symptoms, namely, "rheumatic palsy" of the ocular muscles, which disappears 



874 DISEASES OF THE NERVOUS SYSTEM 

under the free use of the iodides and salicylates, and so-called "recurrent oculomotor 
paralysis," which is probably the result of congestion and edema, and which is 
accompanied by sick stomach, diplopia and fever. 

Ophthalmoplegia or Paralysis of the Internal and External Muscles 
of the Eyeball. — This condition depends not upon disorder of function of any 
single cranial nerve, but upon interference with the action of the third, fourth, and 
sixth nerves. As already stated, the third nerve supplies the ciliary muscle, the 
circular fibres of the iris, the superior rectus, internal rectus, inferior rectus, inferior 
oblique, and the levator palpebral. The fourth nerve supplies the superior oblique, 
and the sixth the external rectus. When morbid changes take place in the nuclei 
of these nerves the normal co-ordinated movements of the eye are impaired or 
lost, that is to say, ophthalmoplegia is developed. 

Fig. 142 




Patient suffering from chronic ophthalmoplegia externa. The wrinkling of the forehead in the effort to 
open the eyes is noticeable. The external strabismus can be seen. (Starr.) 

Ophthalmoplegia is of two forms: ophthalmoplegia externa, when the paralysis 
affects the external muscles of the eyeball and the levator papebrse; and ophthal- 
moplegia interna, when only the pupillary and ciliary muscles are involved. Oph- 
thalmoplegia interna is quite rare, although a modified form of it occurs in that state 
called the Argyll-Robertson pupil, a condition in which the pupil reacts to accommo- 
dation, but not to light. In this condition the lesion exists not in the nuclei of the 
nerves, for if it did there would be no reaction to accommodation, but in the associa- 
tion fibres, whereby the reflex pathway is destroyed. Ophthalmoplegia externa, 
on the other hand, is by no means uncommon. It is a condition depending upon 
a centric lesion, and occurs in an acute and chronic form (see below). Because of 
the fact that the lesion is centric it is usually bilateral, and if all the muscles are 
paralyzed it is. said to be complete external ophthalmoplegia, while, on the other 
hand, if they are simply impaired in function, or if one nerve escapes while the others 
are involved, it is spoken of as partial (Fig. 142). 

Etiology and Pathology. — Ophthalmoplegia is due to a large number of causes, 
such as tumors, areas of degeneration, or inflammatory exudations, where the 
nerves take their exit at the base of the brain. (See Plate XIV.) The additional 
causes are small hemorrhagic extravasations, arteritis, thrombosis, or embolism 
of the small vessels which supply the nuclei of these nerves. In some cases the 



PLATE XV 




Showing Exit of Facial Nerve ( 1 ) from Stylomastoid Foramen and 
its Distribution to the Muscles of the Face. (Rudinger. ) 



DISEASES OF THE CRANIAL NERVES 875 

lesions resemble those of acute poliomyelitis, and belong to the affection called by 
Wernicke " polio-encephalitis superior." 

Symptoms. — The symptoms of ophthalmoplegia externa vary, of course, with the 
nerves which are affected and with the severity of the lesions. When the morbid 
process is severe, there is not only loss of power in the ocular muscles, but in other 
parts as well, so that the symptom-complex of bulbar paralysis may be present; 
or if the tracts to and from the higher areas of the brain are involved, such symptoms 
as hemianesthesia, hemiplegia, or hemiataxia may be present. The pathological 
processes just described are varied not only as to cause and situation, but as to 
acuteness as well. The acute form is ushered in by a train of symptoms which 
necessarily arise when areas of the nervous system so important to life are affected. 
Thus, the patient suffers from vertigo, headache, vomiting, and even coma. Uncon- 
sciousness may last for several days and end in death, or, after a period of a week 
or ten days, consciousness gradually returns and the symptoms connected with 
the eyes alone remain. These consist in double ptosis and various palsies of the 
ocular muscles, or total ophthalmoplegia. The chronic form arises when the nervous 
lesions are gradual in onset, although it may result from the acute type just dis- 
cussed. Here again the degree, of the paralysis depends upon the severity of the 
lesions. In one case a total palsy may be present, in another a partial palsy, and 
in still a third the palsy may be progressive, one muscle after another failing. 
Sometimes one muscle improves as another fails. Ptosis and other forms of ocular 
palsy may be a part of the transient and recurrent paralysis in myasthenia gravis. 
The prognosis depends upon the cause. If syphilis is a factor the outlook is favor- 
able as compared to that type which is due to disseminated sclerosis or bulbar 
palsy. In no case is the outlook anything but grave as to recovery, although 
about one-half of the mild cases recover. 

The treatment also varies with the cause, and yet it may be said that, be the 
cause what it may, the only drugs which offer any promise of relief in the chronic 
form are mercury and the iodides. Hot baths may be useful. 

In the acute form freedom from any cause of excitement, the application of cold 
to the head, and the use of aconite to quiet the circulation, if it is excited, may be 
of some value. 

The Seventh or Facial Nerve. — The nucleus of the facial nerve is found in the 
lower part of the pons. From this nucleus its fibres pass upward and backward 
to the floor of the fourth ventricle, where they make a sharp turn inward and 
forward about the nucleus of the sixth nerve, and finally make their exit between the 
pons and the medulla (Plate XIV) near the eight nerve. Aiter leaving the pons 
the seventh nerve passes into the internal auditory foramen of the petrous portion 
of the temporal bone, and after passing through the aqueduct of Fallopius emerges 
from the stylomastoid foramen upon the surface near the lobe of the ear. (See 
Plate XV.) At this point it is divided into many branches which supply the muscles 
of the face with motor impulses. (See Plate XV.) Upon the fibres of the facial 
nerve just as it enters the auditory foramen a ganglion occurs, commonly called 
the geniculate ganglion. This ganglion consists of an aggregation of cell bodies 
connected with sensory fibres from the chorda tympani nerve, which is a nerve of 
sensation and is concerned with the special sense of taste. The fibres of this nerve 
do not, however, remain in contact with those of the facial, but leave it at once, 
and by way of the Vidian, or superficial petrosal nerve, pass to the superior maxillary 
branch of the trifacial. In addition to these sensory fibres of the chorda tympani, 
the facial nerve also has associated with it the nerve of Wrisberg, which is probably 
sensory in function, and which lies by the side of the facial nerve as its fibres pass 
from the pons to the auditory foramen, where the ganglion of the chorda tympani 
just named exists. The fibres of the nerve of Wrisberg then pass to the nucleus 
of the glossopharyngeal nerve. 



876 DISEASES OF THE NERVOUS SYSTEM 

Etiology. — Interference with the function of the facial nerve arises from many 
causes, of which the chief and most frequent are injuries in its course after it leaves 
the pons. These may be called peripheral lesions, and when the paralysis is per- 
ipheral it is called Bell's palsy. Thus, it not infrequently happens that a child 
is born with facial palsy, which is usually due to injury to the nerve during labor, as 
by the pressure of forceps. So, too, facial paralysis is sometimes seen in children 
and in adults as a result of a severe blow at the lower part of the ear, or of an attack 
of mumps in which the inflammation and swelling has been severe. Tumors of 
the neck and inflammation in the middle ear also may cause facial palsy in this 
manner. 

In adults facial palsy is often due to an inflammation in the stylomastoid foramen 
as the result of exposure. It is thought by some that this takes place in certain 
individuals by reason of the fact that this foramen is so small that very slight 
swelling causes pressure on the nerve and ablation of its function. It is this type 
of paralysis following exposure to cold which has given rise to the belief among 
certain ignorant persons that it is possible to be " moon-struck," because a person 
has slept out-of-doors in the moonlight and has developed facial palsy afterward. 
The real cause is, of course, the exposure to cold, and not the influence of the moon. 
That cold cannot always be the cause of this particular form of facial palsy is, how- 
ever, evident from the fact that the condition is no more frequent in winter than 
in summer. Most commonly it is due to an acute otitis media. 

More serious causes of facial palsy are disease processes inside the skull which 
press upon the nerve before it passes through the aqueduct of Fallopius. These 
conditions are tumor, inflammatory processes at the base of the brain, most com- 
monly arising from injury, syphilis, or tuberculosis, and occasionally one of the 
acute infectious diseases. So, too, a fracture of the base of the skull may produce 
facial paralysis. Facial palsy due to a lesion in the pons is exceedingly rare as a 
single symptom, as is also facial palsy due to a lesion in the cortex. On the other 
hand, facial paralysis is usually present in cases of hemiplegia, but in hemiplegia 
the upper part of the face escapes the paralysis, being innervated from both hemi- 
spheres of the brain. 

The pathological changes which take place in the facial nerve in cases of facial 
paralysis depend, of course, upon the situation of the lesion. If the lesion occurs 
in the nucleus of the nerve, or involves its fibres in such a way that it fails to 
receive its normal trophic impulses, degenerative changes at once ensue, the neuritis 
being of the so-called parenchymatous type. 

Symptoms. — The symptoms of facial paralysis are very characteristic. The 
paralysis is nearly always unilateral and often total, in the sense that all the muscles 
upon one side of the face are impaired in function. It sometimes happens, however, 
that the muscles of the forehead partly escape. Because of the paralysis of the 
muscles of one side of the face the patient is unable to wrinkle the brow upon one 
side, and is not able to close the lids, either as a reflex act, as in winking, or by 
volition. The corner of the mouth on the paralyzed side is drooped, and if the 
patient attempts to smile only one-half of his visage is wrinkled. The nasolabial 
fold is obliterated on the paralyzed side and is usually accentuated on the normal 
side as a result of the contraction of the muscles which are no longer counter-balanced 
by opposing muscles. The condition is not painful. If recovery does not promptly 
ensue the reactions of degeneration speedily develop in the paralyzed muscles, 
and there may be contractures in them. 

Diagnosis. The manifest paralysis of the muscles of one side of the face, which 
is particularly noticeable when the patient attempts to smile or frown, renders the 
diagnosis of facial palsy easy and the symptoms which the patient presents can, 
moreover, be used very successfully in many cases in determining the site of the 
lesion. Thus, in some cases of facial paralysis the sense of taste is modified or lost 



DISEASES OF THE CRANIAL NERVES 877 

upon the anterior two-thirds of the tongue on the side affected. If this symptom 
is present, it indicates that the lesion is one which involves the facial nerve between 
the geniculate ganglion and the point a quarter of an inch above the stylomastoid 
orifice, where the chorda tympani fibres leave it; or, to put the proposition reversely, 
if loss of taste does not accompany a facial palsy the lesion is either in the stylo- 
mastoid foramen within a quarter of an inch of the orifice or it may involve the 
nerve before it enters the bone. So, too, if there is. unusual sharpness of hearing 
with some buzzing in the ear, this also is an indication of a lesion near the pons 
or in the Fallopian canal, since it is due to paralysis of the stapedius muscle which is 
supplied by the stapedius nerve. If deafness and vertigo are present it is probable 
that the condition is due to middle-ear disease or to some lesion which also involves 
the auditory nerve at the base of the brain. A study of the electrical reaction of the 
paralyzed muscles is also of great value for the purpose of localizing the lesions. 
Thus, if the lesion exists in the stylomastoid foramen, the muscles of the face are 
cut off from the trophic impulses which they normally receive from their nuclei in 
the pons, and as a result the reaction of degeneration speedily develops and may 
become complete; whereas, on the other hand, if the lesion which causes paralysis 
is situated in the motor tract above the nucleus of the facial nerve, or, in other words, 
if it involves the fibres which descend from the motor area of the cortex, the reaction 
of degeneration does not develop because the muscles still receive trophic impulses. 
Further than this, in these cases the paralysis is never so complete as in the periph- 
eral type, the patient usually being able to wink and to wrinkle the forehead, 
the muscles of the forehead frequently escaping. Centric facial paralysis is, how- 
ever, exceedingly rare unless associated with other symptoms, as already stated. 
In those rare instances in which the facial paralysis arises from damage to the 
nucleus of the facial nerve in the pons, there are other symptoms of a pontile lesion 
producing in some instances, a crossed hemiplegia, as already described, an asso- 
ciated paralysis of the sixth nerve, or the symptoms of ordinary bulbar paralysis. 
In these cases, too, reactions of degeneration speedily develop. 

Prognosis. — The prognosis in cases of facial paralysis varies, of course, with the 
situation of the lesion and with its severity. The majority of instances get well 
because they have their origin in an inflammatory process in the stylomastoid 
foramen. The outlook when the lesions are back of the stylomastoid foramen 
are not so favorable, and when the nucleus of the nerve or the motor area of the 
cortex is diseased, the prognosis is, of course, very doubtful as to recovery of power 
in the muscles of the face. 

Treatment. — The treatment of paralysis of the seventh nerve depends somewhat 
upon the lesion which produces it. For the relief of that form which is due to 
inflammation in the stylomastoid foramen, it is customary to administer mild 
alteratives, such as small doses of the iodide of potassium or sodium, in order to 
hurry the absorption of the inflammatory exudate. It is also advisable to apply a 
small blister, about the size of a postage stamp, immediately in front of the ear for 
its counter-irritant effect. In those cases in which there is a gouty or rheumatic 
diathesis, the best results are often obtained by the use of the salicylates in moder- 
ately large doses, 10 to 15 grains three or four times a day, or 10 drops of wine of 
colchicum root and 10 grains of iodide of strontium may be administered three times 
a day. The use of electricity for the purpose of maintaining the nutrition of the 
facial muscles in any case of peripheral facial palsy is not only futile, but may be 
harmful, for the cause of the muscular wasting is lack of trophic impulse, and as 
these impulses cannot reach the muscle, it is speedily exhausted if stimulated 
by the electrical current, when deprived of its ordinary means of recuperation. 
If middle-ear disease is present, it must, of course, be treated by those measures 
which are commonly employed by aurists. In cases where the lesion is centric, 
counter-irritation is useless. The only hope is that nature aided by alterative 



878 DISEASES OF THE NERVOUS SYSTEM 

drugs, such as the iodides, may cause an absorption of the results of the local 
inflammatory process. Where the lesion is severe enough to have destroyed the 
nerve cells, treatment is also useless. 

Facial Spasm. — Facial spasm due to irritation of the facial nerve is a frequent 
affection. It may be general or localized in one or two muscles. When the orbicu- 
laris palpebrarum is affected, the condition is called "blepharospasm." As a rule, 
the muscles about the mouth are also affected. When this is the case, the condition 
is called one of " blepharof acial spasm." To this condition the French term "tic 
convulsif" is sometimes applied. The cause of facial spasm is unknown. It 
sometimes develops in nervous individuals as a result of a severe nervous shock. 
In some instances it seems to partake of the nature of a habit spasm, and in these 
cases not infrequently a lightning-like contraction of the muscles of the face takes 
place. Sometimes in addition to facial spasm there is also torticollis. Very rarely 
facial spasm is due to an irritating focus in the motor area of the face in the cortex, 
and sometimes it is the early or first symptom of an oncoming epileptic seizure. 
In ordinary facial spasm the muscles are not persistently contracted, but suffer 
from twitchings which come on in paroxysms, or which occur singly at varying 
intervals. 

The prognosis in a case of this kind is not very favorable, although, as a rule, 
there is no organic lesion to maintain it. 

The treatment of facial spasm consists in a careful investigation to determine 
if there is any localized focus which gives rise to reflex irritation, as, for example 
disease of the middle ear. ■ If such an area is found, it should of course be removed. 
In some instances a hyperesthetic spot in the nasal mucous membrane may be 
discovered. If no such local area of irritation can be found, there is little left for 
the physician to do except to administer nervous sedatives, such as the bromides, 
chloral, and cannabis indica, but these in turn rarely do good in this annoying, 
harmless, but persistent condition. In young persons who have a tendency to 
facial spasm as a result of habit, a powerful mental impression may aid in breaking 
up the habit, particularly if there is a tendency to hysterical manifestations. 

The Eighth or Auditory Nerve. — Disease of the auditory nerve may result in 
deafness, tinnitus, vertigo, and loss of equilibrium. 

When deafness is due to disease of this nerve it commonly arises from some 
degenerative change, which in turn may be due to the effect of an infectious disease. 
In other instances the deafness is due to a congenital defect, but in still others it 
occurs as a part of the course of locomotor ataxia, disseminated sclerosis, or general 
paralysis of the insane. More rarely it arises from a tumor of the brain or from 
cerebral syphilis. In deafness due to these causes the so-called cochlear fibres of 
the auditory nerve are involved. The condition may be differentiated from that 
form of deafness which is due to disease of the middle ear, the peripheral fibres of the 
auditory nerve not being affected, and by the fact that the latter class of patients 
possess the power of perceiving sound transmitted through the bones of the head. 
Thus, if a tuning-fork is placed against the head, or the teeth, the patient can 
perceive the sounds which it generates if the deafness is due to a peripheral cause, 
which produces interference with aerial sound conduction in the external or middle 
ear, but he cannot perceive its sound if the deafness is due to a centric cause, such 
as a lesion of the cochlea of the internal ear, or of the auditory nerve trunk, or of the 
auditory pathway to the cortex. Again, in those cases of disease of the auditory 
nerve of a centric character, the patient does not find it easy to hear in the presence 
of loud Qoises, as he often does in cases of deafness due to a peripheral lesion. 

The prognosis in deafness due to centric disease of the auditory nerve is very bad. 

When tinnitus is present, it arises as the result of irritation of the cochlear portion 
of the auditory nerve which supplies the organ of Corti in the internal ear, or of 
those fibres which pass from this organ in the nerve trunk itself. The sound may 



DISEASES OF THE CRANIAL NERVES 879 

vary from a slight buzzing to a roaring, ringing, or explosive noise which may be 
so severe as to be insufferable. Suicide is sometimes threatened by persons who 
are not only persecuted by these noises during the day, but are unable to sleep by 
night from the same cause. Little can be done for many of these cases. In those 
instances in which tinnitus arises from middle-ear disease or from anemia or from 
the use of drugs, such as quinine and salicylic acid, the condition can often be 
relieved, as it depends upon an irritation and not upon an actual lesion, as a 
rule. 

The treatment depends upon the cause of the tinnitus. If it is due to an actual 
lesion of the internal ear the prognosis is bad and treatment is futile. If it is due to 
gout, anemia, or similar causes, the prognosis is fairly good. 

Vertigo is a condition in which the patient loses the sense of his normal relation 
to surrounding objects. In some instances he seems to be whirled about in space. 
In other instances he seems to remain stationary, while other objects are whirled 
about him. As the patient's conception of his relation to surrounding objects is 
disturbed, he frequently falls, since this conception has much to do with the motor 
impulses by which he controls his muscles in connection with the function of muscle 
sense. The cause of vertigo may be a functional disorder of the branches of the 
auditory nerve which supply the vestibular portion of the internal ear, as when it 
occurs in the course of indigestion (autotoxemia) or under the influence of a drug 
such as quinine, or it may be due to actual lesions in connection with these nerve 
fibres such as hemorrhages into the internal ear, or other damage to the semi- 
circular canals. Sometimes also it seems to be due to reflex irritation produced 
by disease in the middle ear or in the external meatus. In other instances the 
presence of a foreign body in the meatus produces vertigo. When vertigo is severe, 
there may be associated with it great nausea and vomiting, palpitation of the heart, 
profuse sweating, a sense of approaching syncope, and even collapse. The respira- 
tions may be rapid. These symptoms are in part doubtless due to the mental 
distress or fright from which the patient suffers. There is probably no symptom 
which causes so much fright and which is so rarely followed by death as severe 
vertigo. Nothing but the awful apprehension of true angina pectoris approaches 
the mental distress of the patient who suffers from this condition in its well-devel- 
oped form. 

One form of vertigo arising as the result of disease of the internal ear is called 
Meniere's disease. It is usually severe in its nature. Its onset is sometimes sudden, 
the patient being seized with prostration, pallor, vomiting, roaring in the ears, and 
deafness immediately after hearing a loud report which has not, of course, arisen 
from any extraneous source. This form of vertigo is supposed to be due to a 
hemorrhage in the semicircular canals, and resembles in its onset an apoplectic 
stroke, but it is not characterized by paralysis. In some instances it seems to 
depend upon arteriocapillary fibrosis. It may or may not be associated with 
absolute deafness. In the majority of cases the patient suffers from recurrent 
attacks, but as the disease progresses the attacks last longer and longer, and finally 
he not uncommonly has constant vertigo. 

The prognosis in cases of vertigo depends entirely upon the cause of the disorder. 
If it is due to an organic disease, unless that disease exists in the middle or external 
ear and is removable, the outlook is serious. Indeed, the condition may be con- 
sidered incurable if an actual organic and centric lesion is its cause. 

In Meniere's disease the treatment consists in rest in bed, the use of an ice-bag 
on the head, or blister behind the ear, and the employment of large doses of nervous 
sedatives, such as the bromides and chloral. Certain practitioners claim to have 
obtained good results from the administration of large doses of quinine, but it is 
difficult to see how this drug can do good under these circumstances. Indeed, 
one would expect it to make the condition much worse. Babinski claims to have 



880 DISEASES OF THE NERVOUS SYSTEM 

had good results following lumbar puncture, with the withdrawal of a few cubic 
centimetres of cerebrospinal fluid. 

Vertigo which is due to auto-intoxication arising from an abnormal state of the 
bowels or kidneys should be treated by the administration of diuretics, cholagogues, 
purgatives, and free sweatings. 

The Ninth or Glossopharyngeal Nerve. — The ninth nerve is the nerve of sen- 
sation of the pharynx, the palate, and the middle ear. It is also probably connected 
with the special sense of taste in the posterior third of the tongue, although it is 
considered by some physiologists that those fibres which are connected with this 
function join the glossopharyngeal fibres from the fifth nerve. Some of its sensory 
fibres enter the medulla oblongata near the olivary body and terminate in the 
gray matter on the floor of the fourth ventricle, while another set of fibres ends in 
the subtantia gelatinosa. From the latter point some of its fibres ascend into the 
brain. In addition to its sensory function it also contains motor fibres which spring 
from cells known as the nucleus ambiguus. These fibres make their exit from the 
side of the medulla back of the olivary body, and escape from the skull through 
the jugular foramen. The motor fibres supply the muscles of the larynx, the 
esophagus, and pharynx, and are also connected with the function of respiration, 
deglutition, and phonation. 

Paralysis of the glossopharyngeal nerve is exceedingly rare, and therefore we 
possess but little information, either clinical or pathological, concerning its condition 
in disease. Should the nerve itself be damaged, the symptoms consist in loss of 
sensation in the upper half of the pharynx, loss of the sense of taste on the posterior 
half of the tongue, and difficulty in swallowing because of paralysis of the pharyngeal 
muscles and because of the loss of reflex irritability of the mucous membrane of the 
pharynx. Such a condition sometimes develops during postdiphtheritic paralysis. 
When lesions of the nuclei of this nerve take place, the symptoms are practically 
those of bulbar paralysis (which see). 

The Tenth or Vagus Nerve. — This nerve, sometimes called the pneumogastric 
nerve, is composed of both sensory and motor fibres. The sensory fibres pass 
upward from the various portions of the body which they supply and enter two 
ganglia, one of which, the upper, is large and oval, and the other is long and irregular 
in outline. After leaving these ganglia the fibres pass to the medulla, some of them 
terminating in the gray matter which exists in the floor of the fourth ventricle, 
thereby forming the sensory centres connected with respiration and the heart. 
Other of these fibres join the ninth nerve and end in the substantia gelatinosa and 
from this point new fibres ascend to the brain. Those fibres of the pneumogastric 
which are motor in function take their origin from the cells of the nucleus ambiguus 
and escape from the side of the medulla, forming the main trunk of the nerve. The 
distribution of the afferent and efferent fibres of this nerve is well shown in Plate XVI. 

The tenth nerve has a far larger distribution than any other cranial nerve, supply- 
ing the pharynx, the larynx, the heart, the lungs, esophagus, stomach, and intestines, 
and even the external ear through an auricular branch. According to some physi- 
ologists it is the chief motor supply of the palate. It joins the glossopharyngeal 
or ninth nerve, and certain sympathetic nerve fibres, in the formation of the pharyn- 
geal plexus which supplies the pharyngeal muscles. 

The superior laryngeal branch supplies the cricothyroid muscle, the thyroepiglottic 
and aryepiglottic muscles, and the inferior laryngeal branch, sometimes called the 
recurrent laryngeal, supplies the other laryngeal muscles. By means of the sensory 
fibres which exist in the superior laryngeal nerve, the mucous membrane of the 
epiglottis possesses sensation, and by means of those sensory fibres which exist in 
the recurrent laryngeal the mucous membrane below the vocal cords is supplied 
with sensory filaments. If the sensory fibres in the superior laryngeal nerve are 
stimulated, the respirations become slower and deeper, or they may be arrested as 



PLATE XVI 




The Vagus and Sympathetic Fibres of the Right Side and Their 
Anastomoses. (Modified from Rtidinger.) 

1, origin of vagus; 2, anastomosis with sympathetic; 3, superior laryngeal and pharyngeal plexus; 
4, the pulmonary plexus; 5, the inferior cardiac fibres, with sympathetic fibres; 6, the oesophageal plexus. 
The course of the optic nerve (7), the oculomotor (8), the trochlearis (9), the abducens (10), and the facial 
(11) are also shown. 



DISEASES OF THE CRANIAL NERVES 881 

the result of a reflex impulse which passes to the centre in the medulla. Closure 
of the glottis may also be produced in this manner. 

The pulmonary branches of the vagus contain motor fibres which supply the 
unstriated muscles of the bronchi, and sensory fibres for the mucous membrane of 
the bronchi. They apparently also contain fibres centripetal in character, which 
when stimulated diminish the inhibitory action of the pneumogastric nerve upon 
the Jieart, thereby producing tachycardia. Those branches of the vagus which 
supply the esophagus innervate its muscles, on the one hand, and supply its mucous 
membrane with sensory filaments on the other; while those which pass to the 
stomach contain not only fibres which govern its mucles, but also other fibres which 
control its secretion and its blood supply. The same facts hold true of those fibres 
which pass to the intestines. Last, but by no means least, the pneumogastric 
sends fibres to the heart, and through these pathways an inhibitory action is 
exercised which if stimulated may temporarily arrest the heart in diastole. 

Not only is the pneumogastric nerve of very great importance because of the 
multiple functions which it possesses, but it is also of great importance to the 
clinician because it not infrequently suffers from disease. Though it is rarely 
the victim of primary neuritis, cases of rheumatic neuritis of both recurrent laryn- 
geal nerves have been reported, and instances in which this nerve has been involved 
in cases of multiple neuritis due to poison, such as alcohol, for example, are by no 
means rare. So, too, it sometimes suffers in diphtheritic paralysis, and from 
neuritis arising from the poisons of various infectious diseases such as typhoid 
fever, pneumonia, scarlet fever, malaria, and influenza, from tumors and inflamma- 
tion in the mediastinum, disease of the jugular vein, tuberculosis of the mediastinal 
glands, and from pressure upon the nerve exercised by reason of dilatation of the 
left auricle in cases of mitral stenosis. In those instances in which the centres of 
the pneumogastric nerves are affected by disease, we find that tumors, hemorrhagic 
extravasations, the lesions of locomotor ataxia, and disseminated sclerosis are the 
causes. In still other instances the disorder of the function of this nerve develops 
as the result of bulbar paralysis. Cases are also on record in which the fibres of 
the nerve outside of the medulla have been pressed upon by tumors, by the exuda- 
tions due to meningitis, hemorrhages, and by bone disease. 

The symptoms of disorder of the function of the vagus nerve are, of course, very 
varied. If the lesion exists at the base of the brain it nearly always happens 
that there is paralysis of the other cranial nerves, particularly of the ninth, eleventh, 
and twelfth. In such a case if the fibres on one side alone are affected, there is 
unilateral paralysis of the fauces, the palate, and the larynx. The speech is nasal, 
and the act of swallowing may be impaired. There is also interference with the 
action of the vocal cords. If the recurrent laryngeal branch is affected, there is 
laryngeal paralysis. The vocal cord on that side remains midway between adduc- 
tion and abduction, and fails to move during phonation. If both of the recurrent 
laryngeal nerves are paralyzed, the patient suffers from aphonia, inspiratory stridor, 
and dyspnea. When the pulmonary fibres are affected, particularly if the lesions 
are bilateral, the respirations may become rapid and irregular. 

Irritation of the pulmonary fibres, directly or indirectly, may cause spasm of the 
bronchial muscles, and hyperemia and congestion of the bronchial mucous mem- 
brane (asthma). 

If the gastric fibres are involved, there may be vomiting, pain in the stomach, 
and loss of the sense of -hunger and thirst. When the cardiac fibres are severely 
affected, the pulse rate may be markedly accelerated. If they are irritated, an 
exceedingly slow pulse may be present. 

The treatment of disorders of the vagus nerve depends largely upon the cause 
which underlies the disturbance. If there is reason to believe that there is a syphi- 
litic exudate at the base of the brain, or a syphilitic arteritis, the iodides and 
56 



882 DISEASES OF THE NERVOUS SYSTEM 

mercury are, of course, indicated. So, too, in that form of disorder of the vagus 
which results from lead poisoning, the iodides, hot baths, and purgatives are 
required. If it is believed that a gummatous growth exists in the thorax which 
irritates the vagus by pressure, antisyphilitic treatment is necessary. If there is a 
distinct rheumatic history leading one to believe that the recurrent laryngeal 
nerves are suffering from rheumatic paralysis, already mentioned, the iodides and 
the salicylates are advisable. Digitalis may also be useful for the purpose of 
stimulating the pneumogastric nerve in those cases in which tachycardia is present, 
and atropine may be used with the object of diminishing irritation in this nerve by 
depressing its peripheral fibres when the pulse is unduly slow. 

Eleventh or Spinal Accessory Nerve. — The eleventh or spinal accessory nerve 
is composed of two parts, an accessory portion, which goes to the pneumogastric, 
and a spinal portion. The accessory branch is formed by several fasciculi which 
spring from the medulla in series with the roots of the vagus. These fasciculi 
form a trunk, and to this trunk are joined the fibres from the spinal portion. The 
nerve leaves the cranium with the pneumogastric. In its passage through the 
jugular foramen it sends fibres to the root ganglion of the vagus, while others pass 
over the surface of this ganglion into the pharyngeal, superior laryngeal, and recur- 
rent laryngeal nerves. Most of the motor fibres of the pneumogastric are derived 
from this accessory branch. The spinal portion of the nerve arises by a series of 
roots which spring from the lateral portion of the spinal cord, even as low as the 
sixth or seventh cervical nerve roots. They spring from the lateral column near 
the origin of the posterior nerve roots and form an ascending trunk, which enters 
the skull and unites with the accessory portion, as already described. Before 
entering the jugular foramen, however, certain of its fibres leave the accessory 
portion, make a sharp turn backward near the internal jugular vein, and enter the 
deep surface of the sternomastoid muscle, which muscle it supplies. Passing 
through this muscle, it enters under the trapezius, a short distance above the 
clavicle. Here it anastomoses with fibres from the third and fourth cervical 
nerves, forming a plexus, which supplies the trapezius muscle. 

Symptoms. — Disturbances in the function of the acessory nerve, so far as its 
spinal part is concerned, result in torticollis, which occurs as congenital wryneck, 
as wryneck due to injury, and true spasmodic wryneck. The congenital form 
is due to some defect in development or to injury of the sternomastoid muscle 
at the time of delivery. The right side is affected in the majority of cases. 
The sternomastoid muscle is not in the spasm, but the head is drawn to one 
side and rotated to the opposite side as the result of shortening of the muscle 
upon the side to which the head is drawn. Not rarely there is associated with 
this atrophy some wasting of the muscles of the face upon this side. Spasmodic 
wryneck, on the other hand, is due to a true spasm of the muscles supplied by the 
spinal accessory. It is not met with in children, and very rarely in advanced life, 
but occurs most frequently in middle-aged persons. In a certain proportion of 
cases the patients are distinctly hysterical, and the spasm follows some nervous 
shock. In other cases no hysterical stigmata are present, and it is thought that the 
condition is due to that somewhat indefinite state called "rheumatism." This 
form of wryneck differs from the congenital variety in that it is usually accompanied 
by pain. The spasm may not be constant but intermittent. The chin is often 
protruded and raised. At times the spasm extends to the muscles of the face, 
and facial twitching may occur. Often the condition becomes one of tonic spasm 
after having begun as clonic spasm, and if the condition persists for any length 
of time the affected muscles may undergo hypertrophy, and those on the opposite 
side may atrophy from disuse. 

Those forms of wryneck in adults which are characterized by intermittent or 
clonic spasms are rarely due to rheumatism, so called, but depend upon some 



DISEASES OF THE CRANIAL NERVES 883 

neurosis; whereas, the tonic spasm may be due simply to muscular fixation through 
pain. In the latter class of cases the prognosis is exceedingly good, the condition 
usually disappearing under the use of hot applications or counter-irritant liniments, 
and the internal administration of the salicylates and the iodides. Certain persons 
have advised the intramuscular injection of atropine, in the dose of -^q of a grain, 
directly into the belly of the afflicted muscle in order that it may depress the 
peripheral motor nerve endings. While this is efficacious in some cases, it is prone 
to produce moderate systemic symptoms, and is not to be resorted to unless the 
condition fails to yield to the plan of treatment already suggested. 

The type depending upon a neurosis is much more difficult to treat. It often 
remains unchanged for many months, and indeed may become a permanent con- 
dition. Sometimes a nervous shock, or some accident, may suddenly end the spasm. 

Under the unfortunate name of "spurious wryneck," a condition of wryneck 
develops as a result of caries of the spine, the spasm of the muscle being due to the 
lesions in the vertebrae, or the distortion is due to the fact that these bones do not 
properly support the head. 

Under the name of "spasmus Nutans," or "nodding spasm," a condition is met 
with in which the muscles upon both sides of the neck are affected in such a way 
that there is a nodding movement. It occurs in poorly nourished, neurotic individ- 
uals, and closely resembles habit chorea. The symptoms become most marked 
when attention is called to them, and are usually absent during sleep. 

Paralysis of the spinal accessory may be due to injury, disease of the vertebrae, 
muscular atrophy, or any form of disease of the spinal cord in the cervical region. 
As the result of the paralysis there may be loss of power to rotate the head upon 
the vertebral axis. The sternomastoid muscle does not stand out prominently 
as its does when affected by spasm, and there is difficulty in raising the arm at a 
right angle to the body. In those comparatively rare cases in which the para- 
lysis is bilateral, the head may appear to be fixed, as if the fixation were due to 
spasm. 

Twelfth or Hypoglossal Nerve. — The twelfth or hypoglossal nerve arises from 
a group of cells in the floor of the fourth ventricle, at its lowest point. Its fibres 
emerge from the medulla, and escape from the skull through the anterior condyloid 
foramen of the atlas, and so pass to the muscles of the tongue. Injury and disease 
of this nerve rarely take place in its peripheral filaments. Nearly always when 
it is affected, the lesion is in the bulb or in the brain. Thus, out of 79 cases collected 
by Ascoli, in only one-third were the peripheral fibres affected. The causes of 
centric disease of the hypoglossal nerve are an inflammatory process or growth at 
the base of the brain, or in the medulla oblongata. When the lesion is in the 
medulla, there is usually bilateral paralysis with wasting of the tongue, but as the 
nuclei of all the cranial nerves have their origin nearby, it nearly always happens 
that there are evidences of paralysis of the other cranial nerves present. Inside 
the bony casement the causes of hypoglossal paralysis are inflammatory exudates, 
hemorrhages, and disease of the bone. Very rarely the peripheral filaments of 
the nerve, after they take their exit from the atlas, suffer from neuritis. 

In some cases of locomotor ataxia, syringomyelia, and multiple sclerosis, there 
is hemiatrophy of the tongue with paralysis. The same symptom also occurs 
when damage is done to the peripheral fibres of the nerve. The tongue lies on the 
floor of the mouth, and it is impossible for the patient to move the tongue upon the 
paralyzed side. If the tongue is protruded, it deviates to the paralyzed side, but 
sometimes while the main body of the tongue may be deviated in this manner, the 
tip points toward the sound side. Remak points out that while the tongue lies 
on the floor of the mouth apparently paralyzed, it can be easily pushed about 
by the finger if the paralysis is organic; whereas, in hysteria, all attempts to move 
the tongue by the finger-tip cause efforts to resist these movements. The paralysis 



884 DISEASES OF THE NERVOUS SYSTEM 

of the tongue impairs the speech, and also interferes with deglutition and mastica- 
tion when the paralysis is bilateral. 

The prognosis varies with the cause of the lesion. In syphilitic cases recovery 
sometimes occurs under active mercurial treatment. In the so-called rheumatic 
cases, it may take place under the influence of the iodides or salicylates. If an 
actual lesion at the point of origin exists, the prognosis is bad. 



DISEASES IN WHICH THE CHIEF MANIFESTATIONS ARE IN THE 

MUSCLES. 

MUSCULAR DYSTROPHIES. 

Definition. — Under this term are described several related maladies, characterized 
by alterations in the trophic state of the muscles, which are met with almost always 
in early life and which are not due to disease of the nervous system — that is to say, 
they are primarily muscular in origin. The alterations in the muscles cause loss 
of power and the paralysis may be thought to be due to a spinal lesion, but this is 
not the case. 

Muscular dystrophy has been divided by Erb into three forms, namely, pseudo- 
muscular hypertrophy, Erb's juvenile dystrophy, and the Landouzy-Dejerine type 
of dystrophy. Several other types have been described by other writers. (See 
below.) 

Etiology. — The etiology of these dystrophies is not known, but they are all 
believed to be dependent upon faulty development of the muscles affected. In 
other words, it would seem as if the vitality of certain muscles is of such a character 
that they undergo senile changes early in life. When injuries and the acute infec- 
tious diseases seem to be causative factors it is probable that they act only indirectly 
in that they hasten the degenerative changes in the feeble parts. 

Pathology and Morbid Anatomy. — The changes in the muscles in cases in which 
atrophy takes place consist in a wasting and thinning of the muscle fibrils within 
the sarcolemma. They become shortened and pigmented. In other cases a true 
degenerative process goes on, the fibrils become swollen, suffer from fatty or albu- 
minoid changes, and show fatty and granular masses within the sarcolemma, until 
finally the sarcolemma may contain nothing but fatty globules. In a third form 
of dystrophy there is, in addition to fatty degeneration in the fibrils, a deposit of 
fat between the sheaths covering the fibrils. With these changes there is also an 
overgrowth of connective tissue, and as a consequence a muscle which is so large 
as to appear strong and powerful is in reality feeble or powerless. 

Pseudomuscular Hypertrophy. — This form of muscular dystrophy is essentially 
a disease of early childhood beginning between the second and seventh year. It is 
characterized by enlargement of the muscles of the calves of the legs, which soon 
arc seen to be proportionately too large for the rest of the child. It is then noticed 
that these muscles lack power and this weakness causes the patient to walk awk- 
wardly, to stumble over trifling obstacles, to tire easily, and to have difficulty 
in rising from the prone to the erect posture, so that the patient gets on his feet 
very much as a dog does, largely by the aid of the forelimbs. But while inspection 
of the muscles of the calves and of the anterior portion of the thighs reveals that they 
are enlarged, it will also show that the gluteal muscles are atrophied and that the 
muscles of the back arc weakened, with the result that there is developed anterior 
curvature of the spine and a protruding belly. The extension of the hips are 
invariably affected, rendering it difficult for the patient to ascend steps and often 
causing a tilting forward of the pelvis with a compensating curve of the upper 
part of the trunk. 



MUSCULAR DYSTROPHIES 885 

When the disease is still further advanced alterations in the nutrition of the 
muscles about the shoulder-blades is usually present. The deltoid and the supra- 
spinatus, the biceps, and the triceps undergo atrophy and do not appear to be 
increased in size because they seldom have the deposit of fat which makes the 
muscles in the legs seem unusually large. Occasionally, however, such a fictitious 
hypertrophy may be present in these muscles, because of loss of power in the 
rhomboidei, in the levatores anguli scapulse, and in the serrati. The shoulder- 
blades occupy a peculiarly prominent position, and because of the wasting of the 
muscles already named there may be great feebleness in the movements of the upper 
arm. The muscles of the forearm and hand, however, usually escape. 

Contractures appear, which, like contractures in other forms of muscular atrophy, 
result in deformities such as club-foot or flexion of the legs upon the thighs and the 
thighs upon the pelvis. Contractures may also take place in the arms. It is a 
fact worthy of note that, unlike other forms of muscular atrophy, this disease does 
not show fibrillary contractions in the muscles, nor are the reactions of degeneration 
present, even when the muscles are considerably atrophied. Sensation is intact, 
and the reflexes are preserved, unless the muscles are so completely wasted that they 
are unable to contract. 

Prognosis. — The prognosis in these cases is invariably unfavorable. Periods of 
arrest in the advancement of the disease may occur, but ultimately the patient is 
ansolutely helpless. Death never occurs from pseudomuscular hypertrophy 
directly, being caused in most cases by intercurrent diseases which attack the 
enfeebled body. 

Erb's Juvenile Muscular Dystrophy or Scapulohumeral Type. — This form of 
dystrophy begins at about the time of puberty, usually between twelve and sixteen; 
rarely as late as the twentieth year. The pectoral muscles, the trapezii, the latissi- 
mus dorsi, the rhomboidei, and the deltoids undergo apparent hypertrophy with 
progressive weakening. This results in the falling forward of the shoulders, so 
that very much the same attitude is maintained as if there was a fracture of the 
clavicles. The scapulae are prominent. In some cases the disease ceases to develop ; 
but if it does not, the loss of power extends to the muscles of the back, and various 
forms of spinal curvature develop. After this, the gluteal muscles and those of 
the thigh become enfeebled. They may atrophy or may undergo seeming hyper- 
trophy. When the muscles of the leg are enfeebled club-foot may be present. 
The chief difference, therefore, between pseudomuscular hypertrophy and Erb's 
juvenile type of muscular dystrophy is the fact that the latter disease develops later 
in life, that it affects the upper extremities before it affects the lower extremities, 
and that atrophy is more marked than hypertrophy. 

Landouzy-Dejerine Type of Muscular Dystrophy or Facioscapulohumeral Type. 
— This type of muscular dystrophy may appear in early childhood or in adult life. 
It is characterized by the peculiar fact that the atrophy develops in the muscles 
of the face, particularly the orbicularis oris, and extends to the muscles of the cheeks 
and those of the forehead, with the result that the lips lose power; the mouth cannot 
be closed, but has a peculiar pouting expression, and speech, at least so far as labial 
and lingual sounds are concerned, becomes very defective. So, too, the face loses 
its power of expression from a similar cause, and there is dribbling of saliva because 
the lower lip sags. Both sides of the face are usually affected. The orbicularis 
palpebrarum usually escapes, as do also the masseter muscles. Later, the muscles 
of the shoulders become affected, and finally those of the trunk and legs become 
involved until the case closely resembles either one of the forms of muscular 
dystrophy just described, save that the facial symptoms are prominent. 

In some cases the symptoms of these three forms of dystrophy overlap one another 
to such an extent that it is difficult to determine to which type an individual patient 
belongs. 



886 DISEASES OF THE NERVOUS SYSTEM 

Treatment. — No form of special treatment can produce advantageous results. 
The best that can be done is to order for the patient an out-door life, if possible in 
the country, and in a climate where he can remain for many hours in sunshine and 
in a place where he can receive excellent food. Gentle massage and Swedish 
movements may be employed, but care must be taken not to tire the wasting 
muscles. The most that can be expected from this plan of treatment, however, 
is the temporary arrest of the malady. No real improvement usually occurs. 
Efforts to correct deformities produced by contractures are generally useless, since 
the relief is but temporary. 

MUSCULAR ATROPHY OF THE PERONEAL TYPE. 

Definition. — This is a form of progressive muscular atrophy which begins in the 
muscles innervated by the peroneal nerves, and which does not extend higher 
than the knee. After the symptoms in the legs have developed, a somewhat 
similar condition may affect the muscles of the hand and forearms. It is sometimes 
given the name of the " Charcot-Marie-Tooth" form of progressive muscular 
atrophy, or is called the "progressive neural muscular atrophy of Hoffman," 
or primary neuritic or neurotic atrophy. It is an uncommon disease, but not so 
rare as was formerly believed. 

Etiology. — There seems to be a distinct hereditary predisposition, since it fre- 
quently affects several members of a family, and can be traced through several 
generations. It usually develops during the first two decades of life. 

Pathology and Morbid Anatomy. — The condition depends upon degenerative 
changes in the muscles, in the nerves, and sometimes in the posterior columns of 
the spinal cord. There is also sometimes a circumscribed atrophy in the anterior 
horns of gray matter, and perhaps degeneration of the lateral columns of the cord. 
Whether the disease arises in the peroneal nerves primarily, or whether the lesion 
begins in the posterior horns of the gray matter in the spinal cord, is unknown. 

Symptoms. — The symptoms of this form of muscular atrophy consist in weakness 
of the muscles of the foot and of the peroneal muscles of the leg, followed by atrophy 
in the anterior and posterior tibial muscles, with the production of drop-foot, which 
makes it impossible for the patient to walk. Unlike the two forms of muscular 
dystrophy just described, fibrillary contractions are present in the affected muscles, 
and there is a loss of reflex activity and of electric excitability, so that the last stage 
of the reaction of degeneration may finally be present. The various forms of club- 
foot may come on as secondary conditions. When the upper extremities are 
affected, fibrillary contractions can be seen in the muscles of the hand, and after 
loss of power has been present for some time, deformities of the hand may arise 
from contractures. In some cases the progress of the disease is exceedingly rapid 
but in others it is equally slow. In still others the wasting extends so that all the 
muscles of the extremities and trunk, and even -those of the face, may undergo 
atrophy. 

Prognosis. — The prognosis as to recovery is hopeless, but patients may live for 
many years unless destroyed by some intercurrent disease. 

Treatment. — Aside from hygienic measures, no method of treatment can arrest 
the progress of the malady. 

FUNCTIONAL NERVOUS DISEASES AND DISEASES OF DISPUTED 

PATHOLOGY. 

MYOTONIA CONGENITA. 

Definition. Myotonia, congenita, commonly called Thomsen's disease, is an 
exceedingly rare affection not dependent upon disease of the nervous system, and 



PARAMYOCLONUS MULTIPLEX 887 

characterized by hypertrophy of the muscular fibres with the proliferation of their 
nuclei. These changes result in loss of power. The disease usually occurs in several 
members of the same family, and appears in successive generations. 

Symptoms. — The chief symptom of Thomsen's disease is a rigidity of the muscles, 
which develops after they have been quiescent. This spasm of the muscles comes 
on when the patient attempts to move, and may be so severe as to make walking 
practically impossible. Because of the inability of the patient to balance opposing 
muscles in different portions of his body, he may fall. After a time, if the patient 
persists in his endeavor to walk or to make other movements, the spasm passes 
off, and the muscles respond as in the normal individual so that ordinary movements 
can be carried on with ease; but if the muscles are irritated by percussion or are 
allowed to rest and another attempt is made to move, they instantly pass. into 
spasm. The affected muscles develop electrical reactions of a peculiar type, namely, 
a tonic contraction under the galvanic current, which comes on sluggishly and lasts 
longer than in health. If the electrical application is continued contraction waves 
pass over the muscles, but there is no marked atrophy or great loss of power in so 
far as the spasm interferes with ordinary muscular movement. The onset of the 
malady is usually in early childhood, occasionally not appearing until puberty 
or later. The disease is so exceedingly rare that less than 40 cases have been 
reported. A physician named Thomsen, himself a sufferer from the disease, first 
described it. 

PARAMYOCLONUS MULTIPLEX. 

Definition. — Paramyoclonus multiplex is a condition of the motor nervous 
system in which sudden contractions of the muscles take place, the contractions 
resembling those produced by the use of a slowly interrupted faradic current. 
It is sometimes called myoclonus, multiple myoclonus, myoclonus epilepticus, 
spinal epilepsy, and Friedreich's disease, but it is not to be confused in the mind 
of the student with Friedreich's ataxia, a very different malady. It is a rare 
affection. 

Etiology. — The cause is unknown. In a very few instances it has been thought 
to be hereditary, but in all probability this is the case only in the sense that the 
parents or grandparents have suffered from neurotic states. It is not rarely 
associated with epilepsy, and it may develop when a nervous system naturally 
unstable is sapped by excessive mental overwork or other stress. 

The contractions may simultaneously affect similar muscles in both limbs, or 
may occur in series involving first one side and then the other, or pass from muscle 
to muscle. Very rarely only one side is affected. In most instances the face 
and trunk muscles escape as in Friedreich's original case. The ocular muscles 
are never affected. The arms are more commonly affected than the legs and the 
muscles about the arm and shoulder and those of the thigh are more frequently 
and severely affected than those of the forearm or leg. The muscles of the hands 
and those of the feet escape. The severity of the contractions increases greatly. 
In some instances they are so moderate as to be noticeable only when the patient 
is stripped of his clothing. In others they are severe enough to throw him off his 
feet. The motions or attitudes of the patient vary, of course, with the muscles 
affected and the degree of their contractions. The effect of voluntary movements 
upon the contractions is also varied. In some instances, as in Friedreich's first 
case, a voluntary movement inhibits or diminishes the contractions, but in other 
cases voluntary movement seems to exaggerate it. Mental excitement increases 
them. They cease during sleep and are usually less severe when the patient is 
standing than when he is sitting or lying down. If the affected muscles are irritated 
by tapping them a spasm is induced. The deep reflexes may be increased or 



888 DISEASES OF THE NERVOUS SYSTEM 

diminished, but electrical irritability is not altered nor do any trophic changes 
occur. Some superficial vasomotor palsy may be present in the extremities. 

Diagnosis. — Paramyoclonus multiplex is separated from chorea by the fact that 
the movements of chorea resemble those of the will in that certain groups of muscles 
act together and do not contract suddenly as from an electrical shock. Voluntary 
movements are prone to decrease those of myoclonus and to increase those of chorea. 
Chorea is usually a unilateral affection, while myoclonus is usually bilateral. The 
facial muscles, which are so commonly affected in chorea, are rarely affected in the 
malady under discussion. Electrical chorea, or Dubinins disease, is separated from 
paramyoclonus multiplex by the fact that it is accompanied by pyexia, progressive 
muscular atrophy, and paralysis, and by loss of response on the part of the muscles 
to faradic electricity. From hysterical spasm paramyoclonus is separated by the 
presence in hysterical cases of the stigmata of that state, such as disorder of the color 
fields and areas of hyperesthesia or anesthesia. In those cases of hysteria in which 
these stigmata are absent the differential diagnosis may be impossible. 

Paramyclonus multiplex may be separated from the " maladie des tics convulsifs" 
described by French neurologists, by the fact that in that affection the movements 
are more like gestures and not infrequently echolalia is present. 

Prognosis. — The prognosis as to complete and permanent recovery is not good. 
Rarely death ensues in a few months. More commonly the condition persists in 
varying severity for years. 

Treatment. — The treatment consists in measures devoted to the improvement 
of the general health by out-door life, good food, and avoidance of all causes of 
nervous irritation and exhaustion. Remedies like arsenic, phosphorus, iron, and 
similar roborants are useful to this end, but are not curative. Occasionally a care- 
fully regulated course of hydrotherapy at some well-equipped and well-managed 
sanatarium is serviceable. 

PARALYSIS AGITANS. 

Definition. — Paralysis agitans, sometimes called "shaking palsy," or "Parkinson's 
disease," is a condition in which different parts of the body, especially the forearms 
and hands, are affected by a continuous tremor. When the disease is well advanced, 
the patient leans forward, assuming a peculiar attitude, and may suffer from 
festination. 

Etiology. — The precise cause of paralysis agitans is not known. It has been 
thought to follow severe nervous shock and injuries to the central nervous system. 
In other instances it has followed excessive nervous strain. Thus, in one case 
under the writer's care, the treasurer of a very large corporation, after many years 
of hard work, developed a well-marked degree of paralysis agitans. He was quite 
certain that the tremor first began in those muscles which were employed in the 
signing of several hundred papers a day. 

Paralysis agitans develops most frequently between the ages of fifty and fifty-five. 
Gowers analyzed 80 cases and found the average age incidence to be fifty-two years, 
and Wollenberg found that 10 out of 20 cases occurred at ages varying from fifty 
to fifty-five. The disease also not infrequently develops during the fifth and seventh 
decades of life. A few cases occurring in early adult life and in childhood have been 
reported. Hadden, Gowers, Berger, and others have seen the disease in individuals 
whose ages ranged from twenty to thirty, and Weil and Rouvillois have reported a 
case occurring in a child of ten. Lannois also mentions a case occurring in a child 
aged twelve. 

Men are more frequently affected than women. Thus, of 67 cases collected from 
the reports of St. Thomas' and St. Bartholomew's Hospitals, London, 47 occurred 
in men and 20 in women. In 78 American cases Dana found the proportion of 
men to women to be as 5 to 3. 



PARALYSIS AGITANS 889 

The neuropathic constitution may be considered as a predisposing cause, but 
direct inheritance of the disease is rare. A few instances of apparent direct trans- 
mission from parent to offspring have been reported, and Berger cites one in which 
the disease appeared in three successive generations. Borgherini reported 7 cases 
occurring in a family of 9 brothers and sisters. Three children of these individuals 
developed paralysis agitans between their fortieth and fiftieth years. 

Pathology. — Nothing is known of the pathology of this affection which throws 
any light on the cause of the symptoms. 

Symptoms. — The symptoms of paralysis agitans are tremor, muscular rigidity, a 
retardation of ordinary voluntary movements, and a change in the gait. The tremors 
are rhythmical in character, amount to four or five per second, and move the 
part in various directions. Thus, when the hand is affected, the fingers may be 
flexed and extended, abducted and adducted. The most common movement is 
a rubbing of the thumb against the index finger, in much the same way that a pill 
might be made by such a rolling movement. In some instances, particularly 
if the patient becomes excited, the amplitude of the movements becomes greatly 
increased, so that the hand or the head shakes as it does in a severe rigor. Unlike 
the intention tremors of certain forms of organic nervous disease, the tremor of 
paralysis agitans is passive. Be the position of the body and arms what it may, 
the trembling continues, and while certain attitudes may diminish the amplitude 
of the tremor, it is always present except when some definite and active movement 
is attempted, when the tremor diminishes or even ceases. Thus, if the fist is 
clenched, or the patient shakes hands with a friend, the movement may stop 
momentarily. On the other hand, nicely adjusted muscular movements such as 
are involved in writing do not stop the tremor, and for this reason handwriting 
is usually impossible when the disease is well developed. 

The tremor not only involves the head and arms but extends to the legs as well, 
and it may affect the muscles of the thigh. Rarely the muscles of the jaw are 
affected. The tremor continues only during the waking hours, and usually ceases 
in sleep. Not rarely paralysis agitans is associated with insomnia because the 
twitching movements keep the patient awake, or the aching in the affected muscles 
makes the patient so uncomfortable that sleep is postponed until the patient is 
exhausted. As the patient stands in front of the physician, the chin is usually 
pushed forward and the body bent forward. The arms and the elbows are slightly 
flexed. 

After the disease is well developed, chronic muscular rigidity becomes a symptom 
which is even more constant than tremor. It not only involves the parts that we 
have spoken of, but also the muscles of the neck and back, and even those of the 
face. The muscles of facial expression become more or less fixed, causing the 
face to have a peculiar mask-like appearance. As the patient walks, his gait 
usually increases in speed and the attitude is that of a person who is attempting 
to progress rapidly. It is unfortunate that the term "paralysis agitans" is applied 
to the early stages of this disease, for paralysis, in the sense of great loss of power, 
occurs only in its very last stages, and not infrequently the patient will suffer from 
the malady for years without developing paralytic symptoms. The speech is at 
times affected and may be likened to the festinating gait. The patient has difficulty 
in starting to talk, but having commenced, the words follow each other rapidly and 
monotonously, . but without scanning. The skin covering the parts affected is 
not infrequently unduly moist by reason of profuse perspiration. Salivation is a 
not infrequent symptom. There are no disturbances of sensation, and the mind is 
unaffected save by the mental depression which is produced by the annoyance 
of the disease. 

Diagnosis. — Paralysis agitans is to be separated from multiple sclerosis by its 
onset late in life, by the fineness of the tremor, by the fact that it is present when 



890 DISEASES OF THE NERVOUS SYSTEM 

no voluntary movement is made, and by the presence of rigidity. An examination 
of the eyes fails to reveal the nystagmus or the changes in the optic nerve which 
are characteristic of multiple sclerosis. In paretic dementia the tremor is not 
rhythmical, occurs when the patient makes a movement and not when at rest, and 
there is associated with the tremor the mental disturbance, the scanning speech, 
and evidences of paralysis. 

Sometimes in old persons a senile tremor develops. This chiefly affects the head, 
and is increased rather than decreased by active movements; but in some instances 
senile tremor bears a close resemblance to paralysis agitans. Indeed, it has been 
suggested that the latter disease is essentially a premature nervous senility. It 
should be remembered that paralysis agitans may occur without tremor, but the 
muscular rigidity, with the characteristic altitude, gait and mask-like expression 
should be sufficient to establish the diagnosis. 

Prognosis. — Paralysis agitans does not materially shorten life. It frequently 
lasts for twenty years. Recovery practically never occurs. Temporary remissions 
in the severity of the symptoms may take place. 

Treatment. — As in many diseases which apparently depend upon functional 
derangement, treatment is not followed by very satisfactory results. The patient 
should be forbidden to subject himself to nervous stress and worry, which materially 
increase the severity of the malady. Everything should be done to reinstate his 
nervous balance by a healthy out-door life and freedom from care. Massage and 
electricity, as a rule, do little good. In some cases they do harm by increasing the 
exhaustion of the affected muscles. 

A very large number of drugs have been employed with asserted good result, 
but none have the confidence of those members of the profession who have had large 
experience. Of all the remedies which have been recommended, hyoscine seems to 
have received the greatest amount of praise. It should be given in the dose of 
j-jjq- of a grain once, twice, or thrice a day; the size of the dose and the frequency 
of its administration being governed by the severity of the tremor and by the 
susceptibility of the patient to drugs of this character. Duboisine may also be 
given in similar doses. Where there is much aching of the affected muscles, hot 
compresses give relief, and if the patient is in a condition of nervous irritation, 
the bromides and chloral are advantageous. The employment of such powerful 
nervous and vascular sedatives as veratrum viride and gelsemium must be resorted 
to with great caution. In doses large enough to quiet the tremor they are prone 
to produce too much depression. Paralysis agitans is unique among nervous 
diseases in that it is not benefited, but made worse by rest. 



CHOREA MINOR. 

Definition. — Chorea minor, or acute chorea, sometimes called "Sydenham's 
chorea," or "St. Vitus' dance," is a nervous disease characterized by irregular, 
purposeless movements, sometimes limited to certain muscles, but at others involv- 
ing all the muscles of the limbs, face, and trunk. It affects, in the great majority 
of instances, children between the fifth and fifteenth years of life. 

Etiology. — That sex acts is a predisposing cause of chorea is shown by the fact 
that girls arc affected three times as often as boys, and in the period of life from 
the fifteenth to the twenty-fifth year males escape almost entirely. The age 
which predisposes to its development, or is most susceptible, is from the fifth to the 
fifteenth year. After the fifteenth year it steadily decreases in frequency until 
the t went v-fifth year is reached, after which it is very rarely met with. The disease 
may, however, occur at all ages. Nervous, high-strung children suffer from it 
more frequently than those of a more plegmatic temperament, particularly if, in 



CHOREA MINOR 891 

addition, they are anemic, and have a family history indicating that they are prone 
to attacks of acute rheumatism. 

Of the exciting causes may be named sudden shock or acute mental excitement, 
but in all such cases these causes are indirect, that is, they serve to disturb the 
nervous equilibrium, already unstable from other causes. In some cases the 
disease seems to be acquired by association with a choreic child, and in this way a 
large number of children in homes and asylums may become affected. Whether 
many of these cases are true chorea or merely imitations of it, or due to hysteria, 
is difficult to determine. 

That there is a very close relationship between acute articular rheumatism and 
true chorea is certain. Even those physicians who deny that the rheumatism 
produces chorea are forced to admit that the occurrence of chorea after attacks of 
acute rheumatic infection is remarkably frequent. Fraser has shown in England 
that in 300 cases of chorea there was a clear history of an acute articular rheumatism 
in 150 or 50 per cent. Not rarely chorea complicates the development and progress 
of the acute endocarditis produced by this infection. Whether the poison of rheu- 
matism affects the nerve cells of the brain, or whether the disease is due to changes 
in the finer capillaries supplying the brain, or to minute emboli, is unknown. Cer- 
tain clinicians have endeavored to show that chorea is due to a specific infection, 
and Pianese isolated a diplococcus which was capable of producing an experimental 
chorea. There is no proof, however, that such a specific agent exists. 

Under the name of chorea gravidarum, a form of the disease is met with in pregnant 
women, usually only in primiparse. In these cases the gravid state seems to 
develop a condition of lack of nervous equilibrium, for the condition ceases, as a 
rule, with the termination of pregnancy. Occasionally in old age a senile chorea 
develops, but it is a distinct entity from the chorea of childhood. 

Frequency. — Chorea is much more frequently met with in England than in the 
United States. Morris Lewis has shown that its period of greatest frequency is 
March. 

Pathology and Morbid Anatomy. — Cases of chorea come to autopsy infrequently, 
and therefore we have not as much information in regard to postmortem findings 
in this disease as is desirable. In most of those instances in which death occurs 
during an attack of chorea, the autopsy reveals acute endocarditis, or chronic 
endocarditis with an acute exacerbation, and not rarely some degeneration of the 
myocardium. In the great majority of instances the results of examining the brain 
have been negative, and if the positive results which have been obtained are com- 
pared, they are found to be most variable. In some instances an intense hyperemia 
has been present; in others minute hemorrhages; in still others there have been 
small areas of inflammation and softening; while other cases have shown signs of 
meningitis, or thrombosis of the smaller bloodvessels supplying the brain. So, 
too, the changes which have been found in the spinal cord have been too varied 
to lead one to believe that they are in any way closely connected with the disease. 
Some observers have considered that they were the result rather than the cause 
of the condition. Choreiform movements sometimes develop in persons who have 
suffered from an organic brain lesion, but there is no reason to believe that this form 
of chorea and chorea minor have any close anatomical relationship. 

Symptoms. — The onset of chorea may be either sudden or gradual. In those 
cases in which it is gradual, it is first noted that the child is restless, and seems unable 
to keep still. Not rarely it is awkward in its movements, and falls over, or bumps 
into articles of furniture. When the disease is developed the child is continually 
restless, the arm or arms being moved in every possible direction. Sometimes the 
muscles of the shoulders are worked as if the child was uncomfortable by reason of 
ill-fitting clothes. The body is rotated from one side to the other, and the chin 
drawn first to one shoulder then to the other, then elevated, then depressed. When 



892 DISEASES OF THE NERVOUS SYSTEM 

the movements are marked, walking is interfered with and it may be difficult for 
the patient to stand. Unlike most involuntary movements, the movements of 
chorea are not confined to one group of muscles, but usually attack different groups 
alternately. Neither is the movement in the nature of a tremor. It is like a 
voluntary movement, but is purposeless and incomplete. Not infrequently the child 
laughs and cries without adequate cause. The movements affect the upper extremi- 
ties more than the lower extremities. The tongue is sometimes involved, and for 
this reason the speech may be disturbed. The child also frequently gives vent to 
curious guttural or smacking sounds, due to the action of the muscles of the mouth, 
pharynx, and tongue. These sounds may also be increased by spasm of the dia- 
phragm. Occasionally, chorea may be limited to one limb, when it is called mono- 
chorea, or when it is confined to one side of the body it is called hemichorea. These 
motions distinctly interfere with ordinary voluntary movement, and it becomes 
almost impossible for the child to perform an ordinary act slowly; if it is to be 
successfully carried out, it must be done with great rapidity. Any cause which 
produces mental excitement in the patient greatly increases the severity of the jerk- 
ing. Some clinicians have recorded an exceedingly severe form of chorea in which 
the patient has such violent muscular movements that he bites his tongue, cannot 
eat, and is thrown about from side to side as if he were in a violent convulsion. 
The twitchings of chorea may or may not stop with sleep. In those cases in which 
the movements continue at night, the disease is usually severe, and it is in this type 
of cases that death sometimes occurs from exhaustion. 

The mental state of the patient is one of irritablity and peevishness. In adults 
there may be hallucinations, and even a violent delirium. Some have thought that 
those cases in which insanity develops, and to which the name chorea insaniens 
is applied, do not belong to ordinary chorea minor. These mental disturbances 
not rarely complicate the chorea of pregnancy. 

Except for the exhaustion of the general system which is produced by the move- 
ments, there is no impairment of strength, nor is the electric reaction of the muscles 
altered. In some cases of a severe type, leading to a fatal issue, hyperpyrexia 
has been noted, which is probably due to endocarditis. Many years ago I reported 
a case of monochorea in which the temperature of the affected part was raised. 
In some instances weakness or even marked paralysis occurs in one or more of the 
affected limbs, and to this type of cases is applied the term "paralytic chorea." 

Complications. — As already stated, chorea is a disease which is associated with a 
lack of nervous stability. It is manifest, therefore, that it may often be complicated 
by symptoms of hysteria. Indeed, it may be difficult to determine whether the 
patient is hysterical or choreic. That endocarditis frequently precedes, or accom- 
panies, or complicates chorea, has also been stated, but every case of chorea that 
presents a cardiac murmur is not necessarily suffering from endocarditis, since the 
murmur is not infrequently due to anemia, or to relaxation of the fibres surrounding 
the mitral orifice. 

Diagnosis. — Ordinary cases of chorea in childhood are easily diagnosed, particu- 
larly if the history of the patient is borne in mind. Between the ages of fifteen and 
twenty-five care must be taken that it is not confused with hysteria. Sometimes, 
too, choreiform movements develop in those parts which are affected by infantile 
cerebral palsy, but in such cases paralysis is present and muscular rigidity is notice- 
able, while the movements are really different (athetosis). 

Duration and Prognosis. — Chorea minor usually lasts from two to three months, 
and sometimes extends over a year. Mild cases may continue for only a few weeks. 
The prognosis as to recovery is good, the mortality being about 3 per cent., if all 
cases are included, death being due to complications rather than to the disease 
itself. Relapses are not infrequent in chorea. Unfavorable symptoms are rapid 
loss of flesh, fever, and delirium. The prognosis is worse as to duration in adults 



CHOREA MINOR 893 

than in children. In the chorea of pregnancy the prognosis is very much more grave 
than in any other form of the disease, the mortality varying from 20 to 25 per cent- 
Senile chorea is often a permanent affection and is rarely fatal. 

Treatment. — From what has been said in regard to the general condition of the 
patient who suffers from chorea, it is evident that mental and nervous quiet are 
absolutely essential. The child should not be exposed to the excitement or mental 
stress -of school- work, neither should it be subjected to punishment or to criticism 
because of its movements. On the contrary, the fact that it is suffering from choreic 
movements should be ignored unless the physician is convinced that the case is 
one of hysteria and not of chorea. Iron and arsenic are to be given if anemia is 
present, and the salicylates are useful if there is a rheumatic history. If the move- 
ments are severe enough to exhaust the child, it should be kept in bed and sleep 
should be obtained by the use of hypnotics. These drugs, however, must be used 
cautiously lest they produce general depression, and it should always be remembered 
that a hot pack will often put a choreic child to sleep and temporarily or permanently 
arrest the choreic movements. I have seen life saved in at least two instances by 
the hot pack. 

Although there is no specific remedy for chorea, arsenic nearly approaches the 
position of a specific. How it acts is not known. The best way to administer it 
is in the form of Fowler's solution, starting with 2 drops three times a day for a 
child of ten, and increasing it a drop a day until some puffiness about the eyes and 
nose or gastro-intestinal irritation indicates that the full physiological effect of the 
drug is present, when it should be stopped or cut down to one-half the quantity. 
If this is not done an arsenical neuritis may develop. 

Next to arsenic in value are the salicylates. They must be given in full doses 
to be efficient. Antipyrin and acetanilid have also been employed with success. 
Bromides should be tried after the other drugs have failed. 

If the chorea of pregnancy becomes severe it may be necessary to induce labor. 



Other Forms of Chorea. 

Huntington's Disease. — Under the name of "hereditary chorea," or Hunting- 
ton's disease, an affection is met with which must be clearly differentiated from 
chorea minor. It is a rare condition which, as its name indicates, is hereditary, 
although it does not always affect consecutive generations, sometimes passing from 
the grandparent to the child, although in such cases the parent is usually excessively 
neurotic. Both sexes suffer from it equally. The disease begins between the 
thirtieth and fortieth year of life in most instances, and no exciting cause can usually 
be discovered. 

Its early symptoms consist in twitchings of the muscles of the face and upper 
extremities, which gradually increase in severity and in the area which they involve, 
until the entire muscular system may be affected. The patient, under these cir- 
cumstances, carries on a series of grimaces and gesticulations, but it is a noteworthy 
fact that he or she can inhibit these movements at least for a period long enough 
to permit the voluntary movement which it is desired to make. When the muscles 
of the trunk and legs are involved the body is tossed hither and thither with rapid 
movements. Sensation is not involved. Paralysis of a hemiplegic type develops 
very rarely. The mind gradually fails, the mental failure being preceded by depres- 
sion and irritability. 

Huntington's chorea is an incurable disease. It usually ends in the patient 
becoming bedridden and dying from some intercurrent malady. It may, however, 
last for many years. Cases are on record in which the patient has lived thirty 
years after the disease began to manifest itself. The progressive character of the 



894 DISEASES OF THE NERVOUS SYSTEM 

malady, the period of life at which it develops, the progressive dementia, and the 
history of heredity all aid in separating it from chorea minor. 

The morbid anatomy is not understood. In some cases the lesions in the brain 
have resembled those of paretic dementia. 

The treatment consists in a healthy out-door life, and the use of nervous sedatives, 
and tonics, with the object of maintaining the patient's general health. Cases 
apparently identical with Huntington's chorea, but occurring singly, are spoken 
of as chronic chorea. 

Dubini's Disease. — Under the name of "electrical chorea," or "Dubini's 
disease," a form of chorea characterized by severe muscular contractions resembling 
those produced by electricity has been described by Dubini as affecting peasants in 
northern Italy. Occasionally, the movements may be epileptiform in character. 
Paralysis soon develops; pain is suffered in the head, neck, and back, and death 
results, as a rule, form exhaustion. A few cases have been reported as having 
recovered. 

Another form of electrical chorea seen in children has been described by Bergero. 
Such cases usually recover. I showed such a case before the Neurological Society 
of Philadelphia many years ago. The patient, a boy, a little past puberty, suffered 
from violent contractions which were electrical in character. 



HYSTERIA. 

Definition. — Hysteria is a chronic functional disturbance of the nervous system 
in which the motor nervous system may manifest its disorder by convulsions, palsies, 
or contractures, the psychical nervous apparatus by emotional disturbances, and 
the sensory apparatus by lost, diminished, or increased sensibility. It is manifest, 
therefore, that the disease involves both the central and peripheral portions of the 
nervous system, but there can be no doubt that the dominating condition is a 
psychosis. Hysteria undoubtedly depends upon a condition of disturbed nervous 
equilibrium. 

Etiology. — There can be no doubt that this affection is, to some extent, hereditary; 
that is, a parent or parents who possess an unstable nervous system naturally 
transmit a similar condition to their offspring, and in a very large proportion of 
cases it will be found that the patient is a child of parents who have at times mani- 
fested neurotic or hysterical disorders. Age has a distinct influence upon the 
disease. Its most frequent period of occurrence is from fifteen to twenty-five years 
of age in women, although in males it usually appears at from twenty to thirty. 
Occasionally, however, children suffer from it, particularly just before puberty, and 
sometimes much earlier than this. The condition is met with far more frequently 
in females than in males, but statistics vary from 40 to 1 to 4 to 1 or even 2 to 1, 
according to different writers. It is much more common in the very poor and in 
the rich than in the middle classes, and in the Latin races than in the Anglo-Saxon 
race. In America it is most frequently met with in the poorer class of Jews, who 
are often underfed, poorly housed, much confined, and under great nervous excita- 
tion and stress. It is much more common in France and Italy than in Germany 
and England. 

If it be true that the underlying cause of hysteria is a lack of nervous control 
or balance, it is evident that a number of conditions may be considered as direct 
causes of the malady. In other words, any condition which upsets the nervous 
balance may provoke the disease. It is, therefore, frequently found that some 
greal grief or intense joy has been productive of the first manifestation of the disease, 
or, again, that some injury or fright has acted in a similar manner. Great worry 
in business, or over a love affair, may produce a similar result. None of these 



HYSTERIA 895 

causes would so profoundly affect a healthy nervous system. All of them are 
sufficient to disturb the balance of a nervous organization already abnormal. 

Any discussion of the etiology of one of the functional neuroses would be incom- 
plete without a reference to Freud's ideas on the subject. In 1895 Breuer and Freud 
announced their belief that hysterical manifestations were the result of repressed 
psychic traumata, acting like foreign bodies on consciousness and struggling to come 
to the. surface. Later Freud reached the conclusion that the repressed psychic 
traumata represented sexual experiences of childhood, and formulated the hypo- 
thysis that — "In a normal vita sexualis no neurosis is possible." 

At first using hypnotism as the means of investigating his patient's psychosexual 
past, Freud later discarded this method and devised a special technique for psycho- 
analysis. The patient reposes on a couch and is encouraged to secure muscular 
relaxation. The physician seats himself behind the patient's head and instructs 
her to tell whatever comes into her mind, repeating all the thoughts that occur 
to her in the order in which they arise, no matter how distasteful or embarrassing 
the narrative may be. The physician from time to time offers suggestions and 
endeavors to help fill up the gaps until the patient completely unbosoms herself 
and the supposed underlying sexual basis for the malady is discovered. Dreams are 
said to contain the fulfilment of a wish and we are told that sexual ideas are repre- 
sented by dreams in symbols, due to the restraining normal influence of what 
Freud terms a "psychic censor." The interpretation of dreams is said to be a very 
important part of psycho-analysis. 

At present some eminent neurologists are enthusiastic followers of Freud and 
others are equally inclined to put aside his views. 

Pathology. — As already stated, hysteria is a purely functional disease, and the 
central and peripheral nervous systems show no alterations which can be considered 
as responsible for the malady. 

Symptoms. — Hysterical individuals usually present evidences of nervous irritability 
which may manifest itself in great excitement, in violent anger, in undue anxiety, or 
in great mental depression. All of these manifestations may follow one another 
with extraordinary rapidity. The patient also manifests distinct lack of self-control, 
both in regard to her emotions and her impulses, and a markedly increased suscep- 
tibility to suggestion is conspicuous. At times she may seem utterly incapable of 
accomplishing anything which ought to be done. At another time she can develop 
an amount of energy and persistence which is surprising, provided that she conceives 
it to be her duty or her wish to accomplish such an end. The power of thought is 
in no way impaired, but judgment is warped and uncertain. Not infrequently 
the patient has perverse ideas which may seem to amount to delusions, but which do 
not remain constant as in cases of insanity. 

In some instances the first symptoms of the malady are manifested by a hyper- 
sensitiveness, so that the girl cries easily, and perhaps laughs more readily and for a 
longer time than is necessary in the appreciation of a remark which is amusing. 
Restless sleeping also may be present. As the condition develops, attacks of head- 
ache and vomiting may come on, and she may suffer from somnambulism. 

When the condition becomes still more severe, so that it amounts to that state 
which is sometimes called "hysteria major," the disturbances of sensation and 
motion become intense. In addition to attacks of crying and laughter, the patient 
may pass into a trance or into a condition of catalepsy. Or, again, the patient 
may suddenly fall and be seized by a convulsion which is distinctly epileptiform in 
character. Often, however, the convulsion is more largely tonic than clonic, the 
hands and fingers being flexed and the forearm flexed on the arm, while the legs 
and feet are extended and the eyes closed. If the eyelids are lifted, the eyeballs 
are often found to be fixed in convergence or undergo irregular movements. The 
pupils are dilated. The surface of the body is more or less anesthetic. As a rule 



896 DISEASES OF THE NERVOUS SYSTEM 

the patient does not froth at the mouth as much as in true epilepsy, nor does she 
bite her tongue as is done in epilepsy. So, too, she rarely hurts herself when in 
the convulsive seizure. The attack may last from a few minutes to several hours, 
or even longer than this, and may vary in its intensity from semiconsciousness 
with slight twitchings of the muscles to apparent total unconsciousness and severe 
convulsive seizure. The expression of the face is often quite characteristic. In 
some instances it is remarkably peaceful after the convulsion passes by. In others 
it is ecstatic or terror-stricken. In very young patients curious guttural and other 
sounds may be made, and the patient may bark like a dog or mew like a cat. 

It is noteworthy that many of these patients are conscious of what is going on 
around them during the attack, although at the time they may manifest no evidence 
of this. Not rarely a sharply spoken word of command may bring the attack 
to a close, or the threat of applying some instrument which is capable of causing 
pain may do likewise. When the patient returns to consciousness, it may be found 
that there is loss of power in an arm or leg, or upon one side of the body, with or 
without loss of sensation. Frequently the so-called hysterogenic zones may be 
discovered, pressure upon which causes pain and may provoke an hysterical attack, 
or if pressure on these parts is used during the attack it may arrest it. 

The sensory symptoms of hysteria, in distinction from those just described in 
connection with a critical period, consist in anesthesia in all its forms, particularly 
analgesia of the cutaneous and mucous surfaces and disturbances in the special 
senses. The most common form of cutaneous anesthesia is hemianesthesia involving 
exactly one-half the body. After this, the most common type is segmental anes- 
thesia, in which an arm, or leg, or part of the face is anesthetic, the margin of the 
anesthetic area being sharply defined, while the disturbance of sensation does not 
correspond to the distribution of any one nerve trunk. Much more rarely patches 
of anesthesia occur in different portions of the body. In these anesthetic areas 
the senses of touch and of heat and cold are usually preserved to some slight extent. 
Occasionally, the affected part has a subnormal temperature. When the anesthesia 
is limited to one side it affects the left far more frequently than the right half of the 
body. If the anesthesia is of the hemianesthetic, or segmental, type there is usually 
more or less complete loss of motor power in the same limb. 

The disturbances of special sense consist in an anesthetic condition of the retina 
whereby the visual field is greatly narrowed, particularly for certain Colors and 
often for those colors which normally have the widest field, and the color sense is 
disturbed or reversed. These disturbances may or may not complicate those just 
named. When hemianesthesia is present, the eye upon the affected side is some- 
times partly or even totally blind, not as in organic hemianopic hemianesthesia. 
So, too, the acuity of the auditory nerve may be diminished, particularly upon 
that side of the body which is most affected. The sense of taste may also be per- 
verted and the sense of smell may be lost. 

Neuralgic pains are not common in hysteria except when there is present grave 
anemia and other common causes of neuralgia. In certain portions of the body, 
however, hyperesthesia of the skin may be present as in the hysterogenic zones 
described. These zones are most frequently found in females in the groin, whence 
the name "ovarian" tenderness, and under the mammary glands, and in males on 
the scrotum, also along the spine, but they may be found in any part. Paralysis 
of the extra-ocular muscles is sometimes met with. Usually the internal rectus is 
affected, and sometimes the external rectus. Speech may be impaired by paralysis 
of the adductors of the vocal cords. The development of this condition is called 
"hysterical aphonia," the patient being speechless, or able to converse only in a 
whisper. The onset of this condition is usually sudden. 

The paralysis of motion already referred to often persists for a long period of 
time, and in association with this paralysis it not rarely happens that other muscles, 



HYSTERIA 897 

often those which are antagonistic to the ones which are paralyzed, suffer from 
contractures. At first these muscles may be simply abnormally irritable and the 
contractures may be fleeting, or they may last as long as the paralysis of motion 
and sensation, and in this way resemble the contractures which are sometimes met 
with in cerebral diplegia. Tremors may also affect the muscles of an arm, of the 
face, or of a leg, and these tremors may resemble those of paralysis agitans or other 
diseases characterized by tremor, particularly if the patient has been associated 
with such a case. The amount of atrophy or wasting which occurs in a paralyzed 
part is usually very slight, and depends almost entirely upon lack of use. Of the 
internal viscera it may be said that the functions are not gravely impaired in 
most instances, unless perchance these viscera suffer from the chief manifestations 
of the disease. A very common symptom of hysteria, present in the majority of 
cases is the sensation as if a ball or small orange rose into the pharynx. This is 
called "globus." In other instances violent attacks of vomiting develop. In 
still others, the "rifting" of large quantities of gas, or of air which has been swal- 
lowed, takes place, accompanied by much rumbling in the abdomen. In still 
other instances rumination, or, as it is sometimes called, "merycismus," occurs; 
that is, the patient regurgitates food, which has been swallowed, into the mouth 
for a second chewing. At other times intestinal disorders are present. I have seen 
a large phantom tumor of the intestine, in a patient who had constantly refused 
food until she was emaciated to the last degree, give rise to the belief that a malig- 
nant growth was present. At times these patients have a perverse appetite, eating 
chalk or other materials not commonly swallowed. The urine is sometimes very 
limpid and free. At other times it is scanty and high colored. After an acute 
attack of hysteria it is usually limpid. 

Of the circulatory disorders attacks of tachycardia are by no means uncommon. 
Sometimes the patient will complain of severe pain in the neighborhood of the heart. 
This pseudoangina is characterized by a sensation of distention of the heart in 
distinction from the pain of true angina, which is usually described as if the heart 
were being tightly compressed. The peripheral vascular system may also be 
disturbed. Abnormal flushing or blushing or local anemia and pallor may be 
present. At times even edema may develop. In other instances the part becomes 
so pallid or slate-like in color that it resembles Raynaud's disease, but true gangrene 
does not develop. Very rarely, indeed, a sharp febrile movement may take place. 
Sometimes hysterical patients suffer from attacks of hiccough or of sneezing, or of 
rapid breathing, cough, or difficulty in swallowing. 

Under the name of "hystero-epilepsy," a form of hysteria characterized by 
violent convulsions closely resembling those of true epilepsy is described by many 
foreign authors. It is rare in this country. In some instances the convulsive 
seizure is not epileptoid, but cataleptoid or tonic. The patient may lie in bed with 
the arms extended, as in ecstacy, or with the hands tightly clinched, as in terror 
or anger, or the state may resemble simple stupor or even coma. At other times a 
psychical disturbance is manifested so that the patient develops a delirium. Often 
several of these processes are combined. At first the patient experiences an aura 
as in epilepsy. This is followed by the epileptoid form of convulsion, and this 
again by the contortions and emotional attitudes just described. An emotional 
confusion is not rare; hallucinations and delusions may occur and confinement in 
an asylum may be necessary. Finally a stage of delirium may develop. 

Diagnosis. — Under some circumstances there is no more difficult diagnosis than 
the differentiation of hysteria from organic nervous disease, particularly if the 
patient has had an opportunity of studying the symptoms presented by patients 
with organic nervous lesions. The important points in differentiation are the con- 
traction of the visual fields and the alterations in the color fields, the fact that the 
areas of anesthesia are- not confined to any given distribution of sensory nerves, 
57 



898 DISEASES OF THE NERVOUS SYSTEM 

the presence of hysterogenic or hyperesthetic spots, the fact that wasting does not 
develop to any degree in the paralyzed muscles, the absence of the reaction of degen- 
eration, the maintenance or persistence of the deep reflexes, and the peculiar emo- 
tional state. Again, the anesthetic area may be moved from the first place affected 
by the mere placing of a coin or a magnet over the affected part. Hysterical 
contractures also usually disappear in sleep or when the patient is under the influence 
of an anesthetic. In the epileptoid form of attack the tongue is never bitten nor 
the limbs injured. 

Prognosis. — The prognosis as to life is good. The attacks usually diminish in 
frequency and severity with advancing years, but the question of prognosis is always 
governed by the degree of nervous instability in the patient and in her parents. 
When the hereditary influence is bad and the surroundings of the patient are 
unfavorable the malady may last a lifetime. In those who are well-to-do and who 
can afford to take the treatment required by such cases, the outlook is better than 
in those who are continually exposed to bad surroundings, with nervous stress and 
strains. 

Treatment. — The treatment consists in the removal of the patient from those 
causes which tend to produce nervous irritability and stress. If the home surround- 
ings of the patient are such as to increase nervous irritation, the patient must be 
removed from those surroundings. Such a patient should always be taken from 
school and given lessons under a private instructor. If the symptoms are severe 
the Weir Mitchell rest cure is essential. If they are not severe enough for this, an 
out-door life with a moderate amount of healthy exercise carried to the point of 
fatigue, but not of exhaustion, is needful. If anemia is present it must be overcome 
by proper tonics. Insomnia and peripheral nervous irritation should be treated 
by hot and cold packs and the various forms of hydrotherapy. Sedatives may 
be needed, but it must be remembered that the administration of hypnotics to 
neurotic patients frequently produces a drug habit. Local anesthesia, in addition 
to being treated by hydrotherapy, will also be benefited by the use of the rapidly 
interrupted faradic current administered by means of the ordinary wet sponge, or, 
if the anesthesia is marked, through the dry wire brush. The physician must 
exercise a dominant influence over the patient, and she must be put under the 
charge of a trained nurse of strong character, who, on the one hand, will not be 
irritated by peculiarities, but will tactfully discourage them. This mental side of 
the treatment is too frequently overlooked, when it is the most valuable and impor- 
tant therapeutic factor at our command. While the abnormal reaction of the 
patient to suggestion is responsible, as pointed out by Babinski, for the development 
of symptoms, this susceptibility can be taken advantage of in removing the symp- 
toms. The whole atmosphere of the sick room should be one of encouragement and 
optimism. The patient's symptoms should not be ridiculed nor should undue 
sympathy be expressed. Psychotherapy should always be practised, no matter 
what other measures are resorted to. 

The treatment of the hysterical attack itself consists in the administration of 
nitrite of amyl. There are few cases of true hysteria that will not be at once 
relaxed if convulsed, and the attack stopped by this drug, which, on the one hand 
is perfectly safe, and, on the other, produces so powerful a mental impression that 
its use is appreciated by the patient. If nitrite of amyl cannot be employed, ether 
may be used and pushed freely, but chloroform is usually too agreeable to the 
patient to be advantageous. Not rarely the use of the dry electric brush or 
even of the actual cautery, which may be touched at various points on either 
side of the spine, is advantageous through the powerful mental impression it 
produces. 

The Freudian school claim that by their method of psycho-analysis, the bringing 
to the surface of the buried sexual complex will establish a cure for the neurosis. 



NEURASTHENIA 899 

In this connection it may be well to remember that psycho-analysis, as it is practised, 
is a powerful and prolonged method of suggestion and may act in much the same 
way as other forms of suggestion. 



NEURASTHENIA. 

Definition. — Neurasthenia is a condition in which the nervous system suffers 
from various functional disorders due to excessive mental and nervous stress and 
strain whereby the energies of the patient are exhausted. For this reason it is 
often called nervous exhaustion. 

Etiology. — Heredity plays a very important role in the etiology of neurasthenia. 
An individual with a neuropathic ancestry does not have the normal amount of 
nervous energy to begin with and therefore will become nervously exhausted from 
causes which would be inadequate to produce symptoms in one more fortunate 
in his nervous inheritance. The most common cause of neurasthenia in men is 
prolonged mental strain produced by business reverses or the carrying through 
of some important and difficult enterprise. The severity of this strain is by no 
means always in direct proportion to the size of the undertaking. The condition 
is not met with in the lower classes except occasionally, and is largely dependent 
upon the nervous temperament of the individual and the condition of his general 
health and surroundings. In women the condition is commonly met with as a 
result of excessive social duties, as after a winter season devoted to late balls and 
receptions, or it occurs in those who have passed through a long period of nervous 
strain resulting from the nursing of a sick husband, child, or some near relative, 
whereby there is not only physicial exhaustion but mental anxiety to exhaust 
reserve energy. It is evident, therefore, that many causes may produce this con- 
dition provided they result in a great expenditure of nervous energy with so little 
sleep that rest cannot be obtained. 

Every individual may be said to possess two funds, or sources, of nervous energy. 
From one of these he takes daily that force which is necessary for the performance 
of his physiological functions and labor. The second fund is kept in reserve to meet 
the demands of extraordinary occasions and is maintained, as is the reserve fund of 
a bank, to meet conditions which are abnormal. The patient who suffers from 
neurasthenia is one who has not only expended his ordinary fund, but drawn so 
largely upon his reserve fund that he is a nervous bankrupt, and he suffers from a 
large number of more or less serious symptoms because the various parts of his body 
do not receive enough nervous energy to cause them to perfectly perform the 
normal functions. If the strain has been very profound and severe, and the patient 
is one whose nervous balance is not very stable, it can be readily understood that 
a very serious state may develop, and that the life of the patient may be jeopardized 
if any intercurrent disease develops. 

Symptoms. — The symptoms of neurasthenia are exceedingly varied, depending 
in many instances upon the organ, or organs, which are chiefly affected by the state 
of nervous exhaustion. In some cases the mental condition of the patient suffers 
chiefly and the symptoms may vary from mere irritability of temper to great mental 
depression and even to mental aberration. Sometimes persistent insomnia devel- 
ops. In other instances the functions of the digestive tracts suffer chiefly, and in 
others the heart displays the greatest evidence of disturbed nerve supply, so that 
attacks of palpitation ensue, or instead a lack of vasomotor control results in 
attacks of vertigo or syncope. In addition to these definite and specific symptoms 
the patient often complains of a host of subjective symptoms which are quite 
extraordinary in character. Headache, dull in character, and backache, are 
frequently complained of. Walking or other physical exercise rapidly produces 



900 DISEASES OF THE NERVOUS SYSTEM 

fatigue from which the patient does not recover as readily as does the normal individ- 
ual. In fact, the complaint — "I am tired all the time" is a common one. In 
the morning they wake unrefreshed and are usually at their best in the evening. 
Mental exertion becomes equally exhausting, and application and concentration 
are difficult. Except in advanced cases, the appetite is, as a rule, good. In spite 
of the variability of symptoms the following are constantly met with: sense of 
chronic fatigue, of exhaustion, and irritability. Hysteria is not infrequently 
associated with neurasthenia. 

Diagnosis. — The physician should never reach a diagnosis of neurasthenia until 
by repeated examinations and study of the patient, and her secretions, he is con- 
vinced that no grave organic disease exists which may be responsible for the symp- 
toms presented. If cardiac and renal disease are excluded, and no other organic 
malady can be found of sufficient gravity to produce the illness, and if the history 
of the patient reveals the existence of some cause capable of producing nervous 
exhaustion, the diagnosis of neurasthenia may be reached. 

Prognosis. — The prognosis of neurasthenia depends upon the ability of the 
physician to remove the patient from exposure to the causes which have produced 
the condition, upon the ability or willingness of the patient to follow those methods 
of life which are conductive to the re-establishment of nervous balance and reserve 
energy, and upon the age and general physical state, for if the patient be one who 
is far advanced in years, or who by reason of disease or heredity is possessed of low 
recuperative power, it is manifest that complete recovery may be impossible. 
Given a case of neurasthenia in which all the conditions which are unfavorable 
may be excluded the prognosis is favorable, but the physician must be cautious in 
stating the duration of the period of recovery, for the progress toward health is 
governed not alone by the skill displayed in treatment, but by the recuperative 
power of the individual, a power which every physician of experience recognizes 
as a very variable quantity. Not rarely a seemingly frail person recovers speedily, 
whereas another patient of a more powerful build and physique makes progress so 
slowly as to cause great discouragement. 

Treatment. — From what has been said of the causes of this condition it is manifest 
that the chief aim of the physician must be the re-establishment of the normal 
nervous energy or power. As first pointed out by Weir Mitchell, this can only be 
obtained by the accumulation of energy, and this accumulation of energy is to be 
had only by absolute mental and physical rest on the one hand and proper feeding 
on the other, the circulatory and other vital functions being maintained by passive 
exercises and electricity. The patient must so arrange his or her affairs that no 
business worries or family cares will be experienced. For this it is essential that 
the treatment shall be carried out in a health resort far removed from the home and 
office, or in a hospital or "rest-cure house," where the patient will be absolutely 
isolated from ordinary surroundings. An attempt to carry out the "cure" at home 
nearly always ends in failure, because the needed degree of mental discipline is not 
obtainable and the sounds made by the rest of the family annoy the patient or 
develop curiosity or worry as to their cause. It is also essential that a skilled 
trained nurse shall be in absolute control of the patient without any interference 
by members of the family. The patient is not allowed to sit up, but is required to 
remain in bed at perfect rest. The action of the kidneys, bowels, and skin is care- 
fully looked after by suitable remedies, and once every day massage is given over 
the entire body to give the effects of passive exercise. In many cases it is well 
to give massage in the afternoon and faradic electricity in the morning, the slowly 
interrupted current being employed to exercise the muscles, and this in turn followed 
by a general application of the rapidly interrupted current from the head to the 
feet for fifteen minutes. These measures combined with a cool sponging in the 
early morning and an alcohol rub at bedtime, with the administration of small 



EPILEPSY 901 

quantities of food every three hours, will usually cause the patient to complain of 
being "too busy" instead of feeling, as they state they will feel at the beginning 
of the "cure," that time hangs heavily on their hands. The patient must not 
receive or write letters nor must she read, since this requires not only nervous 
but muscular strain. In some cases the nurse is permitted to read aloud to the 
patient for an hour a day. Under such a plan of treatment, in which all the nervous 
energy which it is possible to conserve is secured, and in which every opportunity 
is offered for the addition of units of force by proper feeding, lasting and complete 
recovery is usually obtained. 

EPILEPSY. 

Definition. — Epilepsy is a disease characterized by attacks of unconsciousness, 
which, in the well-developed form of the malady, are accompanied or followed 
by convulsions. The convulsions at the moment of onset are usually tetanic or 
tonic in type, but almost immediately become clonic. Indeed, so typical of epilepsy 
are clonic convulsions that all convulsions of this class are called "epileptiform." 
Epilepsy separates itself from other convulsive conditions associated with uncon- 
sciousness by the fact that it is a chronic malady, whereas epileptiform convulsions 
arising from other causes occur but a few times in the lifetime of the individual, 
as, for example, in puerperal eclampsia or uremic poisoning. Hysterical convul- 
sions, however, closely resemble it. 

Etiology. — The etiology of epilepsy is unknown, although in a certain proportion 
of cases injuries to the brain substance arising from external or internal causes 
undoubtedly predispose to or produce the disease. In some instances it has been 
thought that the condition is hereditary, and this is certainly true in the sense 
that epileptic parents often have epileptic children. By far the largest number 
of cases collected by any one writer, so far as the author is aware, are those 
of Gowers, who analyzed no less than 1450 cases of epilepsy, finding that an inherited 
tendency was indicated by the presence of insanity or epilepsy in ancestors or collate- 
ral relations in rather more than one- third of the cases (35 per cent.), and rather 
less frequently in males than in females, for there was this history in 33 per cent, 
of the males and 37 per cent, of the females. There was a family history of epilepsy 
in two-thirds of the inherited cases, of insanity in one-third, and of both disorders 
in one-tenth of the cases. In the 56 cases recorded by Sieveking heredity was the 
cause in 11. Reynolds, in his collection of cases, found the proportion to be 31 
per cent. Hasse has collected 1000 cases, and has found heredity the cause in 
no less numbers than the others. If we take the average result of the conclusions 
reached by the clinicians just named, who give exact figures, we find that we have 
to deal with 4300 cases of epilepsy, of which a little over 26 per cent, were due to 
heredity. Whether epilepsy can be induced in a child by hereditary influences 
arising from chronic alcoholism or chronic lead poisoning is open to debate. Certain 
neurologists are firmly convinced that these factors are active. 

In other instances, apparently healthy children develop epilepsy after suffering 
from some of the infectious diseases such as scarlet fever. In these cases the 
infection has either produced some definite lesion in the brain or has so impaired the 
normal growth of certain cells in the cerebral cortex that their natural balance is 
destroyed, with the result that periodic explosions of nervous energy take place. 

Syphilis acts as a cause of epilepsy in two w T ays. When the parent is syphilitic, 
the child may suffer from hereditary syphilis or from a syphilitic disease of the 
nervous system, with imperfect cerebral development. In other cases acquired 
syphilis produces epilepsy in adults. Indeed, more than one writer has expressed 
the belief that an epilepsy beginning after the twenty-fifth year is syphilitic in 
origin. This is rather an exaggerated statement, but it is nevertheless true, that 
more than three-fourths of all cases of epilepsy begin before the twentieth year. 



902 DISEASES OF THE NERVOUS SYSTEM 

About half of them begin in the second decade of life. Quite a large proportion 
begin between the seventh and tenth years. 

In some instances the epilepsy dates from the reception of some severe injury 
to the head. Cases that have a traumatic origin, those which are due to syphilitic 
gumma or other form of brain tumor, usually belong to that type which is called 
"Jacksonian" or "localized" epilepsy, although they may ultimately develop all 
the characteristics of the so-called idiopathic form. 

For many years it was considered that a host of conditions tended to produce 
epilepsy by reflex irritation. Such causes as foreign bodies in the ear or in the nose, 
intestinal worms, and uterine disorders have been considered as causative factors, 
but in all such cases these agents act only indirectly in the sense that they provoke 
an irritation which reflexly upsets the nerve balance or equilibrium of an unstable 
motor area of the brain. In other words, in any case of epilepsy it is to be under- 
stood that the underlying factor is a lack of stability or nervous balance. 

The influence of sex is not very great, but males are affected somewhat more 
frequently then females. Althaus has examined an enormous amount of statistics 
to obtain results bearing on this point. He found that in 54,442 cases there were 
28,960 males and 25,482 females. 

Posthemiplegic epilepsy due to cerebral injury may occur at any age, but there 
can be no doubt that it far more commonly occurs in infants than in adults. In 
at least two-thirds of the cases the onset is before the fifth year of age, and in nearly 
one-half it is during the first two years of life. It is not uncommon for the paralysis 
to occur in infancy and the epilepsy to begin at puberty. This prolonged interval 
is rare in adults, in whom the epileptic seizures usually begin in less than one year. 

The frequency with which epilepsy comes on after the hemiplegia of childhood 
has been very exhaustively studied. Thus, in Osier's cases, 20 children out of 97 
suffered from it. In the 80 cases collected by Gaudard 11 children had hemi- 
plegic epilepsy, and 66 children out of 160 cases collected by Wallenberg were 
epileptic after hemiplegia. In another series of cases collected by Osier 15 chil- 
dren out of 23 were thus affected. 

Pathology. — The pathology of epilepsy is not known. It is true that at autopsy 
many cases of epilepsy show atrophic or degenerative changes in the cerebrum 
but this holds true of only a certain proportion, and not of those instances, of 
so-called idiopathic epilepsy in which there is no history of syphilis, or of injury, or of 
damage to the brain through disease of its bloodvessels. In this idiopathic form the 
most careful macroscopic and microscopic examinations of hundreds of cases have 
failed to reveal any alteration which can be considered as responsible for the malady. 
Some of the microscopic lesions which have been described by certain investigators 
are without doubt present, but in these cases the question arises whether they are 
not the result rather than the cause of the affection. 

That epilepsy is a result of an explosive discharge of nervous energy from the 
motor areas of the cortex is proved by the fact that similar convulsions can be 
produced in man and in the lower animals by irritating these areas, and that growths 
and injuries which irritate them produce similar symptoms. The somewhat 
ancient theory that the convulsive disturbance is the result of lesions in the medulla 
and the pons is no longer accepted. 

Symptoms. One of the first and most marked symptoms of an oncoming attack 
of epilepsy is a peculiar sensation felt in some portions of the body, generally below 
the head, which gradually rises up over the patient, either rapidly or slowly, like 
an oncoming cloud, until, the head having been reached, the patient is immediately 
convulsed and unconscious, and almost instantly is seen to be in the very acme 
of the nervous storm. Simultaneously with the arrival of this aura in the cervical 
region (he person utters a peculiar cry or scream, so characteristic that it has been 
called the "epileptic cry," being probably due not so much to a voluntary impulse 



EPILEPSY 903 

as to a sudden expulsion of the air from the thorax by the convulsive contraction 
of the abdominal muscles, as well as those of the thorax, and its rapid passage 
through the glottis narrowed by rapid spasm of the muscles governing this opening. 
Synchronously with this cry the muscles of the whole body, in a widespread attack, 
become strongly contracted until they are in a tonic spasm, and then, having momen- 
tarily relaxed, pass into alternating relaxations and contractions, which throw the 
patient now to this side, now to that. 

During the tonic spasm the muscles of the face often produce marked distortions 
of the features, in some cases bringing about the so-called risus sardonicus; the head 
may be drawn to one side, and under these circumstances the eyes are generally 
turned in the same direction; the jaws are locked one against the other, and the 
lower jaw may also be drawn away from the median line of the face in the same 
direction as the eyeballs. Sometimes the whole body is rotated. In 970 cases 
analyzed by the writer, complete rotation to the right is mentioned as being present 
in 49 persons, and the left in 52 cases. There is, therefore, no difference worthy of 
note in these numbers. 

The arms are strongly flexed at the elbows, while the hand is still more strongly 
flexed at the wrist; the fingers are also so bent into the palm of the hand that not 
unfrequently the skin in this region is found indented by the nails. The arms, legs, 
and body are drawn and jerked in the direction of the most powerful muscles, and, 
as a consequence of this, opisthotonos, during the tonic stage, is by no means 
uncommon. Exceptions to this rule do, however, frequently occur, and when 
present show that the paroxysm is exerting its chief influence on the weaker muscles, 
while the stronger ones are affected at least to a less degree. As a general rule, too, 
the muscles of one side suffer more than those of the other. Unfortunately, in 
the cases collected by me, in only 158 instances were any remarks on this point 
made. In these 158 the right side was most affected in 77 cases, and the left side 
in 81 cases. It is evident, therefore, that both sides suffer about equally. The legs 
may be firmly flexed on the abdomen, while the fingers are rigidly extended. 

The change in the color of the face is very marked and almost typical of the 
disease, being at first pale, then flushed, the flushing deepening often into a livid 
purple, owing to the asphyxia produced by the convulsive contraction of the 
thorax. In some cases the eyelids are widely drawn apart so that the eyes, owing 
to their fixation, have a staring appearance; in others they are so tightly closed that 
the fingers of the onlooker can scarcely force the lids apart. The staring, but 
blank, expression of the eyes is also increased by the slow dilatation of the pupils 
which always accompanies the asphyxia. 

The duration of the tonic contractions rarely exceeds two minutes, and in most 
cases is limited to but a few seconds. It is followed by the clonic spasms, already 
described, which are ushered in by more or less violent tossings, but whose onset 
is forewarned by peculiar vibratory thrills, which run through all the affected 
muscles. The eyelids tremble, the body changes its position never so slightly, 
and then, as if the vibrations gained greater and greater power with each moment, 
the fibrillary tremors give way to muscular contractions. The expression of the 
face, which in the preceding stage was set and firm, is now constantly changed by 
the movements of the facial muscles; the jaws, no longer locked together, are 
gnashed and crunched one upon the other; the tongue is alternately protruded and 
drawn back, and, as a consequence, is often caught between the teeth and bitten 
and lacerated. The excessive movements of the muscles of mastication force the 
increased quantities of liquid secreted by the salivary glands from the mouth in the 
form of froth, which is often stained with blood by reason of the injuries to the 
tongue. The constancy of the convulsive movements now becomes less and less 
marked; well-developed remissions occur between each toss of the body and the next, 
until the movements cease entirely ; but it should be constantly borne in mind that 



904 DISEASES OF THE NERVOUS SYSTEM 

the prolongation of the remissions does not produce any decrease in the severity of 
the intervening spasm, the final spasm often being even more violent than the first. 

The intense discoloration of the face begins to pass away as soon as the remissions, 
by their length, permit the blood to be oxygenated, its disappearance being tem- 
porarily arrested by each paroxysm. Finally, the spasms having ceased, the patient 
lies before us relaxed, unconscious, and exhausted, and passes into a deep sleep or 
coma, which lasts a variable length of time, and from which he cannot be aroused 
except very rarely, and then with great difficulty. 

One of the most interesting and important of all the symptoms is the so-called 
aura. Difference of opinion has arisen as to the frequency of its occurrence, some 
authors stating it to be very rare, while others see it very constantly. There can 
be little doubt that in many cases it is as constantly present as in others it is absent, 
and it would appear that the nationality of the patient has something to do with the 
occurrence of this signal of the attack; at least, if we may judge by the statements 
of the chief authors of each nation. Thus, in America, Wood states that "the 
aura is wanting in a very large proportion of the cases of true epilepsy," and Ham- 
mond agrees with him. In England, Gowers stated it to occur in about one-half 
of the cases, and Bristowe states it to be not uncommon. In France and Belgium 
the aura appears to be present in more than half the cases, in one form or another, 
as it is also in Germany, according to Nothnagel. In 970 cases collected by the 
writer it was found that the aura was recorded as present in 362 cases and absent 
in 138 cases. 

The aura, or warning, while possessing general characteristics common to all 
cases, is by no means identical in each individual. By far the largest number of 
cases, when it is present, have it in an extremity, and if it be not there, then it is 
often in the stomach; and it is not uncommon to see persons suffering from epilepsy 
who have as an aura a general, indefinable sensation all over the body. In much 
more rare instances the aurse are situated in the organs of special sense, and are 
evidenced by sudden attacks of blindness, visual hallucinations or deafness. It is 
worthy of note, however, that whereas the aura may differ in every case in origin, 
seat, and limitation, they are remarkably constant in the same individual, rarely, 
if ever, changing in kind, although they may vary in degree. A careful analysis 
of an enormous number of cases by hundreds of observers shows that the aura most 
commonly met with is that beginning in the hand; next, that beginning in the leg 
or foot; next most common, that arising in some of the viscera, and, after these, those 
which arise in the face and tongue. The rarest form of aura is that which arises 
in the sides of the trunk. 

Not only may the seat of the aura be varied, but its sensations may be even more 
aberrant. Undoubtedly the most common sensation is the indescribable sensation 
of a vapor or cloud, already spoken of; but in a large number of cases the sensations 
are described as being quite painful, or perhaps as partaking of the feeling that the 
part is in active movement when in reality it is still quiet. Others speak of it as a 
sensation of cold, others of heating and burning, and still others of trembling and 
indescribable distress. In certain cases the sensation is confined to the spot where 
it is first noticed, and fails to travel upward or toward the central nervous system. 

Status epilepticus is a condition in which convulsion follows convulsion so rapidly 
that consciousness is not regained. In some instances the patient dies within a 
lew hours as a result of exhaustion or asphyxia. As the case goes on the convulsions 
are replaced entirely by coma, or, in rare cases, violent attacks of mania may 
develop. In this state the body rapidly emaciates, bed-sores develop, and death 
ensues from exhaustion. 

An extraordinary number of fits may occur in a brief space of time without 
causing death, or even very ureal exhausion. A very good example of this fact is 
that of a case reported by Newington, which is as follows: On the twentieth day 



EPILEPSY 905 

of the month, at 5 a.m., the fits began in the woman under his care. By 5 p.m. 
the same day she had had 274 fits, and by 5 a.m. on the 21st she had 384 more, or 
622 fits in twenty-four hours. This makes a rate of one nearly every minute. 
By 5 a.m. on the 22d she had 400 more; by 5 a.m. on the 23d, 525; by 5 a.m. on the 
24th, 355, and from 5 a.m. on this day to 5 a.m. on the 25th she had 214 fits. Alto- 
gether she had 2156 fits in five days and yet survived, being fed by the rectum. 

Motor paralysis may succeed epileptic paroxysms, and this is particularly the 
case in those instances where the convulsive movements are largely unilateral in 
character. 

A very important question, connected not only with the prognosis of epilepsy, 
but also with its relation to medical jurisprudence, lies in the influence which the 
disease may exercise on the mental condition of the sufferer. Russell Reynolds 
has arrived at the following conclusions in regard to the effects of the disease on the 
intellect : 

1. That epilepsy does not necessarily involve any mental change. 

2. That great mental impairment exists in some cases, but this is the exception 
rather than the rule. 

3. That females suffer (in mental vigor) more frequently than males, and also 
more severely. 

4. That the commonest failure is loss of memory, and that this, if regarded in 
all degrees, is more frequent than integrity of that faculty. 

5. That apprehension is more frequently preserved than lost. 

6. That ulterior mental changes are rare. 

7. That depression of spirits is common in males, rare in females, but excit- 
ability of temper is found in both sexes 

Not only may mental deterioration result in epilepsy of long duration, but tran- 
sient qualitative mental change may occur. Thus — delirium may precede, replace 
or follow the convulsion — and the so-called "postepileptic confusion," which may 
last for days or even weeks, is a familiar picture to every alienist. 

It is to be recalled that primary mental weakness is often associated with 
epilepsy. 

Complications. — Naturally enough, a very common variety of complication is 
some traumatism, severe or mild, which is suffered as the result of the fall accom- 
panying the fit, whereby the head is struck against some hard or sharp object. 
The severity of the injury may be anything from fracture to a slight abrasion or 
bruise. When such an accident happens it should not be forgotten that the coma 
of the fit may be dangerously deepened by the concussion, and also that the coma 
may mislead the physician so that it is regarded as the natural sequence of the 
attack rather than the result of the injury. Fractures of the clavicle are very 
common. In the same manner various dislocations may ensue. The presence 
of a fracture in an epileptic is a very much more serious matter than would appear 
at first glance, for even if the fits are not frequent they are almost sure to cause a 
fresh solution of continuity, or even to convert a simple into a compound fracture 
by the jerkings of the muscles. Splints are, of course, of value, and the limb may 
be wrapped in a pillow. Careful watching with quiet rest in bed must always be 
insisted upon, since under these circumstances a second fall is avoided on the advent 
of a new attack. 

In other cases apoplexy may occur, due to the sudden strain upon the cerebral 
bloodvessels during the fit, and if the coma following an attack is prolonged or 
peculiar, this fact should be called to mind. The inequality of the pupils, the ster- 
torous respiration, the fact that the tongue cannot be protruded straight from the 
mouth, all point to a cerebral lesion; but the rise of temperature, the coma, and, 
last of all, the hemiplegia, are characteristic of both states, and cannot be used for 
differential diagnosis. 



906 



DISEASES OF THE NERVOUS SYSTEM 



Diagnosis. — Undoubtedly, the most similar convulsive condition that we have 
is that due to hysteria, and the diagnosis of one from the other is as difficult in some 
cases as it is essential and necessary for treatment and cure. The other conditions, 
with which it might be confused, are uremia, alcoholic epilepsy, tetanus, and 
syncope. In the accompanying table are arranged all these disorders, which 
briefly and succinctly shows the different points between them, although of necessity 
it is somewhat arbitrary on account of the lack of space. 



Table of Differential Diagnosis of Epilepsy from Hysteria, etc. 



Signs. 


Epilepsy. 


Hysteria. 


Uremia. 


Petit mal. 


Alcoholic 
epilepsy. 


Tetanus. 


Syncope. 


Apparent 
cause 


None 


Emotion 


None 


None 


None 


None 


Mental 
shock. 


Aura or pro- 
dromata 


Generally 
present, 
but short 


Globus 

hystericus, 

palpitation, 

choking 


Headache, 
vomiting, 
and dys- 
pepsia 


Faintness 
and dim- 
ness of 
vision 


Tremors 


Nervous- 
ness 


Not so well 
defined as 
in epilepsy 


Onset 


Sudden 


Often 
gradual 


Often 
gradual 


Sudden 


Sudden or 
gradual 


Gradual, 
begins in 
jaw 


Sudden or 
gradual. 


Scream 


At onset and 
sudden 


During 

attack 


Frequently 
none 


Frequently 
none 


May or 
may not 
be present 


None 


None. 


Convulsion 


First tonic, 
then clonic 


Rigidity 
more pro- 
nounced, 
with more 
aching 


Rigidity 
generally 
absent 


No rigidity 


Movements 
more clonic 
than tonic 


Always 
tonic 


None. 


Biting 


Tongue 


Tongue, lips, 
and hands 


Tongue 


None 


Rarely 


None 


None. 


Micturition 


Frequent 


Never 


Never 


Rarely, ex- 
cept when 
bladder is 
affected 


Rarely 


Sometimes 


Never. 


Defecation 


Occasionally 


Never 


Never 


Never 


Rarely 


Rarely 


Never. 


Talking 


Never 


Frequent 


Muttering 


Never 


Never 


Never 


None. 


Duration 


A few 
minutes 


Generally 
many 
minutes 


From a 
minute to 
hours 


Momen- 
tary 


May be 
prolonged 


Hours 


Indefinite 
time. 


Conscious- 
ness 


Lost 


Generally 
preserved 


Lost 


Not lost 
always, 
but 
clouded 


Lost 


Preserved 


Lost. 


Termination 


Spontaneous 


May be 

induced 
by shock 


Spontane- 
ous 


Spontane- 
ous 


Spontane- 
ous 


Spontane- 
ous 


Gradual, 
with no 
somno- 
lence. 



The very irregularity of true epilepsy makes it extremely difficult to give clear 
and well-defined outlines of it against another disease, particularly when we remem- 
ber thai epilepsy and hysteria often go hand in hand. 

By far the most important differential point between the two disorders just 
Darned, when not complicated with still another disease, is the character of the move- 



EPILEPSY 907 

ments. As already pointed out, in epilepsy they are typically at variance with 
those of daily life, while in hysteria they are often equally typical of ordinary muscu- 
lar contractions, or, in other words, are more purposive in character; and frequently 
there is prolonged tonic contraction of the muscles, giving rise to the taking of 
positions which bear more or less resemblance to assumed attitudes. In hysteria, 
also, consciousness is impaired sometimes, but never so completely as in true 
epilepsy. Indeed, most commonly the individual knows all that goes on around 
her, for, while she may give no sign of consciousness by words or looks during the 
attack, she may afterward be able to narrate all that has occurred. Less commonly, 
however, a condition known as automatic consciousness exists, in which, during 
the paroxysm, the patient understands all that is said, but forgets everything 
on the return to quietness. 

The fact that the patient is a female cannot be regarded as affirmative evidence 
of hysteria in the least, but if the fit occurs in a male it may be taken as fairly 
positive evidence of epilepsy; and yet it should always be remembered that males 
may suffer from hysteroid attacks. 

The movements of the hysterical patient after the tonic condition has passed away 
are clonic as are those of epilepsy, but still possess some purposive characteristics, 
and are not so bizarre as are those of the true disease. Thus, the head, arms, 
and legs are struck with evident endeavor against the floor or surrounding furniture. 
Another point, which, when it occurs, is very distinctive, is the onset, toward the 
close of a hysterical convulsion of a second stage of tonic spasm such as occurred 
at the beginning. It will be remembered that this does not occur in epilepsy; 
although it must be borne in mind that in cases of the "status epilepticus" the 
rapid onset of another attack may show a second tonic stage. This can be sepa- 
rated, however, by the fact that it is followed by clonic movements, whereas the 
secondary tonic stage of hysteria is usually followed by relaxation and temporary 
recovery. 

Finally, too, in hysteria, some peculiar emotional position is often assumed, 
as of the crucifix, or of intense grief, or, perhaps, immoderate laughter, with corre- 
sponding movements of the trunk. If the patient is quiet at this time, a smile 
may float across the face, while the eyes, with a look of pleasure, pain, or entreaty, 
may seem to be gazing at some object very far off. In some very well developed 
cases the expression of pleasure is followed by a look of pain, with painful move- 
ments, or an appearance of voluptuous entreaty, with sensual and venereal desire 
evidenced by gestures. Very commonly areas of anesthesia and hyperesthesia 
occur in these patients and are of all degrees of intensity and limitation. Search 
for them generally shows their presence after attacks of convulsions, but they may 
persist from one attack to the other, or develop spontaneously. In nearly all 
cases these areas are unilateral, and may extend over one-half of the body, the line 
of demarcation of the anesthesia or hyperesthesia, from the sound area, being 
clearly and abruptly defined, generally at the median line of the front and back of 
the trunk. It will be called to mind that such conditions are absent in true epilepsy. 
Hallucinations are far more common after the fit in hysteria than in epilepsy, and 
sometimes they occur even during the attacks. 

A very useful differential point, strongly insisted upon by Charcot and Bourne- 
ville, is that in true epilepsy there is generally a very considerable rise of temperature 
during an attack, while in hystero-epilepsy the temperature remains normal or only 
slightly raised. Not rarely malingerers simulate attacks of epilepsy, and very 
serious injuries are sometimes submitted to by these persons to carry out their 
designs. The points to be looked into are: the condition of the pupils, which, in 
the simulated attack, always react normally; nor can the corneal reflexes be held 
back; the color of the face is rarely changed, and the thumbs are rarely flexed as 
they should be. Marc has pointed out that in malingerers the bystander can 



908 DISEASES OF THE NERVOUS SYSTEM 

readily straighten out the thumbs, and that they remain so; whereas in epilepsy 
they instantly become flexed again. 

Suggestions as to movements are sometimes followed by malingerers, and the 
movements generally lack the bizarre character so typical of epilepsy. 

If sulphur fumes or ammonia be held to the nose of the fraud, he generally is 
forced to disclose his true condition. The fact that in malingerers there is no rise 
of temperature is a differential point. 

Prognosis. — The physician can always assure the patient and friends that, so far 
as the disease itself in its ordinary form is concerned, there is little danger of death, 
since, as a general rule, unless the attacks are very severe, death rarely occurs, 
unless indirectly by the fall of the body into a stream or well, or when in some 
position where a steady head is necessary for safety. Accidental asphyxia, due 
to the burying of the face in the pillow at night, or to the impaction of food in the 
larynx, may occur, but even this accident is uncommon. 

The question which the friends will always ask is: What is the prospect of 
ultimate recovery, or, at the least, will there be any progress toward an improve- 
ment? Unfortunately, the reply ought not in any case to be favorable, even for 
ultimate improvement, for the experience in the past of every practitioner has been 
that cures rarely occur. 

Treatment. — By far the most valuable drug in use today for the relief of epilepsy 
is bromide of strontium. In many cases the remedy undoubtedly gives relief when 
it is pushed in a suitable manner, and, in the majority of instances, the seizures 
are so decreased both in violence and frequency that its use may be said to be 
indicated in nearly every case of the disease. In a very small minority, however, 
it signally fails. 

A very important point to be borne in mind is that the drug often seems to have 
produced a complete cure, and this results in carelessness in the regularity of admin- 
istration. The patient should be impressed by the fact that every day passed 
without a fit is a step forward, and that every fit carries him many steps backward. 
He should also be made to use the drug in moderation for at least three years after 
all fits have ceased, and to watch, after that time, for the slightest sign of their 
return. The quantity taken each day should be gradually decreased, not suddenly 
stopped. It has been shown that if ordinary table salt is restricted in the diet a 
smaller amount of the bromide salt is required to control the convulsions. 

The iodide of potassium is entirely useless in epilepsy, unless it is due to syphilis, 
when it is of the greatest service. Under this condition the bromides and all other 
drugs should be set aside while it is pushed to the utmost. As is well known, 
syphilitics usually bear the drug extremely well, and the writer knows of one 
instance where no less than 800 grains were taken every twenty-four hours, with 
rapid improvement as a result. 

When the convulsions are due to a gumma the iodide of potassium is, however, 
too slow in its action, and should be replaced by mercury in order to break down the 
growth without delay, lest a seizure end the scene by asphyxia or some similar 
accident. 

In every case the physician should make careful inquiry as to the presence of 
an aura, and, if it is present, he should order that the patient be provided with 
pearls of amyl nitrite, one of which is to be broken and its contents inhaled the 
moment the warning of an approaching fit develops. By this means attacks can 
often be aborted. 

Crotalin, a protein found in the venom of rattlesnake, has of late been exploited 
as a cure for epilepsy, but is only mentioned here that it may be condemned as 
being both inaffective in relieving the malady and at times dangerous to the 
patient. 

As constipation and indiscretion in diet are potent factors in bringing on the 



ECLAMPSIA 909 

individual attacks, the patient should be instructed to keep the bowels open freely 
and to avoid overloading the stomach. 

Petit Mai or Minor Epilepsy. — Petit mal differs in no way in its essential char- 
acters from epilepsy of a much more highly developed form, but in its minor char- 
acteristics it is sufficiently at variance with haul mal, or grand mal, to separate 
it in the minds of clinicians. In its most common form petit mal consists of a 
momentary loss of consciousness, accompanied by pallor, or, more rarely, flushing 
of the face. The man who is subject to the disease suddenly stops what he is doing 
for a moment or two, and then takes up his work or subject as soon as he recovers, 
and at the point where he ceased, being often unconscious of the break in his con- 
versation or labor. Reynolds has divided this minor form of the affection into 
two divisions. In the first he places those who are attacked and have no evident 
spasm, and in the second group are those who have evident spasm. The seizures 
are characteristically fugacious, and if any spasm is present it is nearly always of 
the tonic variety. Sometimes the disorder of motility lies chiefly in an inhibition 
of an act about to be performed. The fork in a man's hand at a dinner-table may 
be raised half-way to the mouth, then held in mid-air for a moment, and then 
as the attack passes away, continue on its journey to the mouth; or, a woman 
playing the piano may suddenly pause with her fingers raised from the keys, miss 
the time of three or four bars, and then go on exactly where she left off, as if no 
interruption had occurred. 

Jacksonian Epilepsy. — By the term Jacksonian epilepsy we mean an affection 
which separates itself from true or ordinary idiopathic epilepsy by several peculiari- 
ties. By far the most important of the peculiar signs is the character of the onset, 
which always begins, in the typical Jacksonian disease, in some peripheral portion 
of the body, and most frequently in the muscles of the thumb or hand, so that for 
the moment the movements are localized and may remain localized at the point 
of origin, or immediately diffuse themselves over muscle after muscle until all the 
arm, leg, or other groups of muscles are involved. It is of the greatest importance, 
however, that the reader should keep the aura of an attack separated in his mind 
from the onset, remembering that the term onset is here used by the writer to 
designate the beginning of the period following the aura, if there be one. Jacksonian 
epilepsy may be of almost any degree of severity, for in rare cases but one muscle 
may suffer throughout an entire attack, or in others the entire body may be finally 
convulsed. There may or may not be loss of consciousness, its presence or absence 
being dependent upon the severity of the attack. In those instances in which only 
a few localized muscles are involved, consciousness is more commonly preserved 
than lost. 

ECLAMPSIA. 

The term "eclampsia" is applied to convulsions affecting children and pregnant 
women, or women who have just been delivered. 

Infantile Eclampsia. — In infantile eclampsia the attacks are epileptiform in char- 
acter and seem to depend upon a condition of undue irritability of the nervous 
system, which is still further disturbed by some reflex cause. Thus, it is commonly 
supposed that gastric and intestinal indigestion may produce infantile eclampsia, 
and certainly the presence of foreign bodies in the stomach and intestines may act 
in this manner. Again, many physicians believe that the first dentition, by reason 
of the irritation in the gums, may result in such a seizure. This is doubtful. A 
host of other sources of peripheral irritation have also been held responsible. Not 
rarely the underlying cause is rickets. It is often stated, in text-books on medi- 
cine, that the acute infectious fevers are frequently initiated by a convulsive 
seizure. As a matter of fact this rarely occurs in an ordinary child when infected 
in this manner. 



910 DISEASES OF THE NERVOUS SYSTEM 

The convulsive attack varies in severity from a mere clinching of the fingers and 
the drawing of the thumb into the palm of the hand to a severe clonic or tonic 
convulsion closely resembling epilepsy or hysteroepilepsy. In many instances 
the child has a single attack and no more. In other cases several attacks occur 
within a few days. In still others the occurrence of one or more attacks of convul- 
sions seems to develop a convulsive habit, and in these instances the child may 
become a confirmed epileptic. In such cases, however, it is probable that the con- 
dition of indigestion, or other direct cause, simply induces a nervous explosion on 
the part of a brain which has an impaired stability. 

Diagnosis. — The condition must be separated from the convulsions produced 
by organic cerebral disease (which see). 

Prognosis. — The prognosis in infantile eclampsia is good for single attacks, and 
becomes grave in direct proportion to their severity and repetition. Such attacks 
occurring in feeble, poorly nourished children are more grave than in those who are 
better able to withstand an illness. 

Treatment. — This consists in removing the cause of local irritation, if it can be 
found. If it exists in the stomach or the bowels, it should be removed by an emetic 
or a purge. If the gums are inflamed they should be lanced. If rickets is the cause 
it must be cured if possible. 

The treatment of the attack itself consists in the administration by the mouth, 
if swallowing is possible, of 5 or 10 grains of bromide with from 2 to 4 grains of 
chloral, or by the use of 20 grains of sodium bromide with 5 grains of chloral in 
starch-water, by the rectum. If laryngeal spasm is marked, and is a dangerous 
symptom an inhalation of nitrite of amyl may be used, or chloroform may be 
employed if the heart is not weak. 

Puerperal Eclampsia usually occurs in young primiparse. The convulsions 
are tonic and clonic. The pathology of the condition is not understood. Without 
doubt the condition is toxic. In some instances it is probably due to perverted 
functional activity, or actual disease, of the liver or kidneys. In other instances 
it seems to be dependent upon perverted metabolism. Not infrequently, in asso- 
ciation with the albuminuria of pregnancy, there is albuminuric retinitis, and even 
blindness with general anasarca. That the presence of fetus in utero exercises some 
influence is shown by the fact that not infrequently the convulsions cease as soon as 
the uterus is emptied. 

Puerperal eclampsia is an exceedingly dangerous condition. The mortality 
varies from 20 to 30 per cent., or even more than this. In a certain proportion of 
cases it can be prevented, and for this reason the physician should repeatedly 
examine the urine of the pregnant woman for several months before the termination 
of pregnancy to determine that the kidneys are carrying out their eliminative 
function properly. The blood pressure if above 160 systolic is to be taken as 
threatening eclampsia. 

Treatment. — The uterus must be emptied, the poisons must be eliminated, and 
the nervous system must be quieted. For the best method of emptying the uterus, 
the reader is referred to books upon obstetrics. If arterial tension is high and there 
is much cyanosis, the patient should be freely bled and the intravenous injection 
of normal saline solution employed, unless there is a tendency to pulmonary edema, 
when the intravenous injections should not be used. Copious irrigation of the large 
bowel or the injection of an ounce of magnesium sulphate dissolved in a half-pint 
of water and 2 ounces of glycerin are also useful. If the convulsions are severe 
in these cases may physicians treat the condition by the use of large doses of 20 to 
30 minims of the tincture, or even of the fluid extract, of veratrum viride, giving it 
in some cases hypodermically. A useful preparation for hypodermic use is 
strophanthine. This drug lowers arterial tension quiets the spinal cord, and 
produces sweating. Pilocarpine is never to be employed, as it almost invariably 
causes pulmonary edema. 



AMOK 911 



LATAH. 



Latah is a state very closely allied to the saltatory spasm described by Bam- 
berger, and the patients described by Beard as " jumpers." The chief symptom 
of latah is involuntary and uncontrollable mimicry by the patient of everything 
she sees or hears. There is also frequent coprolalia or the spasmodic ejaculation of 
filthy words. The disease is common among the Malay races, and its geographical 
distribution corresponds with the countries inhabited by these people. It occurs 
commonly enough among the Filipinos and is known by the Tagalogs as "mali- 
mali." It is seen in Ceylon and Burmah, and the disease known in Siberia as 
"myriachit" is probably identical with it. Kraepelin allies latah with hysteria. 

The subjects of latah are almost invariably women in early adult life. Men 
rarely, if ever, suffer from the disease. There is a distinct hereditary tendency, 
but the cases show no evidence either of hysteria or epilepsy. It is a very common 
spectacle indeed, in Malay villages, to see one of these unfortunate women pursued 
by a crowd of tormenting boys. They dance in front of her, going through all sorts 
of grotesque and obscene movements, and the unfortunate victim, apparently 
struggling to the utmost to resist the impulse, exactly imitates all their actions to 
her own great rage and mortification. Besides such examples of complete echo- 
chinesia, or mimicry of motion, there frequently is echolalia, or mimicry of speech. 
When startled or frightened these patients utter irrelevant words or incoherent 
noises and make involuntary movements. Consciousness is never lost during these 
attacks. This latter type closely resembles the "jumping Frenchmen" of Maine 
and Canada, who jump violently and suddenly with a loud cry when startled or 
when under strong emotion. Jumpers, and latah patients as well, will frequently 
obey any sharp, sudden command given them. Undoubtedly, this represents some 
form of psychic suggestion acting on a weak and unstable will. The Malay is 
notoriously unstable in his mental makeup. Such patients are markedly neurotic. 
They are pusillanimous and easily startled. As a rule, both the superficial and 
deep reflexes are increased. Many of these patients suffer later from serious mental 
disorders. Among the Philippine natives "mali-mali" patients are believed to be 
particularly prone to the outbreaks of maniacal furor known as amok. 

AMOK (RUNNING AMOK). 

This term is used, in Malayan countries, to designate cases of maniacal furor 
in which a native rushes out in the streets of his village with kris or barong, cutting 
down everyone in his path, until he himself is dispatched or commits suicide. 
It is a question whether these outbreaks should be considered as evidences of a 
specific disease. Preceding the attack the patient is in a stupid, morose, or melan- 
cholic condition for several days. During this period there frequently is amnesia, 
and during the attack itself complete amnesia is the rule. The exciting causes of 
the outbreak are usually psychical; grievance over some real or fancied wrong, 
over financial losses, marital difficulties, fear of disgrace or punishment, and the 
sight or smell of blood. The disease almost always attacks young adult males. 
Various causes have been advanced for this condition. Alcoholism may be 
excluded, as the Malay, although not a total abstainer, is very frugal in the use 
of liquors. So, too, opium smoking cannot be considered the cause of the disease. 
Bevan Lewis believes it to be a psychical epilepsy, and, indeed, transitory furor 
very much resembling the attacks of amok are frequently seen in epileptics. Earlier 
travellers and writers ascribed these attacks to religious mania. Schuebe discredits 
this idea on the ground that the Koran does not justify the killing of unbelievers, 
and he quotes Ellis to the effect that amok-running occurred among Malays before 
they were converted to Mohammedanism. The Malayan races chiefly subject 



912 DISEASES OF THE NERVOUS SYSTEM 

to amok are the Bugis, Illanums, and the Sulus, or Joloanos, in the Southern 
Philippines. In many instances among this last tribe the motive is undoubtedly 
religious. During the service of the United States army in the Philippines a most 
melancholy case occurred in an officer, corresponding exactly to the typical amok 
cases. This man, an excellent soldier, and a man of exemplary personal habits, 
after a few days of brooding and melancholy, suddenly appeared on the veranda of 
his quarters with a rifle and began to shoot into his company formed up in close 
proximity. He could not be secured, and after wounding a number of his men he 
was shot and killed by one of his own sergeants. With regard to the responsibility 
of these cases no general rule can be laid down. The responsibility cannot be 
affirmed in all cases, nor can it be denied. Most of the cases of amok are clearly 
irresponsible. Mention has been made, under Latah, of the occasional outbreaks 
of furor resembling amok that take place in that disease. 

According to Kraepelin, who has studied this condition in Java very completely, 
amok is not an entity, but embraces a variety of conditions in which sudden, 
violent, impulsive acts are committed while consciousness is clouded. Some cases 
belong to the class of the "insanity of adolescence," some are epileptics, a few may 
be instances of "malarial psychosis," but there are rare cases of amok that Kraepelin 
cannot explain. Latah is distinguished from it by the complete preservation of 
consciousness in that state. 

ASTASIA-ABASIA. 

Definition. — Astasia-abasia is a symptom of hysteria. It occasionally follows 
disturbance of the nervous system produced by injury, and in that sense might 
be considered a traumatic neurosis. Occasionally it has followed the acute infect- 
ious diseases. 

Symptoms. — The symptoms consist in a partial or complete inability to use the 
lower limbs in standing or in walking, although if the patient lies upon her back in 
bed she can move her legs perfectly. Examination fails to reveal any alteration 
from the normal as to motion, co-ordination, or sensation. When the condition 
simply interfers with walking, it is called "dysbasia." Patients who may be quite 
unable to walk can, nevertheless, swim perfectly. 

The prognosis is as favorable as that of ordinary hysteria, and the treatment is 
the same as that which is employed for patients who are suffering from hysteria 
or neurasthenia. 

TRAUMATIC NEUROSES. 

Definition. — Under the term traumatic neuroses there is described a condition in 
which an individual, after exposure to some severe mental shock or physical injury, 
develops a train of symptoms which do not depend upon any demonstrable lesion of 
the nervous system. As the result of functional disorder of the nervous system in 
various parts of the body, following the accident, the patient presents symptoms 
which are chiefly subjective, though they may be somewhat objective, and he may be 
actually and completely incapacitated from performing the ordinary acts of life for a 
long period of time. Rarely the disability may be permanent, but in these cases the 
question always arises as to whether there has not been in addition to the functional 
disturbance an actual organic lesion. It is evident, therefore, that cases of this 
character may, and do, present to the physician very difficult problems in differential 
diagnosis, for not only may functional disorders exist side by side with those due 
to true organic change, but in addition the functional disturbances may simulate 
organic; disease so closely as to cause great confusion in symptomatology. When to 
these natural difficulties are added the desire of the patient to obtain heavy damages 
from the individual or corporation responsible for the injury, it at once becomes 



TRAUMATIC NEUROSES 913 

evident that malingering or unintentional and subconscious production of symptoms 
may be commonly met with. 

Etiology. — The most common cause of traumatic neuroses are railroad accidents, 
trolley-car accidents, falls, and injuries received from falling bodies. As a result 
of exposure to one of these causes, with associated mental shock due to terror or 
horror, the nervous system develops the perversions about to be described. 

Symptoms. — It is manifest from what has already been said that the symptoms 
may be most varied as to severity, distribution, and duration. Probably the most 
common statement of the patient is that he has lost power in one or more parts of 
his body, or he may suffer from disturbances of sensation, with or without loss of 
power. In males it is not infrequently claimed that the injury has resulted in a 
loss of sexual power, particularly if the back has received a blow or strain, even if 
the genital apparatus is itself entirely unaffected. In women the most common 
complaint is of pain or weakness in the back, of pelvic pain or displacement of the 
pelvic organs, and of vesical disorders. In other cases the chief claim is that more 
or less violent pain or tingling in the limbs is suffered. When loss of power is 
suffered from it appears usually as a hemiplegia or a brachial monoplegia, but if it 
be a hemiplegia the face nearly always escapes. Paraplegia is very rare and the 
sphincters of the bladder and rectum always escape. 

Those paralyses which are not truly organic can be separated from those that 
are such by the facts that the reactions of degeneration do not develop in the 
paralyzed parts and the deep reflexes are usually preserved. Anesthesia is practic- 
ally always present if the paralysis of motion is complete, and it is of the type of 
hysterical paralysis in that it has often a sharp line of degeneration which is not 
coincident with the distribution of the sensory nerves of the part. Paraplegic 
cases do not suffer from anesthesia of the genital organs. Again, it sometimes 
occurs that the symptoms complained of are not constantly in the same part or 
that positive suggestions may cause their development elsewhere. Not rarely an 
examination of the color fields of such a patient will reveal the reversals commonly 
found in hysteria. Disorders of all the special senses may also occur and total 
disappearance of these functions may take place — as complete deafness, blindness, 
or loss of taste or smell. Occasionally the patient may develop attacks which 
resemble to some degree ordinary epilepsy or catalepsy, but these attacks are 
separated from true epilepsy by the points already named when discussing that 
disease. 

If we carefully exclude from any case of nervous disorder following an injury the 
presence of an actual organic lesion, we may unhesitatingly state that the patient 
is suffering from hysteria or neurasthenia due to injury, and we can treat him 
accordingly. On the other hand, it is not to be forgotten that the patient who 
suffers from the symptoms he describes is often a most miserable and unfortunate 
individual, as deserving of our pity as if we found him the victim of an incurable 
malady due to destruction of a part of his body. His functional disorders are as 
real to him and cause him as much suffering as if they depended upon organic 
causes, and a nervous system functionally perverted may be as useless as one 
actually grossly diseased, just as a watch which needs regulating may be as useless 
to its owner as one in which a spring is broken. While, therefore, it is our duty 
to relieve such patients by every means in our power, and to bear in mind that their 
sufferings are often very real, we are forced to recollect that the condition may not 
be permanent, as it would be after a destructive injury, and so when the case has 
become one of medicolegal importance it may not be possible to testify that the 
patient is incurable and permanently disabled. Not only is this true, but it is also 
a fact that the very continuance of litigation, and the frequent appearance of the 
patient before attorneys and experts for both sides and before a crowded court-room, 
may make recovery impossible by still further exciting and disturbing nervous 
58 



914 DISEASES OF THE NERVOUS SYSTEM 

balance, for aside from this form of excitement the description of the scene of the 
accident impresses its terrors, over and over again, upon a mind already horror- 
stricken by the original occurrence. Perfectly sincere persons often suffer all the 
symptoms they describe up to the period when the trail of the case is finished and 
then speedily improve. 

Treatment. — The treatment varies, of course, with the character of the symptoms, 
but it may be said to be practically identical with that already advised in cases of 
hysteria and neurasthenia. 

OCCUPATION NEUROSES. 

An occupation neurosis is a state in which the innervation of a part becomes 
functionally disturbed by the exhaustion of the nervous centres supplying it, and 
in all probability by exhaustion of the nerve endings as well. The causes of this 
exhaustion are exceedingly numerous. Almost every pursuit in life which involves 
the continuous use of muscles of the hand and wrist may produce an occupation 
neurosis of these parts. As a result we find spasm, cramp, or palsy developing to 
such a degree as to incapacitate the patient. The most common neurosis, because 
the pursuit is most common, and because small and accurate movements are 
required, is that due to writing, the so-called scriveners' palsy or writers' cramp. 
Another form is telegraphers' cramp, and a third is hammerers' palsy. Less com- 
mon forms are violinists' cramp, pianists' cramp, flute-players' cramp, and " sewing 
spasm." Milkers and cigarmakers sometimes suffer from neuroses of this character. 
In writers' cramp the flexor muscles suffer chiefly, while in telegraphers' cramp 
the extensors are the ones most involved. Various disorders of sensation in the 
hands are also present and consist in sensations of tingling, tension, or numbness. 
Localized sweating or excessive dryness of the skin may be present. Occasionally 
the condition depends upon, or is associated with, a true neuritis, which may involve 
the entire brachial plexus and cause pain in the upper arm and even in the muscles 
of the neck and head on the affected side. The history of the case in many instances 
is that the patient first experiences for some days a feeling of stiffness and lack of 
pliability in his fingers, which is generally accompanied by a certain lack of co-ordi- 
nation in the movements required. This inability to move the fingers rapidly and 
accurately is only present when the sufferer attempts to perform the movements 
which are the cause of the trouble, and almost all other motions can be gone through 
with without difficulty. If the patient now insists on keeping on with his duties, 
the stiffness is replaced by violent cramps, more or less painful, which come on 
suddenly and with considerable power. Co-ordination is still further disordered 
and all attempts at a repetition of the offending act are resented by the -affected 
centres and muscles in such a positive manner as to make all movements irregular 
and often jerking in character. Unless absolute rest and avoidance of former 
movements is permitted, the cramps, etc., are followed by loss of power, deepening 
into partial paralysis. Even when paralysis exists, however, it is surprising to 
see how many unoffending movements can be performed without discomfort and 
failure. 

Some discussion has arisen as to whether the several symptoms which the disease 
presents are each in their turn an indication of a more advanced stage in the disorder 
or are merely more prominent in one case than another by chance or tendency on 
the part of the individual to any one of them. Thus, some observers have held 
that the first sign of the disorder was the feeling of distress or fatigue in the over- 
worked extremity/and that the tremors followed because the warning given by the 
fatigue was not heeded. Finally, the disregard of this second symptom brought 
about the spasm or cramp, or, in other cases, the palsy. Other writers, especially 
those of the present day, have attempted to prove that there is no distinct onward 



OCCUPATION NEUROSES 915 

march of the symptoms from fatigue to tremor and from tremor to palsy or cramp, 
but rather than the disorder is to be divided into four varieties, each one of which 
may assert itself without the development of another. 

Thus, Lewis tells us that in some cases cramps come on, in others palsy, and in 
others tremors, while still another variety is separated from its fellows by the 
predominance of certain symptoms associated with disturbances of sensation. 
He states, however, that the disorder of sensation is always present in all forms of 
the trouble in some degree, and that it is only in cases where the trouble consists in 
a neuritis that the symptom rises to the importance of marking a separate variety. 

Many very prominent writers on scriveners' and hammerers' palsy assert that 
predisposition is one of the prime factors in the causation of these maladies. While 
this is doubtless true to a certain extent, it is nevertheless a fact that all persons, 
be their temperaments nervous or otherwise, are affected, and in view of this fact 
the writer thinks that predisposition should not be accorded the leading position 
in the causation of the malady. It is, of course, probable that persons whose 
temperaments are nervous and excitable are naturally susceptible to nervous dis- 
orders, whereas the phlegmatic temperament is rather opposed to the conditions 
which are necessary for the presence of this disease. 

Rosenthal calls attention to the fact that the loss of power is limited entirely 
to those centres which are the directors of the particular muscles involved, and 
states in substantiation of this assertion that the surrounding centres for other 
groups of muscles always escape, as is proved by the fact already mentioned, that 
other acts can be performed without difficulty. While it is true that the surround- 
ing centres are not affected, it is also true that the centre governing like movements 
in the opposite hand is, by sympathy or other cause, affected with its fellow to a 
certain extent. This is proved by the fact that if the operator learns to send 
messages with this well hand, that hand very soon follows the fate of its fellow. 

Experiments performed by the late Dr. N. A. Randolph bear so strongly on this 
subject that they may be quoted at this point. His object was to discover if 
exhaustion of one centre in the brain produced any effect on the corresponding 
centre on the opposite side of the brain; and to this end he proceeded as follows: 
He attached a small lever to a meter, and resting the hand of the subject on the 
table, as when writing, he directed him to place the tip of his forefinger on the end 
of the lever and to depress it as often as he could. Each depression was, of course, 
registered in this way. Dr. Randolph found that, normally, the right forefinger 
possessed power for 100 movements, the left forefinger for 75 movements. Having 
decided this primary point he proceeded to search after the main object of his 
examination. He found that if the left forefinger was set to work after the right 
forefinger had performed* its 100 depressions, it became exhausted at 50 movements, 
and that if the right hand was set to work after the left forefinger had moved 75 
times it could only move 75 times. In other words, exhaustion of one centre 
produced exhaustion of the corresponding centre on the opposite side of the brain. 

Careful tests prove that in most instances exaggerated reflexes are present, 
denoting a hyperexcitability of the spinal cord, and in other cases evidences of 
neuritis of the nerve trunks have undoubtedly been observed. In some cases of 
the disease a species of pseudomuscular hypertrophy comes on, due, probably, to 
some centric nervous lesion, and, perhaps, in part to the congested condition which 
is nearly always present in the affected muscles. Thus we find the bellies of the 
muscles hard, firm, and projecting, yet devoid of power. 

Treatment. — In the way of treatment rest is the best measure that we possess 
for the cure of the affection; but although absolute rest from the exciting cause is 
one of the essential factors for a complete recovery, the affected arm should be 
used in every other motion which is natural and easy, so that it may not become 
useless from disuse. Next to rest we have as a therapeutic agent electricity, 



916 DISEASES OF THE NERVOUS SYSTEM 

which is, however, indicated only in those cases where very slight or no inflammatory 
conditions are present, either in the muscle, nerve, or nerve centre; and it should 
be the invariable rule to use that current which causes the most contraction with 
the least pain. Galvanization of the affected muscles should be performed in such 
a way that the disordered nerve centres are not disturbed, and care should be taken 
to gradually increase the exercise, so as not to exhaust or overfatigue the muscles 
which are out of order. Movements which are slowly performed with the affected 
parts are also useful, following the method of muscle training proposed by Fraenkel 
in the treatment of locomotor ataxia. 

Finally, the administration of tonics, such as arsenic, iron, and strychnine, is 
to be resorted to, and these measures combined with massage are the best methods 
we have for effecting a cure. 

RAYNAUD'S DISEASE. 

Definition. — Raynaud's disease is a condition in which one or more of the fingers 
or toes, and rarely the nose and ears, suffer from a disorder of the local bloodvessels, 
with the result that these parts become bloodless and pallid or slate colored and 
mottled in appearance. The affected parts are cold and sometimes painful. The 
malady usually affects persons under thirty years of age, and females more com- 
monly than males. The cause is unknown save that it seems to be of the nature 
of a paroxysmal neurosis involving the bloodvessels of the parts affected. Various 
conditions, all of them capable of causing a loss of normal nerve tone, have been 
considered as etiological factors, varying from diabetes and neurasthenia to fright 
and exposure to cold air or cold water. 

Etiology. — The onset begins with a sense of tingling, or of heat or cold, in the 
parts which are to suffer from the well-developed state. The skin looks shrunken 
and ashen in hue and numbness is present to a more or less well-developed degree, 
but complete anesthesia does not occur. The condition may last for a few hours 
or for weeks. When it disappears it nearly always returns in a short time. 

When the disease occurs in its severe form local gangrene may ensue. The 
part becomes livid and dusky and small blebs develop on the fingers. These may 
dry up and recovery take place, only the skin being destroyed, or the process may 
become so deep that the entire part may be lost. 

This condition is to be separated from senile gangrene by the youth of the patient, 
from frost-bite by the absence of a history of exposure to cold, and from chronic 
ergotism by the absence of any history of eating rye bread contaminated by ergot. 

Treatment. — The treatment consists in the use of tonics and every possible 
measure designed to re-establish good general health. Hydrotherapy is often of 
value. Locally the nutrition of the affected part may be maintained to some 
extent by the use of dry or moist heat. Great care should be taken to protect 
those parts which are usually affected, from extremes of heat and cold. 

ANGIONEUROTIC EDEMA. 

Definition and Symptoms. — Angioneurotic edema is a condition characterized 
by the suddea appearance, in a limited area in one or more parts of the body, of 
well-defined swelling due to some perversion of the normal functional activity of 
the vasomotor nerve supply, so that the bloodvessels of the part become dilated, 
and, in all probability, ;m extravasation of fluid takes place. The condition is to 
be clearly separated from that characteristic of inflammation. The temperature 
o!' the pari is often lower, but sometimes it is higher than normal. The dimensions 
of the affected part vary greatly, but it is rarely more than a few inches in circum- 
ference 1 . The hue of the area affected may be a deep red, as if suffering from intense 



ERYTHROMELALGIA 917 

congestion, or so pallid as to be cadaveric. It may be the seat of a sense of tingling, 
or heat, or itching, but actual pain does not occur, and pitting on pressure, to the 
extent that it appears in ordinary edema, is absent. 

Angioneurotic edema occurs most commonly on the face or hands. It may 
affect the body and quite rarely the larynx and pharynx, when it may produce 
alarming symptoms by interfering with respiration. Instances of death due to this 
cause have been reported. The attacks last a few hours to several days, and are 
prone to occur at irregular intervals. 

Angioneurotic edema occurs more frequently during the third decade of life 
than at any other period, and in the United States affects females more frequently 
than males, although the reverse of this holds true in Europe. We do not know 
what the causative factor is, but it is known that exposure to cold and causes 
which diminish nervous tone bring on an attack in those who are susceptible. 

In some cases the condition is induced by digestive disorders, or by the ingestion 
of some food which is toxic, as lobster, fish, or other animal food that is not fresh. 
In nearly all cases the patient is neurotic, and not rarely has a neurotic family 
history, or even a direct inheritance of the disorder from the parents. 

Diagnosis. — Angioneurotic edema must be separated from the local vasomotor 
disturbances of hysteria. This is done by the fact that in hysteria there are asso- 
ciated paralysis of motion or anesthesia and, it may be, hysterical contractures. 
Again, the edema of hysteria is often persistent, whereas this is temporary. From 
severe attacks of urticaria it is differentiated by the fact that "hives" are usually 
scattered widely over the body, and if they appear on the hands are characterized 
by multiple lesions. In most cases of hives, or urticaria, additional lesions can be 
produced by rubbing a part. Some of these suffer from severe attacks of abdomi- 
nal pain resembling appendicitis. 

Prognosis. — The prospect of complete cure in the sense of an escape from all 
future attacks is not encouraging. The general health is usually good between the 
attacks, and unless the part affected be the larynx the prospect of any serious result 
is unlikely. 

Treatment. — The treatment can be directed only along those lines which will 
tend to improve the general health, of which the most useful are an out-door life, 
hydrotherapeutics, and the internal use of tonics, such as iron and arsenic if there 
is anemia, and nux vomica and quinine if the nervous system is atonic. Phosphorus 
may also be useful. When lithemic or gouty conditions are present, the iodides, 
salicylates, and colchicum may be of great value. It is needless to add that all 
causes known by the experience of the patient to be provocative of an attack should 
be sedulously avoided, for there can be little doubt that the occurrence of one attack 
predisposes to another. 

ERYTHROMELALGIA. 

Definition. — This condition was first described by Weir Mitchell in 1872. It 
consists of a hyperemia of the foot and leg, rarely the hand, associated with pain 
which may vary in degree from a sense of weight and heaviness to exceedingly 
severe suffering. The malady first affects the neighborhood of the ball of the foot, 
and thence it spreads to the entire plantar surface. In other cases the heel is first 
affected. Although exercise greatly increases the suffering, it is, as a rule, worse 
at night. The pain may be intermittent or continuous. The skin is often not 
only hyperemic, but is often marbled or mottled in appearance. Elevation of the 
part, by decreasing the congestion, diminishes the pain. 

Etiology. — The causes of the malady are several. In rare instances it seems 
to depend upon lesions in the spinal cord, in others it apparently depends upon 
diabetes mellitus, and in still others arteriocapillary fibrosis seems to be the under- 
lying factor. 



918 DISEASES OF THE NERVOUS SYSTEM 

Diagnosis. — Before determining the diagnosis of erythromelalgia it is essential 
that gout and diseases of the soft and hard tissues of the foot be excluded. In 
the vast majority of cases the symptoms will probably be due to such causes, for 
true erythromelalgia is a very rare malady indeed, and but few cases have been 
recorded. 

Treatment. — Treatment often fails to give much relief. The part should be kept 
in an elevated posture as much as possible, cool lotions may be applied to it, and 
if the patient be lithemic the alkalies and salicylates should be given. 

MIGRAINE. 

Definition. — Much confusion exists as to the exact nature of the condition which 
is called migraine. By all authors it is used to describe a condition of severe pain, 
more or less limited to one side of the head, often accompanied by some disturbance 
of vision in one or both eyes, and by nausea and vomiting, which often do not 
develop until toward the end of the attack. Certain clinicians have expressed the 
belief that migraine is an hereditary affection, and even go so far as to regard it as 
a manifestation of nervous instability not far removed from epilepsy. This, how- 
ever, is certainly incorrect in the vast majority of cases. It may be true that certain 
neurotic individuals who are subject to hysterical or epileptic manifestations often 
suffer from migraine. But, on the other hand, it cannot be denied that in the 
majority of instances the condition is a toxic neurosis due to the production and 
retention in the body of abnormal products of metabolism. These products are 
chiefly the result of a disturbed action of the liver, either in the sense that the 
liver fails to destroy poisons which are absorbed from the intestines, or in the sense 
that it develops substances which it does not produce when in health. As a matter 
of fact migraine, as a toxic condition, is rarely the result of any disorder of function 
in a single organ, but is produced by several causes, an undue development of 
poison, a deficient action of the liver in destroying these poisons, and a torpid 
condition of the kidneys, whereby toxins are not speedily eliminated. It naturally 
follows that in highstrung, nervous individuals, and in those who have neurotic 
tendencies, these toxic products can readily disturb the functions of the sensory 
nerves of the head and so produce a seizure. 

Among the active causes in provoking an attack of migraine, aside from the 
effects of autointoxication, there can be no doubt that nervous tire, or exhaustion, 
aids materially in causing an attack, particularly if in addition to such stress there 
is added undue sexual activity, or other forms of abuse. All these factors diminish 
the nervous energy which supports vital processes and so tend to cause perversions 
of metabolism, and at the same time they diminish the resistance of the nervous 
and vascular system to the action of such poisons. 

The disease occurs most frequently in women and rarely develops before the age 
of puberty. It is particularly prone to attack those who have a gouty ancestry. 
Certain schools of ophthalmologists have strongly urged the view that all cases 
of migraine are due to errors of refraction. There can be no doubt that in many 
instances this cause of nervous exhaustion is a potent factor. The important point 
for the physician to remember in studying this malady is that various causes may 
be responsible for it; and if the patient is to be permanently relieved, one or more 
of these causes must be discovered and removed. 

Symptoms. — The mode of onset of an attack varies greatly. Some patients 
state that for several days prior to a paroxysm they feel generally out-of-sorts and 
anything but well. Often the chief symptom is mental depression. Other patients 
have no premonitory symptoms whatever. Arising in the morning in perfect 
health, they are seized at some time during the day with blurring of the vision in 
one or both eyes, soon followed by a sharp attack of pain, or pain may be the first 



MIGRAINE 919 

and only symptom, and its onset may be so sudden and severe as to completely 
incapacitate the patient. To this form of migraine the terms "fulgurating" or 
"fulminant" have been applied. In most cases the pain exists chiefly in one side 
of the head, and involves the supraorbital region and the eyeball. When it is fully 
developed the entire head may suffer. The character of the pain is throbbing and 
the sensation in the head is tense. Not rarely photophobia is present, and in some 
cases vision may be so much interfered with that actual hemianopsia is described by 
the patient. In addition to the pain the patient not infrequently has some vertigo, 
is mentally heavy and dull, and not rarely slightly aphasic. 

After the attack has lasted from one to several hours the patient quite frequently 
becomes nauseated and then vomits. As a rule, the stomach does not contain 
undigested food; on the contrary, digestion seems to have gone on with undue 
rapidity. The material vomited is usually small in amount and excessively acrid 
and acid. I am firmly convinced that this fluid is the result of an attempt on the 
part of the stomach to eliminate poisonous materials, just as this organ eliminates 
oxydimorphine in morphine poisoning. If the vomiting persists for any length 
of time bilious materials may be brought up by reason of the drawing of bile through 
the pylorus in the act of retching. It is a question whether this vomiting is the 
result of the action of the poison which produces the symptoms, or whether it is in 
large part due to the severity of the pain which, when it affects the eyeball, closely 
resembles the sickening pain produced by an injury to the testicle. During an 
attack the patient's face is usually pallid and betokens severe pain, having an 
anxious and hunted expression or one of profound depression. Sometimes the 
radial pulse is small and hard, and not rarely the temporal artery on the affected 
side stands out like a whipcord. The attacks rarely come oftener than once a week, 
and sometimes much more rarely than this, unless the patient by errors in diet 
and by various excesses produces the provoking condition frequently. Sometimes 
patients state that the attack comes on in the midst of perfect health. Thus, I 
have heard a patient remark that she felt so well that she was sure she was going 
to be sick the next day, as it had been her experience that a sensation of well-being 
was not rarely followed by a nervous explosion. In rare cases a certain degree 
of paralysis of the extraocular muscles may be present during the attack. In still 
more rare instances the face is flushed instead of being pallid. Not rarely during 
the attack the urine is scanty and high colored, but as the attack subsides the urine 
is frequently passed in large quantities and is exceedingly limpid. Speedy recovery 
usually follows the vomiting of the acrid fluid already named. 

Treatment. — The treatment depends upon the underlying cause of the malady. 
All excesses as to eating and sexual activity must be prevented. If the patient 
is run down and neurasthenic, a vacation or a rest cure is essential. If the kidneys 
fail to excrete a sufficient quantity of urinary solids per day, the various potassium 
salts, such as the acetate, citrate, or bitartrate of potassium, must be given in 5 or 
10 grain doses three or four times a day, in copious draughts of water to increase 
urinary elimination. If there are any evidences that the liver is persistently or 
occasionally inactive, its function should be stimulated by the use of calomel, blue 
mass, or podophyllin. Many of these cases do very well if 5 to 10 grains of blue 
mass are taken every week or ten days, and then followed by a saline purge. In 
those instances in which the patient leads a sedentary life, active out-door exercise 
to ensure perfect oxidation processes in the body are essential. In those patients 
who suffer from gastrointestinal catarrh, a dose of Hunyadi or Apenta water, taken 
hot and in sips, before breakfast, will often be efficient not only in moving the bowels, 
but preventing the attacks. Often diluting one of these waters one-half with hot 
water makes it an efficient purgative. The use of salol in the dose of 5 to 10 grains 
a day as an intestinal antiseptic is often advantageous. 

Of all forms of preventive treatment, that which is devoted to the increased 



920 DISEASES OF THE NERVOUS SYSTEM 

activity of the intestines, the liver, and the kidneys is of most importance. If 
the patient is gouty, or suffers from that condition commonly but erroneously called 
"uricacidemia/' not only should the treatment just recommended be employed, 
but the use of other more active salicylates, such as the salicylate of strontium 
in 5 or 10 grain doses three times a day, is advisable. If errors in refraction exist, 
carefully fitted glasses should be provided, and if the nasal mucous membrane is 
hypertrophied or other abnormalities exist in this region, they should be treated. 
For the relief of the attack many measures have been suggested. In those instances 
where the patient has prodromal symptoms, a brisk saline cathartic, such as Seidlitz 
powder, citrate of magnesia, or Rochelle salt, should be given, with the idea of 
sweeping out from the bowels poisonous material. This may be followed in half 
an hour to an hour by 2 grains of caffeine with 10 grains of bromide of sodium. 
The best way to give this is in granular effervescent salts. In some instances a 
small dose of phenacetin or acetanilid should be added. If high arterial tension 
is present, nitroglycerin is valuable. For the relief of the pain when it is very 
severe phenacetin, antipyrin, and acetanilid are useful, but it must always be remem- 
bered that the stomach is, as a rule, excreting rather than absorbing, and that the 
mere administration of a palliative at this time may be fruitless for this reason. 
Under these circumstances it may be necessary to give these drugs by the rectum, 
or to empty the stomach by vomiting or by the use of the stomach tube before 
they are administered. Sometimes the stomach can be stimulated to absorption 
by 4V grain of strychnine. In certain cases the use of a full dose, 10, 15, or 20 drops, 
of the tincture of gelsemium with a grain of an active extract of cannabis indica 
gives the greatest relief. The use of cologne-water containing 5 to 10 grains of 
menthol to the ounce applied over the course of the painful nerve may give some 
relief. In many instances it is impossible for any of these remedies to do good 
unless the patient will rest in a quiet and dark room for several hours. 



SUNSTROKE. 

Definition. — Sunstroke, more accurately called heatstroke, insolation, or thermic 
fever, and by the French coup de soleil, is a condition of the body produced by 
exposure to great heat. In rare instances the temperature of the patient does 
not rise, but falls, and to this condition is given the name heat exhaustion. 

Etiology. — The chief factor in producing heatstroke is the presence of great 
heat associated, as a rule, with marked humidity of the atmosphere. It is important 
to bear in mind the fact that exposure to the rays of the sun is not necessary for the 
development of heatstroke. Cases are constantly met with in which the illness 
of the patient is due to artificial heat, and heatstroke may occur in the night as 
well as in the day if the atmosphere is hot and moist. Dry heat is better borne 
by all persons than is moist heat, probably because evaporation on the skin proceeds 
rapidly in dry air, and so the body is cooled by the function of perspiration, whereas 
in a moist atmosphere the imperfect evaporation results in an accumulation of 
heat in the body. For this reason heatstroke is very rare on the western plains 
of the United States, where the temperature in summer often reaches 105° in the 
shade, whereas- in Philadelphia, where the air is humid, heatstroke is exceedingly 
common when the thermometer registers a temperature of 90°. In the one case 
evaporation is so rapid that the heat of the body is kept at a normal level, whereas 
in the latter case the perspiration lies on the skin in great beads. A second factor 
in producing heatstroke is the use of alcoholic drinks in any form. There can 
be 110 doubt that all such beverages greatly predispose to the development of this 
state. So, too, renal disease and a feeble heart may act as predisposing factors. 
Loss of sleep and torpidity of the bowels are also possessed of an evil influence. 



SUNSTROKE 921 

Certain French clinicians have asserted, with notable facts in support of their 
views, that sunstroke is really a form of infection which develops under the atmo- 
spheric states already named. 

Pathology and Morbid Anatomy. — While a very considerable number of clinicians 
in America and in the East Indies described sunstroke symptomatically in the early 
part of the last century, it was not till H. C. Wood collated our knowledge and 
enriched it by further experimentation that the profession began to fully grasp the 
facts concerning its production and the lesions which ensued. 

The pathology of the disorder resides in the inability of the heat-regulating 
mechanism of the body to maintain a normal body temperature. The primary 
difficulty lies in a decreased power of the body to carry out an efficient heat dissipa- 
tion, and this is followed by an unrestrained heat production, due, in Wood's 
opinion, to failure of the inhibitory heat centres, in the pons, to check oxidation 
processes. With diminished heat dissipation and increased heat production it is 
not difficult to perceive why the temperature of the body rises until a state of 
hyperpyrexia is reached. 

The morbid anatomy consists in changes in the tissues which in turn permit 
decomposition to set in very rapidly, being preceded by well-marked rigor mortis. 
The veins of the brain and lungs are found distended with fluid blood, and every- 
where the blood fails to clot as it does in the vessels of the ordinary cadaver. If 
an autopsy is made very soon after death, the left ventricle is found in firm systole, 
but the right ventricle is distended with blood. The liver and kidneys are also 
found to be intensely engorged. 

Symptoms. — The symptoms of sunstroke consist, in the preliminary stage, in 
oppression and dizziness. If these evidences of heat are ignored, the stage of sudden 
unconsciousness develops, and is often ushered in by a convulsion which may be 
exceedingly violent. In other cases no convulsion develops, but deep stupor with 
stertorous breathing comes on. The face is at first livid and later deeply cyanotic, 
the great vessels of the neck and upper extremities being distended. The tempera- 
ture of the patient speedily rises to a height never seen in any other disease, some- 
times reaching 112° or more, the average being from 105° to 110°. The pupils 
may be contracted or widely dilated. If the fever cannot be reduced and the cardiac 
and pulmonary congestion are not relieved, death ensues within twelve to thirty- 
six hours. When improvement takes place, a relapse some hours later often ensues. 
A patient who has sunstroke may subsequently become very ill and die from a 
secondary meningitis. Persons who -have had sunstroke are very susceptible to 
high temperatures, and when exposed in after years may be greatly distressed by 
an atmospheric temperature as low as 80°, if the air is moist. 

Diagnosis. — There are only two other states that resemble heatstroke, namely, 
uremia and apoplexy. The first can be excluded by the absence of hyperpyrexia 
and albumin and casts in the urine. The second is excluded by the same lack of 
temperature, except in those cases in which the pons is involved, when the fever 
may be high, but pontile hemorrhage is usually speedily fatal and the paralysis 
severe. Sunstroke and uremia may, however, exist simultaneously. The history 
of the patient will exclude epilepsy which is also excluded by the high fever. 

Prognosis. — The prognosis depends on the height of the fever and the resistance 
which it offers to treatment. Do what we will a large number of these cases die. 

Treatment. — The treatment of sunstroke, if it is to be followed by satisfactory 
results, must be bold and vigorous. In most cases three things are essential : First, 
that the temperature must be reduced until it is at a safe level, by the application 
of cold water or ice. This is best carried out by stripping the patient, laying 
him upon a canvas cot, and then directing a stream of cold water upon his body 
from a hose, the patient being actively and vigorously rubbed at the same time 
by one or more attendants, with the object of producing reaction, of overcoming 



922 DISEASES OF THE NERVOUS SYSTEM 

internal congestion, of bringing the blood to the surface, whereby it may be cooled, 
and of increasing the dissipation of heat, for frictions increase the dissipation of heat 
during the application of cold nearly fifty per cent. During this procedure ice 
should be applied to the head constantly. In other instances, the patient may be 
immersed in a tub of cold water, and if necessary pieces of ice may be placed in 
this water. If the tub is used, active frictions are as essential as in the case just 
stated. Care should be taken that the temperature, when it once begins to fall 
does not drop too rapidly, so that the patient passes into hypothermia and collapse. 
If the patient is robust and there is evidence of venous engorgement, free venesection 
should be practised. Many physicians of large experience believe that venesection 
is of almost equal importance with the use of cold. Venesection may be followed 
by hypodermoclysis or by the intravenous injection of normal salt solution. By 
these two measures engorgement of the right side of the heart is diminished and 
toxemia combated. If the circulation on the left side of the heart seems failing, 
hypodermic injections of Hoffmann's anodyne and strychnine may be administered. 
The use of alcohol should be avoided. If the bowels are confined, citrate of mag- 
nesia should be given in full purgative dose to relieve them, and where the patient is 
unconscious and unable to swallow so large a dose, J of a grain of elaterium may be 
used not only to move the bowels, but diminish cerebral congestion. The violent 
headache which often follows sunstroke may, in some instances, yield to the ordinary 
coal-tar products combined with the use of bromide of sodium and caffeine. Where 
it does not do so, and there are any evidences of meningeal or cerebral congestion, 
free venesection should be practised, not only for the relief of pain, but in order to 
prevent the development of secondary meningitis. This is a matter of very great 
importance, but is often treated as of little moment. 

In the after-treatment of the patient it is essential that the temperature should 
be carefully watched, as it nearly always has a tendency to rise a second time. 
Such a tendency should be combated by the application of cold to the head, and by 
cold bathing if actual hyperpyrexia develops. Perfect rest in bed for a number of 
days after the sunstroke should be insisted upon, and the patient should be warned 
that any exposure to heat for several days will be liable to produce another attack. 



HEAT EXHAUSTION. 

Heat exhaustion is a condition produced by the same causes as heatstroke, but 
instead of hyperpyrexia developing the temperature becomes subnormal, the 
patient's skin may be bedewed with a cold sweat, and all the evidences of severe 
collapse may be present. This condition is to be treated by immersing the patient 
in hot water and by the application about his body, after the removal from the bath, 
of hot bottles or hot bricks to maintain body temperature. A failing circulation 
should be supported by hypodermic injections of Hoffmann's anodyne and atropine. 
Care should be taken that coldness of the extremities is not mistaken for true heat 
exhaustion, for it sometimes happens that the extremities are cold in thermic fever, 
although the temperature of the body may be far above normal. This point 
must be determined by taking the rectal temperature. If the rectal temperature is 
found to be very high, the treatment for heatstroke should be instituted and the 
circulation equalized by active rubbing. A hot bath in such a case is not advisable 
except for a few moments to warm the extremities. 



FACIAL HEMIATROPHY. 

This is a condition in which one side of the face undergoes a slowly progressive 
wasting. As a rule it begins between the ages of ten and twenty years. The cause 



PERIODICAL PARALYSIS 923 

is unknown, although it is without doubt due to some localized degenerative change 
in the nervous system. In an autopsy upon a case of this character Mindel found 
degeneration of the trifacial nerve in its efferent fibres and atrophy of the substantia 
nigra. 

When the malady first develops, the skin of the affected part begins to be thin 
and glossy and seems to be stretched. The fine hairs fall out and the sebaceous 
glands atrophy, so that the part is unduly dry. After that the subcutaneous tissues 
atrophy so that the natural fulness of the face is diminished, and, in the later stages 
of the affection, even the underlying bone may be atrophied or absorbed. The 
muscular tissues escape the atrophy to a greater extent, and do not undergo degen- 
erative changes. The eye may become sunken from wasting of the orbital fat, 
and the pupil may be in a state of mydriasis. Usually the condition is painless, 
but local spasm of the muscles of the part may occur. No treatment is of any 
avail in arresting the progress of the disease. 



PERIODICAL PARALYSIS. 

This term is applied to an extraordinary condition of paralysis involving widely 
distributed groups of muscles in the arms, legs, and trunk, which develops rapidly 
in apparently healthy individuals without any apparent exciting cause. Not rarely 
several members of a family are affected by the malady. The patient may go to 
bed in perfect health and wake to find himself paralyzed, or the paralysis develops 
after a preliminary sense of weakness in the affected parts. As a rule, the legs 
suffer chiefly. Very rarely the muscles of the neck are affected, but the cranial 
nerves always escape. The reflexes are minus, and the muscles and nerve trunks 
lose their reaction to faradic stimulation. The paralysis lasts from a few hours to a 
day, and speedy and perfect recovery ensues, but relapses frequently take place. 

The condition is apparently a form of auto-intoxication, and is said to be benefited 
by the use of alkaline diuretics. 



INDEX. 



Abdomtnal facies in ascites, 600 
Abducens nerve, paralysis of, 873 
Abscess in appendicitis, 574 
of brain, 809 
in bronchiectasis, 378 
in erysipelas, 170 

hepatic, 602. See Hepatic abscess, 
of liver in dysentery, 205 
of lung, 407 

in croupous pneumonia, 132, 140 
of mediastinum, 431, 433 
in metastatic pneumonia, 397 
parotid, 514 
perinephritic, 672 

treatment of, 672 
peritoneal, 594 
pulmonary, in septicemia, 172 

in typhoid fever, 39 
in smallpox, 70 
of spleen, 703 
Acetone in urine, test for, 732 
Achylia-gastrica nervosa, 559 
Acquired idiocy, 798 

syphilis, 302 
Acromegaly, 699 

definition of, 699 
diagnosis of, 699 

from gigantism, 699, 701 

from leontiasis ossea, 699, 701 

from myxedema, 699, 701 

from osteitis deformans, 699, 701 

from pulmonary hypertrophic osteo- 
arthropathy, 699, 701 
etiology of, 699 
symptoms of, 699 
treatment of, 701 
types of, 701 
Actinomycosis, 233 
cerebral, 234 
definition of, 233 
diagnosis of, 235 
etiology of, 233 
morbid anatomy of, 233 
pathology of, 233 
ray fungus in, 233 
streptothrix actinomyces in, 233 
symptoms of, 233 
treatment of, 234 
Acute anterior poliomyelitis, 111 
atrophic paralysis, 111 
infantile palsy, 111 
poliomyeloencephalitis, 111 
Addison's anemia, 710 
disease, 695 

anemia in, 697 

asthenia in, 697 

atrophic changes in, 696 

definition of, 695 

diagnosis of, 697 



Addison's disease, diagnosis of, from diabetes 
bronze, 697 
from hypertrophic cirrhosis of 

liver, 697 
from pregnancy, 697 
from prolonged use of arsenic, 697 
etiology of, 695 
history of, 695 
languor in, 697 
morbid anatomy of, 696 
pathology of, 695 
pigmentation of skin in, 697 
prognosis in, 698 
symptoms of, 697 
treatment of, 698 
tuberculosis in, 698 
Adenitis, cervical, 246 

tropical, 200 
Adenoma of kidney, 668 
of pancreas, 637 
of thyroid gland, 683 
Adhesions of colon, 592 
Adhesive pericarditis, chronic, 440 
Adiposis dolorosa, 764 
Adrenal apoplexy, 696 

iEstivo-autumnal parasite of malarial fever, 319 
African itch, 69 

lethargy, 331, 333. See Sleeping sickness. 
Agglutometer for agglutination test in typhoid 

fever, 44 
Agraphia, 800 

Ague cake in malarial fever, 321, 326 
Ainhum, 766 

treatment of, 766 
Albuminuria, 675 

in acute diffuse nephritis, 642 
of adolescence, 676 
cyclic, 676 

in diabetes mellitus, 729 
in diphtheria, 157 
orthostatic, 676 
in pneumonic plague, 198 
tests for, 676 
in tick fever, 298 
in typhoid fever, 38 
in ulcerative endocarditis, 459 
in yellow fever, 191, 192 
Albuminuric neuroretinitis, 653 
papillitis, 653 

retinitis in chronic parenchymatous nephri- 
tis, 646 
degenerative, 653 
hemorrhagic, 653 
typical, 653 
Albumosuria, myelopathic, 680 
Alcoholism, 771 

acute, symptoms of, 771 

treatment of, 772 
chronic, 772 

morbid anatomy of, 772 
symptoms of, 773 

(925) 



I 



926 



INDEX 



Alcoholism, chronic, treatment of, 773, 774 
dietetic, 773 
definition of, 771 
etiology of, 771 
subacute, 772 
Aleppo boil, 336 
Alexia, 800 
Algid form of pernicious malarial fever, 325 

yellow fever, 191 
Alimentary canal, tuberculosis of, 278 
Allochiria in locomotor ataxia, 827 
Alopecia, syphilitic, 309 
Amaurosis, uremic, 660 
Amaurotic family idiocy, 798 
Amblyopia in "whooping-cough, 104 
Ameba carriers, 203 
Amebiasis, intestinal, 201 
Amebic abscess of liver, 604 

dysentery, 201, 202 
Amimia, 800 
Amok, 911 

Amphoric breathing, 264 
Amyloid degeneration of heart, 449 
disease of kidney, 657 
liver, 614 
Amyotrophic lateral sclerosis, 838 
Anaphylactic manifestations in scarlet fever, 84 
Anaphylaxis from diphtheria antitoxin, 163 
Anemia, 707 

Addison's, 710 

disease, 697 
aplastic, 713 
brickmakers', 338 
in chronic lead poisoning, 780 
definition of, 707 
in diphtheria, 159 
essential, 708 
in gastric ulcer, 539 
infantum, 718 

blood changes in, 718 
definition of, 718 
treatment of, 718 
miners', 338 
pernicious, 710 

blood changes in, 711 
definition of, 710 
diagnosis of, 712 
etiology of, 710 
* history of, 710 

morbid anatomy of, 711 
prognosis in, 712 
symptoms of, 712 
treatment of, 712 
Porto Rican, 338 
primary, 708 
secondary, 707 
cause of, 707 
diagnosis of, 708 
symptoms of, 708 
treatment of, 708 
in septicemia, 172 
splenic, 704 

blood in, 704 

clinical characteristics of, 705 
definition of, 704 
diagnosis of, 704 
H iology of, 704 
morbid anatomy of, 704 
pathology of, 704 
prognosis in, 705 
spleen in, 704 
symptoms of, 704 
treatment of, 705 
in sprue, 590 



Anemia in syphilis, 309 
in typhoid fever, 30 
tunnel, 338 
in uncinariasis, 341 
Anesthesia in hysteria, 896 
Anesthetic leprosy, 293 
Aneurysm, 500 

of abdominal aorta, 507 

cardiac, 453 

definition of, 500 

"dissecting," 500 

embolic, 500 

etiology of, 500 

false, 500 

frequency of, 501 

fusiform, 500 

hematemesis in, 559 

of hepatic artery, 507 

morbid anatomy of, 500 

mycotic, 500 

pathology of, 500 

of renal artery, 507 

sacculated, 500 

of splenic artery, 507 

of superior mesenteric artery, 507 

of thoracic aorta, 501 

complications of, 504 
diagnosis of, 504 
prognosis in, 505 
sequelae of, 502, 503 
symptoms of, 502 
treatment of, 505 
operative, 506 
Tufnell, 505 
varicose, 500 
Aneurysmal varix, 500 
Angina, Ludwig's, 520 
pectoris, 491 

definition of, 491 
diagnosis of, 492 
etiology of, 491 
pathology of, 491 
prognosis in, 492 
symptoms of, 491 
treatment of, 492 
Vincent's, 521 
Angiomata, cavernous, of liver, 615 

of kidney, 668 
Angioneurotic edema, 916 
definition of, 916 
diagnosis of, 917 
prognosis of, 917 
treatment of, 917 
Angiosclerosis, 498 
Ankle clonus in lateral sclerosis, 837 
Ankylosis in gonorrheal arthritis, 166 
Ankylostomiasis, 338 
Ankylostomum duodenale, 338 
Annular stricture of esophagus, 523 
Anorexia nervosa, 558 
Anthracosis, 398 
Anthrax, 219 

bacillus of, 219 
definition of, 219 
diagnosis of, 221 
etiology of, 219 
frequency of, 219 
history of, 219 
lesion of, 220 
morbid anatomy of, 220 
edema, malignant, 220 
pathology of, 220 
prevention of, 219 
prognosis in, 221 



INDEX 



927 



Anthrax, symptoms of, 220 

treatment of, 222 
Anticholera vaccine, 182 
Antigonococcic serum, 167 
Antiplague inoculations, Haffkine's, 197 
Antirabic serum, 226 
Antisepsis, intestinal, in typhoid fever, 50 
Antistreptococcic serum in erysipelas, 171 
in pulmonary tuberculosis, 275 
in septicemia, 173 
Antitetanic globulin, 229 

serum, 229 
Antitoxin, diphtheria, 162, 163 
Antityphoid vaccination, 20 

vaccine, 50 
Anuria, 672 

treatment of, 673 
Aorta, abdominal aneurysm of, 507 

thoracic, aneurysm of, 501 
Aortic regurgitation, 476 

Corrigan pulse in, 479 
definition of, 476 
diagnosis of, 480 
Duroziez sign in, 480 
etiology of, 477 
murmur in, 479 
ox-heart in, 478 
pathology of, 477 
physical signs of j 478 
pistol-shot sound in, 480 
prognosis in, 480 
Quincke's pulse in, 478 
symptoms of, 478 
trip-hammer pulse in, 479 
water-hammer pulse in, 479 
stenosis, 474 

definition of, 474 
diagnosis of, 476 
etiology of, 474 
physical signs of, 475 
prognosis in, 476 
symptoms of, 475 
Aortitis, 495 

treatment of, 496 
Aphasia, 799 

in apoplexy, 791 
in brain tumor, 802 
conduction, 800 
definition of, 799 
symptoms of, 799 

transitory, in croupous pneumonia, 142 
Aphemia, 800 
Aphonia, hysterical, 896 
in smallpox, 70 
in tuberculous laryngitis, 369 
Aphthae tropicse, 588 
Aphthous stomatitis, 509 
Aplastic anemia, 713 
Apoplectiform attack, 785 
bulbar paralysis, 785 
type of yellow fever, 191 
Apoplexy, 785 
adrenal, 696 
aphasia in, 791 
astereognosis in, 791 
athetosis in, 792 
bed-sores in, 791 
contractures in, 791 
definition of, 785 
in diabetes mellitus, 730 
diagnosis of, 792 

from acute alcoholism, 793 
from coma of diabetes, 793 
of uremia, 793 



Apoplexy, diagnosis of, from embolism of cere- 
bral vessels, 792, 794 
from epilepsy, 792 

from general paralysis of insane, 793 
from opium poisoning, 793 
from sunstroke, 793 
from syncope, 792 

from thrombosis of cerebral vessels, 
792, 793 
etiology of, 785 
frequency of, 785 
hemianesthesia in, 791 
hemianopsia in, 791 
hemiplegia in, 790 
Hutchinson's pupil in, 792 
ingravescent, 792 
muscular atrophy in, 792 
ocular symptoms of, 790 
paralysis in, 790, 791 
pathology of, 786 
prognosis in, 794 
pulse in, 790 
reflexes in, 790 
sequelae of, 791 
stertorous breathing in, 790 
symptoms of, 789 

premonitory, 789 
treatment of, 794 
unconsciousness in, 790 
uremic, 793 
Appendicitis, 572 
abscess in, 574 
catarrhal, 573 
definition of, 572 
diagnosis of, 576 

from hepatic colic, 576 
from intestinal obstruction, 576 
from ovarian inflammation, 576 
from renal colic, 576 
from tuberculosis, 577 
from typhoid fever, 576 
etiology of, 572 
gangrenous, 573, 574 
history of, 572 
McBurney's point, 575 
morbid anatomy of, 573 
muscular rigidity in, 575 
obliterative, 573 
pathology of, 573 
perforative, 573 
prognosis in, 577 
symptoms of, 575 
treatment of, 577 
in typhoid fever, 28, 36 
ulcerative, 573, 574 
vomiting in, 576 
Apraxia, 800 

Aran-Duchenne type of chronic anterior polio- 
myelitis, 834 
Argyll-Robertson pupil in dementia paralytica, 
818 
in disseminated sclerosis, 821 
in locomotor ataxia, 827 
Army itch, 69 
Arrhythmia, 488 
Arsenical poisoning, 777 

chronic, etiology of, 777 
prognosis in, 777 
pseudotabes in, 777 
symptoms of, 777 
treatment of, 778 
Arteries, diseases of, 495 
Arteriocapillary fibrosis, 496 
Arteriosclerosis, 496 



928 



INDEX 



Arteriosclerosis, definition of, 496 
etiology of, 496 
morbid anatomy of, 497 
pathology of, 497 
symptoms of, 499 
treatment of, 499 
Arteritis, syphilitic, 306 
Artery, hemorrhage of cerebral, 786 
Arthritis in cerebrospinal fever, 123 
in croupous pneumonia, 143 
deformans, 749 

definition of, 749 
diagnosis of, 752 
etiology of, 749 
Haygarth's nodosities in, 751 
Heberden's nodes in, 751 
morbid anatomy of, 750 
prognosis in, 753 
symptoms of, 751 
treatment of, 753 
gonorrheal, 165 

ankylosis in, 166 
chronic, 165 
endocarditis in, 166 
symptoms of, 165 
treatment of, 167 
serum in, 167 
infections in cholera, 185 
in mumps, 101 

in rheumatic fever, acute, 176 
rheumatoid, 749 

in bronchiectasis, 378 
septic, in scarlet fever, 87 
in smallpox, 71 
in typhoid fever, 40 
Articular rheumatism, acute, 174. See Rheu- 
matic fever, acute. 
Ascariasis, 336 

symptoms of, 336 
treatment of, 337 
Ascaris lumbricoides, 336 
Ascending myelitis, 840 

paralysis, acute, 854 
Ascites, 599 

definition of, 599 
diagnosis of, 600 

from hepatic enlargement, 601 
from ovarian cyst, 600 
from splenic enlargement, 601 
dyspnea in, 600 
etiology of, 600 
paracentesis abdominis in, 602 
physical signs of, 600 
symptoms of, 600 
treatment of, 601 
Asiatic cholera, 181 
Aspiration pneumonia, 387 
Astasia-abasia, 912 
definition of, 912 
symptoms of, 912 
Astereognosis in apoplexy, 791 
Asthenia In Addison's disease, 697 
\ai lima, bronchial, 381 

Charcot-Leyden crystals in, 383 
Curschmann's spirals in, 383 
definition of, 381 
diagnosis of, 383 

from pulmonary edema, 384 
etiology of, 381 
Earrison's groove in, 382 
morbid anatomy of, 382 
pathology of, 382 
pigeon-breast in, 382 
prognosis of, 384 



Asthma, bronchial, sputum in, 382 
symptoms of, 383 
treatment of, 384 

bronchitis tent in, 386 

cardiac, 382 

renal, 382 
Asymmetrical stricture of esophagus, 523 
Ataxia, family, 830 

Friedreich's, 830 

hereditary, 830 

locomotor, 823 

Marie's cerebellar hereditary, 833 
Atheroma, 497 
Athetosis in apoplexy, 792 
Athyrea, 688 
Atonic dilatation of esophagus, 524 

gastrectasis, 535 
Atrophic cirrhosis of liver, 606 

emphysema, 400 

enteritis of tropics, 588 

nasal catarrh, 361 

paralysis, acute, 111 

rhinitis, 361 

spinal paralysis, chronic, 833 
Atrophy in apoplexy, 792 

of heart, 449 

of liver, red, 613 

yellow, acute, 616 

muscular, progressive, 833 
of peroneal type, 886 

optic, 866 
Atypical forms of typhoid fever, 28 
Auctioneer's sore throat, 517 
Auditory nerve, disease of, 878 
deafness in, 878 
tinnitus in, 878 
vertigo in, 879 
Aura in epilepsy, 902, 904 
Auricular fibrillation, 472 
Autumnal catarrh, 362 

fever, 17 

B 

Babinski reflex in amyotrophic lateral sclerosis, 
839 
in apoplexy, 790 
in lateral sclerosis, 837 
Bacillary dysentery, 201 

Bacillus aerogenes capsulatus in pneumoperi- 
cardium, 443 

of amebic dysentery, 201 

of anthrax, 219 

of Asiatic cholera, 181, 183 

coli communis in typhoid, 17 

of diphtheria, 152 

dysenteriae, 17, 204 

of Eberth, 17 

lactamorbi in milk sickness, 296 

lepra?, 290 

mallei in glanders, 231 

para-colon, 18 

paratyphosus, 21, 54 

pertussis, 102 

pestis, 194, 195 

of Pfeiffer in influenza, 106, 107 

of Shiga, 201 

of tetanus, 227 

of tuberculosis, method of staining, 265 

typhosus, 17 

of typhoid fever, 17 
Bagdad sore, 336 
Balantidium coli, 201, 203 

dysentery, 203 



INDEX 



929 



Banti's disease, 705 
Barlow's disease, 760 

Barrel-shaped chest in chronic hypertrophic 
tonsillitis, 521 
in emphysema, 400 
Basedow's disease, 683 
Basilar meningitis, 248 
Bath, Brand, in typhoid fever, 48 
Baths, Nauheim, in myocarditis, 452 
Bean itch, 69 

pox, 69 
Bed-sores in apoplexy, 791 
in smallpox, 70 
in typhoid fever, 30 
Beef-worm, 350 
Benign endocarditis, 455 

goitre, 681 
Beriberi, 766 

acute pernicious, 769 
atrophic, 768 
blood in, 769 
cardiac changes in, 769 
definition of, 766 
diagnosis of, 770 
distribution of, 767 
dry, 768 
etiology of, 767 
forms of, 768 
frequency of, 767 
history of, 767 
mild, 769 

morbid anatomy of, 767 
paraplegic, 768 
pathology of, 767 
prognosis in, 770 
rudimentary, 768, 783 
symptoms of, 768 
treatment of, 770 
urine in, 769 
Bilateral salivary swelling, 514 
Bile-ducts, catarrh of, acute, 617 
chronic, 618 

treatment of, 618 
constriction of, 619 
inflammation of, suppurative, 619 
diagnosis of, 619 
symptoms of, 619 
treatment of, 619 
occlusion of, 619 
congenital, 620 
Bilharzia disease, 353 

diagnosis of, 355 
distribution of, 353 
etiology of, 353 
hematuria in, 354 
history of, 353 
pathology of, 354 
prognosis in, 355 
Schistosoma hematobium in, 353 
symptoms of, 354 
treatment of, 355 
Biliary calculi, 621 
colic, 623 

passages, malignant growths of, 627 
tract, diseases of, 617 
Bilious fever, 324 

remittent fever, 324 
Bilocular heart, 494 

stomach, 555 
Birth palsy, 860 
"Black" measles, 95 
smallpox, 68 

vomit in yellow fever, 191 
water fever, 325 
59 



Bladder, tuberculosis of, 282 
Blepharofacial spasm, 878 
Blepharospasm, 878 
Blindness, word-, 800 
Blood in beriberi, 769 

in cerebrospinal fever, 123 
changes in anemia infantum, 718 

in pneumonic plague, 198 
in chlorosis, 709 
in diabetes mellitus, 728 
in diphtheria, 156 
diseases of, 707 
in Hodgkin's disease, 288 
in malarial fever, changes in, 320 
in pernicious anemia, 711 
in septicemia, 172 

-spitting in mitral regurgitation, 467 
in splenic anemia, 704 
in splenomedullary leukemia, 715 
in stools, tests for, 541 
in typhoid fever, 24, 30 
in urine, 673 

in malarial fever, 325 
in yellow fever, 190 
Blood pressure in angina pectoris, 491 
in aortic regurgitation, 478 
in arteriosclerosis, 499 
in myocardial degeneration, 449 
Blue line on gums in chronic lead poisoning, 779 
Boas' reagent, 549 

test meal in gastric cancer, 549 
Boils in typhoid fever, 30 
Bold hives, 69 
Bone-marrow changes in typhoid fever, 25 

in malarial fever, 320 
Bones, syphilis of, 312 
Bossy frontals in rickets, 757 
Bothriocephalus cordatus, 352 
cristatus, 352 
latus, 352 
Bouquet fever, 117 
Bouton d'Orient, 336 
Bovine tuberculosis, 237 

Bowel, hemorrhage from, in typhoid fever, 33 
treatment of, 51 
obstruction of, 579 

by congenital malformations, 579 
by fecal impaction, 579 
by foreign bodies, 579, 582 
by internal strangulation, 579, 581 
by intussusception, 579 
by stricture, 579 
by tumors, 579 
by volvulus, 581 
perforation of, in typhoid fever, 29, 34 
diagnosis of, 35 
treatment of, 52 
Bradycardia, 488 
Brain, abscess of, 809 

in bronchiectasis, 378 
definition of, 809 
diagnosis of, 810 
etiology of, 809 
morbid anatomy of, 809 
pathology of, 809 
prognosis in, 811 
symptoms of, 810 
treatment of, 811 
cancer of, 801 
diseases of, 785 
echinococcus cyst of, 801 
fibroma of, 801 
glioma of, 801, 802 
gumma of, 801 



930 



INDEX 



Brain, hemorrhage into, 785 
neuroma of, 801 
sarcoma of, 801 

softening of, in croupous pneumonia, 143 
syphilis of, 308, 310 
tabes of, 817 
tubercle of, 801 
tuberculosis of, 286 
tumors of, 801 

aphasia in, 802 
diagnosis of, 807 

from localized meningitis, 807 
etiology of, 801 
frequency of, 801 
headache in, 802 
hemianesthesia in, 804 
hemianopsia in, 803 
hemiatoxia in, 804 
hemiplegia in, 804 
morbid anatomy of, 801 
optic neuritis in, 802 
paralysis in, 803 
bilateral, 803 
crossed, 803 
pathology of, 801 
prognosis in, 807 
symptoms of, 802 
table of cerebral localizing symptoms 

in, 806 
treatment of, 808 
surgical, 808 
vascular, 801 
vertigo in, 802 
vomiting in, 802 
Weber's syndrome in, 803 
Brand bath in typhoid fever, 48 
Breakbone fever, 118 
Breathing, stertorous, in apoplexy, 790 
Brickmakers' anemia, 338 
Blight's disease acute, 641 

chronic, 643 
Bromatotoxismus, 781 
Bronchi, diseases of, 370 
Bronchial asthma, 381 
Bronchiectasis, 375 

brain abscess in, 378 

bronchopneumonia, septic in, 378 

complications of, 378 

cough in, 376 

in croupous pneumonia, 141 

cyanosis in, 378 

definition of, 375 

diagnosis of, 378 

from pulmonary tuberculosis, 378 
dyspnea in, 378 
etiology of, 375 
forms of, 375 
hemoptysis in, 378 
morbid anatomy of, 375 
pathology of, 375 
physical signs of, 377 
prognosis in, 378 
pulmonary gangrene in, 378 

osteo-arthropal hy in, 378 
rheumatoid arthritis in, 378 
sputum in, 377 
symptoms of, 376 
treal menl of, 378 
Bronchitis actinomycotica, chronic, 234 
capillary, 3 ( .)l 
catarrhal, acute. 370 

definition of, 370 
distribution of, 371 
el iology of, 371 



Bronchitis, catarrhal, acute, history of, 370 
morbid anatomy of, 372 
pathology of, 372 
prevention of, 372 
symptoms of, 372 
treatment of, 372 
chronic, 374 

definition of, 374 
treatment of, 375 
in croupous pneumonia, 133 
fibrinous, 379 

definition of, 379 
diagnosis of, 381 

from diphtheria, 381 
etiology of, 379 
pathology of, 380 
prognosis of, 381 
symptoms of, 380 
treatment of, 381 
in influenza, 107 
in measles, 93, 95 
in smallpox, 70 
tent in bronchial asthma, 386 
in whooping-cough, 105 
Bronchocele, 681 
Bronchopneumonia, 386 
complications of, 392 
definition of, 386 
diagnosis of, 393 

from acute bronchitis, 393 
from croupous pneumonia, 393 
from malarial infection, 393 
from tuberculous infection, 393 
in diphtheria, 156, 158, 159 
distribution of, 387 
duration of, 392 
etiology of, 387 
frequency of, 388 
in measles, 93, 96 
morbid anatomy of, 388 
pathology of, 388 
prevention of, 388 
prognosis of, 394 
in scarlet fever, 88 
septic, in bronchiectasis, 378 
in smallpox, 70 
symptoms of, 389 
treatment of, 394 
types of, 387 
in whooping-cough, 103 
Bronzed diabetes, 739 
Brown induration of heart, 449 . 
Bubo, climatic, 200 
parotid, 514 
tropical, 200 
Buboes in bubonic plague, 198 
Bubonic plague, 194 
Buccal psoriasis, 513 
Bucket fever, 117 
Bulbar paralysis, 835 

apoplectiform, 785 
Bulimia, 558 
Bumps, 69 



Cachexia, miners', 338 
in pellagra, 783 
strumipriva, 688 
Cecum, tuberculosis of, 279 
Caisson disease, 855 

treatment of, 856 
palliative, 856 
prophylactic, 856 



INDEX 



931 



Calcareous degeneration of heart, 449 
Calculi, biliary, 621 
Calculus, coral, of kidney, 669 
" hemp-seed," of kidney, 670 
mulberry, of kidney, 670 
pancreatic, 636 
renal, 669 
Cancer of brain, 801 
of kidney, 668 
of esophagus, 525 
of peritoneum, 599 
of stomach, 545 
Cancrum oris, 511 
Canker, 509 

Capillary bronchitis, 391 
Capsular cirrhosis of liver, 612 
Carcinoma of biliary ducts, 627 
of gallbladder, 627 
of liver, 614 
in lung, 412 
of mediastinum, 431 
. of thyroid gland, 683 
Carcinosarcoma of thyroid gland, 683 
Cardiac aneurysm, 453. See Heart, aneurysm of. 
asthma, 382 • 
changes in beriberi, 768 

in croupous pneumonia, 133 
in whooping-cough, 104 
in yellow fever, 190 
complications in rheumatic fever, 177, 178 
defects, congenital, 494 
dilatation, 444. See Heart, dilatation of. 
disorders not due to valvular lesions, 487 
hypertrophy, 444. See Heart, hypertrophy 

of. 
neuroses, 487 

treatment of, 490 
palpitation, 487 
valvular anomalies, 494 
Cardiospasm, 556 

treatment of, 557 
Caseative nephritis, 663 
Cataract in diabetes mellitus, 730 
Catarrh, autumnal, 362 

of bile-ducts, acute, 617 

chronic, 618 
gastric, acute, 525. See Gastric catarrh, 
nasal, atrophic, 361 

definition of, 361 
etiology of, 361 
pathology of, 361 
prognosis of, 362 
symptoms of, 362 
treatment of, 362 
chronic, 360 

definition of, 360 
etiology of, 360 
pathology of, 361 
symptoms of, 361 
treatment of, 361 
suffocative, acute, 389, 391 
Catarrhal appendicitis, 573 
bronchitis, acute, 370 

chronic, 374 
cholecystitis, 617 
dysentery, acute, 201 
enteritis, 566 
jaundice, 617 
laryngitis, acute, 364 

chronic, 366 
pneumonia, 386 
pyelonephritis, 664 
stomatitis, 509 
Cedar itch, 69 



Celiac disease, 702 
Cerebral actinomycosis, 234 
embolism, 785 
hemorrhage, 785 

artery of, 786 
meningitis, 813 
paralysis, infantile, 795 
syphilis, 308, 310 
thrombosis, 785 
Cerebritis, acute, 811 

definition of, 811 
diagnosis of, 812 
etiology of, 811 
morbid anatomy of, 811 
pathology of, 811 
prognosis of, 812 
symptoms of, 811 
treatment of, 812 
Cerebrospinal fever, 120. See Meningitis, men- 
ingococci . 
meningitis, 120 
Cervical adenitis, 246 
Cervicobrachial neuritis, 859 
Cestodes, 350 
Ceylon sour mouth, 588 
Chalicosis, 398 
Chancre, 302, 306, 308 

leprous, 292 
Charcot joint in locomotor ataxia, 828 
Charcot-Leyden crystals, 383 

in distomatosis of lung, 356 
uncinariasis, 340 
Charcot-Marie-Tooth form of progressive mus- 
cular atrophy, 886 
Cheyne-Stokes respiration in cerebrospinal 

fever, 123 
Chicken-breast in rickets, 757 
Chicken-pox, 77. See Varicella. 
Chigger, 357 

treatment of, 357 
Chloroma, 718 
Chlorosis, 708 
blood in, 709 
complications of, 710 
definition of, 708 
diagnosis of, 710 

from pernicious anemia, 710 
Egyptian, 338 
etiology of, 709 
florida, 710 
pathology of, 709 
prognosis in, 710 
symptoms of, 709 
tarda, 709 
treatment of, 710 
tropical, 338 
Cholangitis, acute, 617 

diagnosis of, 617 
etiology of, 617 
prognosis in, 617 
symptoms of, 617 
treatment of, 617 
chronic, 618 

treatment of, 618 
suppurative, 619 

diagnosis of, 619 

from catarrhal cholangitis, 619 
from hepatic abscess, 619 
symptoms of, 619 
treatment of, 619 
Cholecystitis, acute, 620 
definition of, 620 
diagnosis of, 621 

from acute appendicitis, 621 



932 



INDEX 



Cholecystitis, acute, diagnosis of, from acute 
pancreatitis, 621 
from gastric ulcer, 621 
from hepatic colic, 621 
from intestinal obstruction, 621 

etiology of, 620 

morbid anatomy of, 620 

symptoms of, 621 

treatment of, 621 
catarrhal, 617 
in typhoid fever, 37 
Cholelithiasis, 621 
colic in, 623 
complications of, 624 
Courvoisier's law in, 625 
definition of, 621 
diagnosis of, 625 

from appendicitis, 625 

from gastralgia, 625 

from gastric crises of ataxia, 625 
ulcer, 625 

from pleurisy, 625 

from renal stone, 625 
enlargement of gallbladder in, 624 
etiology of, 621 
jaundice in, 623 
pathology of, 621 
perforation in, 624 
sequelae in, 624 
symptoms of, 623 
treatment of, 626 
in typhoid fever, 37 
urine in, 623 
Cholera, 181 

arthritis, infectious, in, 185 
Asiatic, 181 
bacillus of, 181, 183 
collapse in, 184 
complications of, 185 
definition of, 181 
diagnosis of, 185 
diarrhea in, 183 
distribution of, 181 
edema of lungs in, 185 
etiology of, 181 
facial expression in, 184 
gangrene in, 185 
history of, 181 
incubation in, 183 
infantum, 569 

definition of, 569 

etiology of, 570 

morbid anatomy of, 570 

pathology of, 570 

prognosis in, 570 

symptoms of, 570 

treatment of, 570 
intestinal changes in, 183 
liver in, 183 

morbid anatomy of, 182 
nephritis in, 185 
parotitis in, 185 
pathology of, 182 
prevention of, 181 

antichol&a inoculations for, 182 
prognosis in, 185 
purging in, 184 
sequels of, 1X5 
sicca, 185 
stools in, 183 
symptoms of, L83 
treatment of, L86 

irrigal ion of bowel in, 187 
variations in symptoms of, 185 



Cholera, visceral changes in, 183 

vomiting in, 183 
Cholerine, 185 
Chondroma in lung, 412 
Chorea, acute, 890 

in acute rheumatic fever, 178 
electrical, 894 
gravidarum, 891 
hereditary, 893 

prognosis in, 893 
symptoms of, 893 
treatment of, 894 
Huntington's, 893 
insaniens, 892 
minor, 890 

complications of, 892 
definition of, 890 
diagnosis of, 892 

from hysteria, 892 
from infantile cerebral palsy, 892 
duration of, 892 
endocarditis in, 892 
etiology of, 890 
exciting causes of, 891 
frequency of, 891 
hysteria in, 892 
mental state in, 892 
morbid anatomy of, 891 
movements in, 891 
pathology of, 891 
prognosis in, 892 
symptoms of, 891 
treatment of, 893 
paralytic, 892 
Sydenham's, 890 
Chvostek's sign in gastric tetany, 534 

of tetany, 692 
Chyluria, 678 

" Cinder-sifting" kidney, 638 
Circulatory disturbances in kidney, 640 

system, diseases of, 435 
Circumscribed peritonitis, 594 
Cirrhosis of kidney, 650 

of liver, 606 
Claw-hand in chronic anterior poliomyelitis, 834 
Clergymen's sore throat, 517 
Climatic bubo, 200 

definition of, 200 
symptoms of, 200 
treatment of, 200 
treatment of pulmonary tuberculosis, 270 
Coffee-ground vomit, 559 
Coin sound in hydropneumothorax, 431 
Cold bathing in typhoid fever, 47 
Colic, biliary, 623 

in chronic lead poisoning, 780 
painters', 780 
renal, 671 
Colica pictonum, 780 
Colitis, 586 
acute, 586 

symptoms of, 586 
treatment of, 586 
croupous, 587 

treatment of, 588 
follicular, 587 
mucous, 586 

definition of, 586 
treatment of, 587 

counter-irritation in, 587 
diet in, 587 
rest in, 587 
nodular, 587 
pseudomembranous, 588 



INDEX 



933 



Collapse in cholera, 184 
''Collar of brawn" in scarlet fever, 84 
Colloid goitre, 681 
Colon, adhesions of, 592 
dilatation of, 591 

by foreign bodies, 591 
by gas, 591 

treatment of, 591 
idiopathic, 592 
by obstruction, 591 
displacements of, 592 
redundancy of, 592 
Coma in chronic parenchymatous nephritis, 646 
diabetic, 730 
in uremia, 659 
vigil in typhoid fever, 39 
in typhus fever, 57 
Comatose form of pernicious malarial fever, 325 
Comma bacillus of Asiatic cholera, 181, 183 
Compensatory emphysema, 400, 404 
Compression of spinal cord, 848 
Conduction aphasia, 800 
Condylomata, syphilitic, 309 
Confluent smallpox, 68 
Congenital cardiac defects, 494 
hydronephrosis, 665 
malformations of bowel, 579 
myxedema, 688 
stenosis of pylorus, 553, 554 
wryneck, 882 
Congestion of lungs, 409 
definition of, 409 
diagnosis of, 411 

from catarrhal pneumonia, 411 
from croupous pneumonia, 411 
from pleural effusion, 411 
dyspnea of, 411 
etiology of, 410 
hypostatic, 410 
pathology of, 410 
prognosis of, 411 
symptoms of, 411 % 
treatment of, 411 
Conjunctiva, diphtheria of, 158 
Conjunctival hemorrhages in whooping-cough, 

104 
Conjunctivitis in measles, 96 
Constitutio lymphatica, 694 
Contracted kidney, 650 
Contractures in apoplexy, 791 
Convulsions in acute anterior poliomyelitis, 115 
in chronic lead poisoning, 779 
in croupous pneumonia, 138 
in epilepsy, 903 
in hysteria, 895 

in infantile cerebral paralysis, 796 
in mumps, 101 
in typhoid fever, 40 
in uremia, 659 
in yellow fever, 190 
Cor bovinum in aortic regurgitation, 478 
Cordylobia anthropophagia, 358 
Corrigan pulse in aortic regurgitation, 479 
Corynebacterium granulomatis maligni in Hodg- 
kin's disease, 287 
Hodgkini, 287 
Coryza, acute, 359 
definition of, 359 
diagnosis of, 360 
diplococcus coryzse in, 359 
etiology of, 359- 
in measles, 94 

micrococcus catarrhalis in, 359 
morbid anatomy of, 359 



Coryza, pathology of, 359 

symptoms of, 359 

transmission of, 359 

treatment of, 360 
Coup de soleil, 920 
Courvoisier's law, 625 
Cracked-pot sound, 263 
Cramp, flute-players', 914 

pianists', 914 

telegraphers', 914 

violinists', 914 

writers', 914 
Cranial nerves, diseases of, 865 
Craniotabes, 757 
Craw-craw, 344 
Cretinism, 689 

definition of, 689 

diagnosis of, 690 

prognosis in, 690 

symptoms of, 689 

treatment of, 690 

thyroid gland in, 690 
Crises in croupous pneumonia, 139 

in locomotor ataxia, 826 
Croup, false, 368 

spasmodic, 368 
Croupous colitis, 587 

pharyngitis, 517 

pneumonia, 128. See Pneumonia, croup- 
ous. 
Cuban itch, 69 
Curschmann's spirals, 383 
Cyanosis in croupous pneumonia, 136 

in edematous laryngitis, 367 

in mitral regurgitation, 467 
Cyclic albuminuria, 676 

vomiting, 560 
Cylindrical stricture of esophagus, 523 
Cynache gangrenosa, 520 
Cyst, hydatid, of spleen, 703 
Cystadenoma of pancreas, 636 
Cystic adenoma of peritoneum, 599 

disease of kidney, 667 
of liver, 615 

epithelioma of pancreas, 636 

goitre, 681 
Cysticercus mediocanellata, 351 
Cystitis in typhoid fever, 38 
Cysts of mediastinum, 431 

of pancreas, 636 
Cytoryctes vaccinae as a cause of smallpox, 61 
Cytoscopy in pleurisy with effusion, 421 



D 



Dactylitis, syphilitic, 312 
Dandy fever, 117 
Deafness, 878 

word-, 800 
Delhi boil, 335 

Delirium in acute rheumatic fever, 178 
in cerebrospinal fever, 123 
cordis in diphtheria, 158 
in croupous pneumonia, 134, 136, 138 
ferox in typhus fever, 57 
in relapsing fever, 331 
in smallpox, 67 
in typhoid fever, 27, 39 
Dementia paralytica, 816 

Argyll-Robertson pupil in, 818 
definition of, 816 
diagnosis of, 819 
etiology of, 816 



934 



INDEX 



Dementia paralytica, morbid anatomy of, 817 
pathology of, 817 
prognosis in, 819 
symptoms of, 818 
treatment of, 819 
Dengue, 117 
chill in, 118 
crisis in, 118 
definition of, 117 
desquamation in, 118 
diagnosis of, 119 

from influenza, 119 
from rotheln, 119 
from scarlet fever, 119 
from syphilitic roseola, 119 
distribution of, 117 
eruption in, 118 
erythema in, 118 
etiology of, 117 
fever in, 118 
history of, 117 
prognosis in, 119 
relapse in, 118 
symptoms of, 118 
treatment of, 119 
Dentition in rickets, 757 
Dermatobia cyaniventris, 358 
Dermoid cyst in lung, 412 

of mediastinum, 431 
Descending myelitis, 840 
Desquamation in dengue, 118 

in scarlet fever, 89, 92 
Desquamative nephritis, chronic, 645 
Dhobie itch, 69 
Diabetes, bronzed, 739 

definition of, 739 
insipidus, 739 

definition of, 739 
diagnosis of, 740 
etiology of, 739 
morbid anatomy of, 739 
prognosis in, 740 
symptoms of, 739 
treatment of, 740 
urine in, 740 
mellitus, 723 

albuminuria in, 729 
blood changes in, 728 
carbuncles in, 729 
coma in, 730 
complications of, 729 
dyspeptic, 730 
nervous, 730 
ocular, 730 
pulmonary, 730 
definition of, 723 
diagnosis of, 730 

blood tests in, 731 
urinary tests in, 732, 733 
distribution of, 723 
dyspeptic symptoms in, 730 
emaciation in, 728 
etiology of, 724 
frequency of, 723 
gangrene in, 729 
glycosuria in, 725, 728, 729 
history of, 723 
kidney changes in, 727 
Knssmaul's coma in, 730 
morbid anatomy of, 727 
nervous system in, changes in, 727 
pathology of, 725 
prognosis in, 732 
sequels of, 721) 



Diabetes mellitus, symptoms of, 728 

treatment of, 734 

dietetic, 734, 736 
medicinal, 737 

urine in, 729 
"phosphatic," 679 
Diaphragm, spasm of, in tetanus, 228 
Diarrhea, 565 
alba, 588 
in cholera, 183 
hill, 214 

definition of, 214 

etiology of, 214 

pathology of, 214 
- symptoms of, 214 

treatment of, 214 
in influenza, 108 
in measles, 96 
serous, 565 

causes of, 565 

treatment of, 565 
Simla, 214 
in sprue, 590 

in typhoid fever, 26, 27, 28 
Diazo reaction of urine in typhoid fever, 45 
Dibothriocephalus latus, 350, 352 
Diet in typhoid fever, 48 
Dietl's crises in movable kidney, 639 
Digestive tract, diseases of, 509 
Dilatation of colon, 591 
of heart, 446 
of esophagus, 523 
of stomach, 531 

acute, 535 

paralytic, 535 
Diphtheria, 151 

albuminuria in, 157 
anemia in, 159 
antitoxin, 162, 163 

administration of, 163 

anaphylaxis after, 163 

disagreeable effects of, 163 

results of administration, 163 
bacillus of, 152 
blood in, 156 

bronchopneumonia in, 156, 158, 159 
circulation in, 157 
complications of, 158 
of conjunctiva, 158 
definition of, 151 
"delirium cordis" in, 158 
diagnosis of, 159 

bacteriological, 160 

from tonsillitis, 160 
distribution of, 152 
emphysema in, 156 
etiology of, 152 
glandular enlargement in, 157 
heart failure in, 15S 

lesions in, 155 
hemorrhage in, 159 
history of, 152 
kidney lesions in, 156 
laryngeal, 157 
local lesion of, 154, 156 
lymphatic enlargements in, 157 
in measles, 96 
morbid anatomy of, 154 
myositis, acute, in, 155 
nasal, 157 
nephritis in, 156 

nervous manifestations of, 156, 157 
neuritis in, 156 
paralysis, facial, in, 159 



INDEX 



935 



Diphtheria, paralysis, local or widespread, in, 
159 
of phrenic nerve in, 159 
pathology of, 154 

poliomyelitis, anterior, acute in, 156 
prognosis of, 161 
prophylaxis of, 161 
renal disease in, 159 
Schick test of natural immunity to, 161 
sequelae of, 158 
sore throat in, 156 
spleen in, 156 
symptoms of, 156 
systemic lesions in, 155 
transmission, mode of, 152 
treatment of, 162 
local, 164 
serum, 162, 163 
visceral lesions of, 155 
Diphtheritic dysentery, 201 

gastritis, 527 
Diplegia, spastic, 795, 797 
Diplococcus coryzae, 359 

of Weichselbaum in cerebrospinal fever, 120 
Diplopia, in locomotor ataxia, 827 
Diptera, infection by larvae of, 357 
Dipylidium caninum, 350 
Displacements of colon, 592 . 
"Dissecting aneurysm," 500 
Disseminated myelitis, 840 

sclerosis, 820 
Distomatosis, 353 
of liver, 356 

symptoms of, 356 
treatment of, 357 
of lung, 353, 355 

pathology of, 356 
prognosis of, 356 
symptoms of, 356 
treatment of, 356 
Diverticula of esophagus, pressure, 523 

traction, 523 
Dracontiasis, 346 
Dracunculus medineusis, 346 
Drop-foot in chronic anterior poliomyelitis, 834 
Dropsy in mediastinal tumor, 432 
Dry mouth, 514 

pleurisy, 413, 414, 415 
Dubini's disease, 894 

Duchenne's type of ascending paralysis, 834 
Ductless glands, diseases of, 681 
Ductus arteriosis, patent, 494 
Dum dum fever, 335 
Dumb rabies, 224 

Duodenal ulcer, 561. See Ulcer, duodenal. 
Dura mater, hematoma of, 814 
Duroziez sign in aortic regurgitation, 480 
Dwarf tapeworm, 350 
Dysbasia, 912 
Dysentery, 200 
bacillary, 201 

pathology of, 203 
Shiga's bacillus in, 201 
specific treatment of, 210 
catarrhal, 201 

pathology of, 205 
symptoms of, 206, 207 
complications of, 207 
definition of, 200 
diagnosis of, 207 
diphtheritic, 201 

pathology of, 205 
symptoms of, 207 
entamebic, 201. 202 



Dysentery, entamebic, diagnosis of, 204, 208 

hepatic abscess in, 205 
changes in, 205 

intestinal perforation in, 207 

pathology of, 204 

peritonitis "in, 207 

symptoms of, 207 
etiology of, 201 
frequency of, 203 
morbid anatomy of, 203 
pathology of, 203 
prevention of, 203 
prognosis in, 208 
sequelae in, 207 
serum in, 203, 210 
stools in, 206 
symptoms of, 206 
treatment of, 209 

diet in, 209 

local, 212 
Dysphagia in dilatation of esophagus, 524 

in tuberculous laryngitis, 369 
Dyspituitarism, 699 

Dyspnea in acute pernicious beriberi, 769 
in ascites, 600 
in congestion of lungs, 411 
in croupous pneumonia, 136 
in emphysema of lung, 403 
in exophthalmic goitre, 688 
in Hodgkin's disease, 288 
in mitral regurgitation, 467 
in pleurisy with effusion, 418 
in pneumothorax, 430 
in pulmonary tuberculosis, 261 
in tumors of mediastinum, 432 
in uremia, 660 
Dystrophy, muscular, 884 

definition of, 884 

Erb's juvenile, 885 

etiology of, 884 

Landouzy-Dejerine type of, 885 

morbid anatomy of, 884 

pathology of, 884 

Treatment of, 888 



E 



Earache in smallpox, 70 
Echinococcic strumitis, 681 
Echinococcus cyst of brain, 801 

exogena, 351 

multilocularis, 351 
Eclampsia, 909 

infantile, 909 

diagnosis of, 910 
prognosis in, 910 
treatment of, 910 

puerperal, 910 

treatment of, 910 
Ectopia cordis, 495 
Eczema of tongue, 512 
Edema in acute diffuse nephritis, 642 

angioneurotic, 916 

in Hodgkin's disease, 288 

of larynx, 366 

of lungs in cholera, 185 

malignant anthrax, 220 

in mitral regurgitation, 467 
Edematous laryngitis, 366 
Effusion, pericardial, 438 

pleural, 417 

bloody, 429 
Egyptian chlorosis, 338 



936 



INDEX 



Ehrlich's reaction in typhoid fever, 45 
Electrical chorea, 894 
Elephant itch, 69 
Elephantiasis, 344, 345 
Elephantoid fever in fllariasis, 345 
Embolic aneurysm, 500 
Embolism, cerebral, 785 

in croupous pneumonia, 143 
in metastatic pneumonia, 397 
in typhoid fever, 32 
Embryocardia in typhoid fever, 32 
Emphysema in diphtheria, 156 
of lungs, 400 

acute, 400, 404 
atrophic, 400 

barrel-shaped chest in, 400 
chronic, 400 
compensatory, 400, 404 
definition of, 400 
diagnosis of, 403 
dyspnea in, 403 
etiology of, 400 
frequency of, 400 
hypertrophic, 400 
interstitial, 400, 405 
morbid anatomy of, 401 
pathology of, 401 
physical signs of, 401 
prognosis in, 403 
senile, 400 
small-lunged, 405 

treatment of, 405 
subjective signs of, 402 
surgical, 400 
symptoms of, 401 
treatment of, 403 
venesection in, 404 
in whooping-cough, 103 
Emprosthotonos in tetanus, 229 
Empyema, 413, 423 

complications of, 426 

in croupous pneumonia, 139 

definition of, 423 

diagnosis of, 426 

from serous effusion, 426 
etiology of, 423 
micro-organisms in, 423 
necessitatis, 426 
perforation in, 426 
physical signs of, 426 
prognosis in, 427 
in scarlet fever, 88 
sepsis in, 426 
in septicemia, 172 
symptoms of, 425 
in typhoid fever, 39 
treatment of, 427 

aspiration in, 427 
Encephalitis, acute, 811 
Encephalomyelitis, 840 
Encephalopathia saturnina, 779 
Endarteritis, obliterative, 498 

in typhoid fever, 25 
Endemic oemal una, 353 
hemoptysis, 353, 355 
mull iple neuritis, 784 
Endocardil is, 454 

acute, 455 

complical ions of, 457 

diagnosis of, 457 
et iology of, 455 
malignant , 455 
morbid anatomy of, 456 
pat I iology of, 456 



Endocarditis, acute, prognosis in, 457 
symptoms of, 457 
in tonsillitis, 519 
treatment of, 458 
benign, 455 
chronic, 460 

valvular disease as result of, 461 
in croupous pneumonia, 133, 141 
definition of, 454 
in erysipelas, 170 
gonorrheal, 166 
lenta, 459 
mural, 454 
papillary, 455 

in rheumatic fever, acute, 177, 178 
simple, 455 
in smallpox, 70 
tuberculous vegetative, 285 
ulcerative, 458 

albuminuria, 459 
cerebral type of, 459 
complications of, 460 
definition of, 458 
diagnosis of, 460 
in erysipelas, 170 
etiology of, 458 
hematuria in, 459 
malarial type of, 459 
morbid anatomy of, 458 
pathology of, 458 
prognosis in, 460 
septic form of, 459 
splenic enlargement in, 459 
symptoms of, 459 
treatment of, 460 
serum in, 460 
typhoid type of, 459 
valvular, 454 
verrucous, 456 
Endothelioma of kidney, 668 
in lung, 412 
of thyroid gland, 683 
Entameba histolytica, 202 
Entamebae dysenterise in hepatic abscess, 602 
Entamebic dysentery, 201 
Enteric fever, 17. See Typhoid fever. 

intussusception of bowel, 579 
Enteritis, atrophic, of tropics, 588 
catarrhal, 566 

symptoms of, 566 
treatment of, 566 
Enteroptosis, 582 

definition of, 582 
diet, 585 
etiology of, 582 
symptoms of, 584 
treatment of, 585 
surgical, 585 
Ephemeral fever, 295 
Epidemic gangrenous proctitis, 213 
definition of, 213 
etiology of, 213 
pathology of, 213 
symptoms of, 213 
treatment of, 214 
parotitis, 99 
poliomyelitis, 113 
roseola, 98 
sore throat, 518 

definition of, 518 
etiology of, 518 
symptoms of, 518 
treatment of, 518 
Epididymitis in typhoid fever, 38 



INDEX 



937 



Epilepsy, 901 

apoplexy, 905 

aura in, 902, 904 

complications of, 905 

convulsions in, 903 

cry in, 902 

definition of, 901 

diagnosis of, 906 

from alcoholic epilepsy, 906 
hysteria, 906 
from petit mal, 906 
from syncope, 906 
from tetanus, 906 
from uremia, 906 

etiology of, 901 

Jacksonian, 902, 909 

localized, 909 

minor, 909 

motor paralysis in, 905 

pathology of, 902 

prognosis in, 908 

risus sardonicus in, 903 

spinal, 887. See Paramyoclonus multiplex. 

symptoms of, 902 

traumatisms in, 905 

treatment of, 908 
Epiphysitis, syphilitic, 312 
Epistaxis, 364 

etiology of, 364 

in leprosy, 292 

in tick fever, 298 

treatment of, 364 
serum in, 364 
Epithelioma, cystic, of pancreas, 636 
Erb's juvenile muscular dystrophy, 885 

sign in gastric tetany, 534 
of tetany, 692 
Ergotism, 781 
Erosive, 529 

Eructation, nervous, 558 
Eruption in cerebrospinal fever, 123 

in dengue, 118 

in frambesia, 235 

in leprosy, 293 

in measles, 94, 95 

in miliary fever, 300 

in pellagra, 783 

in rubella, 99 

in scarlet fever, 85 

in smallpox, 64, 65 

in tick fever, 298 

in typhus fever, 57 

in varicella, 78 

in verruga, 301 
Eruptive itch, 69 
Erysipelas, 168 

abscess in, 170 

complications of, 170 

definition of, 168 

endocarditis in, 170 

etiology of, 168 

facial, 169 

frequency of, 168 

incubation of, 169 

migrans, 170 

morbid anatomy of, 169 

pathology of, 169 

pericarditis in, 170 

pleuritis, purulent in, 170 

prognosis in, 170 

sequelae of, 170 

in smallpox, 70 

symptoms of, 169 

treatment of, 170 



Erysipelas, treatment of, antistreptococcic 
serum in, 171 
local, 171 
in typhoid fever, 30 
in varicella, 78 
Erythema in acute rheumatic fever, 178 
in dengue, 118 
endemicum, 783 
scarlatiniform, 89 
Erythremia, 713 
Erythromelalgia, 917 
definition of, 917 
diagnosis of, 918 
etiology of, 917 
treatment of, 918 
Esbach's method for quantitative estimation of 

albumin in urine, 676 
Esophagismus, 524 
Esophagitis, 522 
chronic, 523 
membranous, 522 
in typhoid fever, 33 
Esophagus, cancer of, 525 
prognosis in, 525 
symptoms of, 525 
treatment of, 525 
dilatation of, 523 
atonic, 524 
diagnosis of, 524 
diffuse, 523 
dysphagia in, 524 
etiology of, 523 
localized, 523 
symptoms of, 524 
treatment of, 524 
diseases of, 522 
spasms of, 524 

treatment of, 524 
stricture of, organic, 523 
annular, 523 
asymmetrical, 523 
cylindrical, 623 
multiple, 523 
single, 523 
symmetrical, 523 
symptoms of, 523 
treatment of, 523 
tuberculosis of, 278 
ulceration of, in typhoid fever, 33 
Essential emphysema, 400 
Ewart's sign of pericardial effusion, 438 
Exercise in treatment of pulmonary tubercu- 
losis, 270 
Exhaustion, heat, 922 
Exophthalmic goitre, 683 
Exophthalmos in exophthalmic goitre, 684 
Exudative nephritis, 642 

Eyeballs, protrusion of, in exophthalmic goitre, 
684 



Face, lion-like in leprosy, 293 
Facial erysipelas, 169 

expression in cholera, 184 

in typhoid, 26 
hemiatrophy, 922 
nerve, paralysis of, 875 

diagnosis of, 876 
etiology of, 876 
prognosis in, 877 
symptoms of, 876 
treatment of, 877 
spasm, 878 



938 



INDEX 



Facial spasm, prognosis in, 878 

treatment of, 878 
Fallopian tubes, tuberculosis of, 285 
False aneurysm, 500 

croup, 368 
Family ataxia, 830 
Famine fever, 329 
Farcy, 231 

buds, 232 

chronic, 232 
Fat necrosis in acute pancreatitis, 631 
Fatty degeneration of heart, 448 

liver, 614 
Febricula, 295 

definition of, 295 

diagnosis of, 295 

etiology of, 295 

symptoms of, 295 

treatment of, 295 
Febris recurrens, 329 

Fecal impaction as cause of intestinal obstruc- 
tion, 579 
Fehling's solution, 732 
Fetid stomatitis, 510 
Fibrillation, auricular, 472 
Fibrinous bronchitis, 379 

pericarditis, 437 

pleurisy, 413 

pneumonia, 128 
Fibroma of brain, 801 

in lung, 412 

of mediastinum, 431 
Fibromata of kidney, 668 
Filaria diurna, 344 

loa, 344 

nocturna, 343 

perstans, 344 

sanguinis hominis, 343 
Filariasis, 343 

definition of, 343 

elephantiasis in, 344, 345 

elephantoid fever in, 345 

filaria dermarquaii in, 343 
diurna in, 343 
loa in, 343 
magalhesi in, 343 
nocturna in, 343 

microscopic demonstration of, 344 
ozzardi in, 343 
perstans in, 343 

hematochyluria in, 345 

history of, 343 

lymph scrotum in, 346 

morbid anatomy of, 344 

pathology of, 344 

symptoms of, 345 

treatment of, 346 

varicose groin glands in, 346 
Filipino itch, 69 

Fingers, club-shaped, in mitral regurgitation, 467 
Flatulence in sprue, 590 
Flea, sand, 357 
Floating kidney, 638 
Fluke, genito-urinary, 353 

liver, 353, 356 

lung, 355 
Flukes, 353 

Flute-players' cramp, 914 
Follicular colitis, 587 

pharyngitis, 517 

stomatitis, 509 

tonsillitis, 518 
Food poisoning, 7SI 
Foot-and-mout li disease. '2\)[) 



Foot-and-mouth disease, definition of, 299 
Foramen ovale, persistence of, 494 
Forchheimer's spots in rubella, 99 
Foreign bodies in bowel, 579, 582 
Frambesia, 235 

definition of, 235 
diagnosis of, 236 

from syphilis, 236 
from verruga, 236 
eruption in, 235, 236 
etiology of, 235 
history of, 235 
incubation of, 235 
prognosis of, 236 
symptoms, 235 
treatment of, 236 
tropica, 235 
Friedreich's ataxia, 830 

definition of, 830 
diagnosis of, 832 

from hereditary cerebellar ataxia, 
833 
etiology of, 831 
gait in, 832 
history of, 830 
inco-ordination in, 832 
morbid anatomy of, 831 
pathology of, 831 
prognosis in, 833 
speech in, 832 
symptoms of, 832 
treatment of, 833 
disease, 830, 887. See Paramyoclonus 
multiplex. 
Fulminant migraine, 919 
Fulminating purpura, 720 
Fungus foot of India, 234 

ray, 233 
Funnel chest in chronic hypertrophic tonsillitis, 

521 
Fusiform aneurysm, 500 

G 

Gait in Friedreich's ataxia, 832 

in locomotor ataxia, 825 
Galactotoxismus, 782 
Gallbladder, carcinoma of, 627 

diagnosis of, 629 

etiology of, 627 

jaundice in, 628 

morbid anatomy of, 627 

pathology of, 627 

prognosis in, 629 

symptoms of, 628 

treatment of, 629 
inflammation of, acute, 620 
malignant growths of, 627 
perforation of, 624 
Gallstone crepitus, 624 
Gallstones, 621 
Gangosa, 302 
Gangrene in cholera, 185 
diabetic, 729 
of lung, 405 

cough in, 407 

in croupous pneumonia, 132, 140, 144 

diagnosis of, 407 

etiology of, 405 

frequency of, 406 

morbid anatomy of, 406 

odor of breath in, 406 

pathology of, 400 

septic diarrhea in, 407 



INDEX 



939 



Gangrene of lung, sputum in, 406 
symptoms of, 406 
treatment of, 407 
surgical, 407 
pulmonary, in bronchiectasis, 378 
in Raynaud's disease, 916 
of skin in smallpox, 70 
in tick fever, 298 
in typhoid fever, 30 
Gangrenous appendicitis, 573, 574 
pancreatitis, 632 
proctitis, epidemic, 213 
pyelonephritis, 664 
stomatitis, 511 
Gastralgia, 558 
Gastrectasis, 531 
acute, 535 

diagnosis of, 536 

from acute indigestion, 536 
from volvulus, 536 
etiology of, 535 
lavage in, 536 
morbid anatomy of, 535 
prognosis in, 536 
symptoms of, 535 
treatment of, 536 
atonic, 535 
toxic, 535 
Gastric cancer, 545 

diagnosis of, 548 

from gastric ulcer, 548 
from pernicious anemia, 548 
microscopic, 551 
test meal in, 549 
duration of, 551 
etiology of, 545 
hematemesis in, 548, 559 
mode of spreading, 546 
morbid anatomy of, 545 
Oppler-Boas bacillus in, 551 
prognosis in, 551 
symptoms of, 547 
treatment of, 551 
vomiting in, 548 
catarrh, acute, 525 

definition of, 525 
diagnosis of, 526 
etiology of, 526 
symptoms of, 526 
treatment of, 526 
chronic, 528 
changes in yellow fever, 190 
crises in locomotor ataxia, 826 
dilatation, 531 
acute, 535 
definition of, 531 
diagnosis of, 534 
etiology of, 531 
morbid anatomy of, 532 
pathology of, 532 
physical signs of, 532 
symptoms of, 532 
treatment of, 534 
vomiting in, 532 
fever, 17 
ectasy, 531 
hyperperistalsis, 557 

treatment of, 557 
juice, hypersecretion of, 558 

hyposecretion of, 559 
neuralgia, 558 
neuroses, 556 
tetany, 533 

Chvostek's sign in, 534 



Gastric tetany, Erb's sign in, 534 
Trousseau's sign in, 534 
ulcer, 536 

anemia in, 539 
classes of, 537 
chronic, 539 
definition of, 536 
diagnosis of, 540 

from duodenal ulcer, 541 

tests for blood in stools, 541 
from gallstone colic, 540 
from gastric cancer, 541 
from gastric crises of locomotor 

ataxia, 541 
from gastric neuralgia, 541 
rc-rays in, 540 
etiology of, 536 
frequency of, 536 
gastroenterostomy in, 542 
hematemesis in, 539, 559 
hemorrhage in, treatment of, 544 
hour-glass contraction in, 538 
morbid anatomy of, 537 
pathology of, 537 
perforation in, 539 
prognosis in, 541 
symptoms of, 538 
treatment of, 542 

dietetic, 543, 544 
surgical, 542, 545 
in typhoid fever, 33 
Gastritis, catarrhal, acute, 525 
chronic, 528 

definition of, 528 
diagnosis of, 529 

from gastric cancer, 529 
diet in, 531 
etiology of, 528 
lavage in, 530 
morbid anatomy of, 528 
pathology of, 528 
prognosis in, 530 
symptoms of, 529 
tongue in, 529 
treatment of, 530 
diphtheritic, 527 
erosive, 529 
mycotic, 528 
phlegmonous, 526 
definition of, 526 
diagnosis of, 527 
etiology of, 526 
symptoms of, 527 
treatment of, 527 
polyposa, 528 
Gastrodynia, 558 
Gastro-intestinal paralysis, 535 
Gastroptosis, 582 
Gastrorrhagia, 559 
Gaucher's disease, 705 
etiology of, 706 
symptoms of, 705 
treatment of, 706 
Genito-urinary complications of typhoid fever, 
38 
system, tuberculosis of, 281 
Geographical tongue, 512 
Gerhard's test for acetone in urine, 732 
German measles, 98. See Rubella. 
Gibraltar fever, 215 

Girdle sensations in locomotor ataxia, 826 
Gland, thymus, diseases of, 693 
Glanders, 231 

bacillus mallei in, 231 



940 



INDEX 



Glanders, chronic, 232 
definition of, 231 
diagnosis of, 232 

from carbuncles, 232 
from multiple abscesses, 232 
etiology of, 231 
morbid anatomy of, 231 
pathology of, 231 
symptoms of, 232 
treatment of, 233 
Glands, ductless, diseases of, 681 
salivary, diseases of, 513 
suprarenal, diseases of, 695 
Glandular enlargement in bubonic plague, 198 
in diphtheria, 157 
in rubella, 99 
in scarlet fever, 84, 88 
in whooping-cough, 104 
fever, 296 

definition of, 296 
diagnosis of, 297 
etiology of, 297 

glandular enlargements in, 297 
history of, 296 
nephritis in, 297 
prognosis in, 297 
treatment of, 297 
tuberculosis, 245 
Glaucoma, hemorrhagic, in chronic interstitial 

nephritis, 653 
Glenard's disease, 582 
Glioma of brain, 801, 802 
Globulin, antitetanic, 229 
Globus in hysteria, 897 
Glomerular nephritis, 641 

chronic, 645 
Glosso-labio-laryngeal paralysis, 835 
Glossopharyngeal nerve, paralysis of, 880 
Glottis, spasm of, in tetanus, 229 
Glycosuria, 725, 728, 729 
Goitre, 681 

benign, 681 
colloid, 681 
cystic, 681 
definition of, 681 
etiology of, 681 
exophthalmic, 683 
definition of, 683 
dyspnea in, 686 
etiology of, 683 
exophthalmus in, 684 
frequency of, 683 
Mobius' sign in, 685 
morbid anatomy of, 684 
nervous symptoms of, 686 
operative, 687 
pathology of, 684 
prognosis in, 686 
serum in, 687 
Stelwag's sign in, 685 
symptoms of, 684 
tachycardia in, 685 
treatment of, 686 
tremor in, 686 
von Graefe's sign in, 685 
x-rays in, 686 
hyperplastic, 681 
Lingual, 681 
malignant, 681 
mixed, 681 

neoplastic, 681 
parenchymatous, 681 

simple, OX] 
symptoms of, 682 



Goitre, treatment of, 682 

vascular, 681 
Gold-dust complaint, 399 
Gonorrheal arthritis, ankylosis in, 166 
chronic, 165 
symptoms of, 165 
temporary, 186 
treatment of, 167 
antigonococcic serum in, 167 
endocarditis, 166 
infection, 165 

diagnosis of, 166 
fascia in, 166 
prognosis of, 167 
symptoms of, 165 
pyemia, 165 
rheumatism, 167 
Gout, 740 

acute, 745 

symptoms of, 745 
cardiovascular changes in, 744 
chronic, 746 

symptoms of, 746 
definition of, 740 
diagnosis of, 747 

from arthritis deformans, 747 
etiology of, 741 
frequency of, 741 
irregular, symptoms of, 746 
joint changes in, 743 
morbid anatomy of, 743 
pathology of, 741 
prognosis in, 747 
retrocedent, 747 
symptoms of, 745 
treatment of, 748 
dietetic, 748 
Gouty lesions in chronic lead poisoning, 779 
Grain shovellers' disease, 398 
Grand mal, 901 
Granular kidney, 650 

meningitis, 247 
Graves' disease, 683 
Green sickness, 709 
Grindstone consumption, 399 
Ground itch, 339 
Guinea-worm, 346 
disease, 346 

definition of, 346 
distribution of, 346 
symptoms of, 347 
treatment of, 347 
Gull's disease, 688 
Gumma, 801 

of pancreas, 637 
Gummata, syphilitic, 306, 309 
Giinzburg's reagent, 549 



H 



Haffkine's antiplague inoculation, 197 
Hammerer's palsy, 914 
Hanot's cirrhosis of liver, 611 
Harrison's groove in bronchial asthma, 382 

in rickets, 757 
Haut mal, 901 
Hay fever, 362 

definition of, 362 

distribution of, 362 

etiology of, 362 

morbid anatomy of, 362 

pathology of, 362 

prognosis of, 303 






INDEX 



941 



Hay fever, symptoms of, 363 

treatment of, 363 
Haygarth's nodosities in arthritis deformans, 751 
Head tetanus, 231 
Heart, aneurysm of, 453 
causes of, 453 
forms of, 453 
symptoms of, 454 
atrophy of, 449 
bilocular, 494 
-block, 450 

brown induration of, 449 
congenital defects of, 494 
degeneration of, amyloid, 449 
calcareous, 449 
fatty, 448 
hyaline, 449 
parenchymatous, 448 
dilatation of, 444, 446 
causes of, 446 
definition of, 444 
physical signs of, 447 
prognosis in, 447 
symptoms of, 447 
treatment of, 447 
diseases of, 444 
failure in diphtheria, 158 
fragmentation of, 449 
hypertrophy of, 444 
definition of, 444 
diagnosis of, 445 

from cardiac dilatation, 445 
from pericardial effusion, 445 
from tobacco heart, 446 
physical signs of, 445 
prognosis in, 446 
symptoms of, 445 
treatment of, 446 
-muscle, changes in, in typhoid fever, 25 
neuroses of, 487 

definition of, 487 
treatment of, 490 
palpitation of, 487 
pulmonary valves of, disease of, 482 
segmentation of, 449 
-sounds in typhoid fever, 32 
trilocular, 494 
tuberculosis of, 285 
in typhoid fever, 32 
valves of, mechanism of, 462 
valvular anomalies of, 494 
disease of, chronic, 461 
causes of, 461 
treatment of, 483 
valves affected in, 461 
wounds of, 454. 
Heat exhaustion, 922 
Heatstroke, 920 

Heat test for albumin in urine, 676 
Heberden's nodes in arthritis deformans, 751 
Hemameba malarise, 316 
in man, 318 
in mosquito, 319 
Hematemesis, 559 
in aneurysm, 559 

diagnosis of, from hemoptysis, 560 
in gastric cancer, 548, 559 

ulcer, 539, 559 
in hemophilia, 559 
in hepatic cirrhosis, 559 
in purpura, 559 
in smallpox, 559 
in yellow fever, 191, 559 
Hematinuria, 674 



Hematinuiia, treatment of, 675 
Hematitis, suppurative, 714 
Hematochyluria in filariasis, 345 
Hematoma of dura mater, 814 
Hematura, 673 

in bilharzia disease, 354 
causes of, 673 
endemic, 353 
in malarial fever, 325 
in movable kidney, 639 
treatment of, 674 
in ulcerative endocarditis, 459 
Hemianesthesia in apoplexy, 791 

in hysteria, 896 
Hemianopsia, 867 
in apoplexy, 791 
binasal, 867 
bitemporal, 867 
in brain tumor, 803 
homonymous, 867 
Hemiatrophy, facial, 922 
Hemiplegia in apoplexy, 790 
in croupous pneumonia, 142 
in malarial fever, 326 
pneumonique, 142 
spastic, 795 
in typhoid fever, 40 
in uremia, 660 
Hemoglobinuria, 674 

in croupous pneumonia, 138 
in malarial fever, 325 
Hemolytic splenomegaly, 706 
Hemopericardium, 443 
Hemophilia, 721 

definition of, 721 
epistaxis in, 721 
etiology of, 721 
hematemesis in, 559 
morbid anatomy of, 721 
pathology of, 721 
prognosis in, 721 
symptoms of, 721 
treatment of, 721 
Hemoptysis, 560 

in bronchiectasis, 378 
endemic, 353, 355 
parasitic, 353, 355 
in pulmonary tuberculosis, 261 
Hemorrhage, cerebral, 785 
in diphtheria, 159 
in duodenal ulcer, 563 
from lungs, 560 
into pancreas, 637 
in pneumonic plague, 198 
in pulmonary tuberculosis, 261 
retinal, in malarial fever, 326 
into spinal cord, 846 
definition of, 846 
diagnosis of, 847 
etiology of, 846 
prognosis of, 847 
symptoms of, 846 
treatment of, 847 
membranes, 847 
from stomach, 559 

symptoms of, 559 
subconjunctival in whooping-cough, 104 
in typhoid fever, 29, 33, 34 
diagnosis of, 34 
symptoms of, 34 
treatment of, 51 
Hemorrhagic affections of newborn, 720 
albuminuric retinitis, 653 
cysts of pancreas, 636 



942 



INDEX 



Hemorrhagic glaucoma in chronic interstitial 
nephritis, 653 
internal pachymeningitis, 814 
measles, 95 
nephritis, 642 
pancreatitis, acute, 637 
peritonitis, 594 
smallpox, 68 
Henoch's purpura, 720 
Hepatic abscess, 602 
amebic, 602 

entamebse dysenteriae in, 602 
diagnosis of, 605 

from empyema, 606 
from infection all gall-ducts, 605 
from malarial infection, 605 
in dysentery, 205 
etiology of, 602 
fever in, 605 
morbid anatomy of, 603 
multiple, 603 
pathology of, 603 
prognosis in, 606 
pyemic, 602 
single large, 603 
symptoms of, 605 
traumatic, 602 
treatment of, 606 
tropical, 602 
artery, aneurysm of, 507 
bloodvessels, affections of, 612 
changes in croupous pneumonia, 133 
in malarial fever, 37 
in yellow fever, 191 
cirrhosis, 606. See Liver, cirrhosis of. 

hematemesis in, 559 
complications in typhoid fever, 320 
congestion, 612 

fever of Charcot, intermittent, 624 
tuberculosis, 281 
Hepatitis, acute, 602 

definition of, 602 
etiology of, 602 
Hepatization of lung, 410 

in croupous pneumonia, 132 
Hereditary ataxia, 830 

Marie's cerebellar, 833 
ataxic paraplegia, 830 
chorea, 893 
syphilis, 302, 304, 312 
Herpes in cerebrospinal fever, 123 
in croupous pneumonia, 136 
in typhoid fever, 30 
Hill diarrhea, 214 

definition of, 214 
etiology of, 214 
pathology of, 214 
symptoms of, 214 
treatment of, 214 
Hip-joint, dislocation of, in scarlet fever, 87 
Hip, spontaneous dislocation of, in typhoid 

fever, 40 
Hippocratic facies in acute peritonitis, 595 
in cholera, 184 
in yellow'fever, 191 
Hob-nail liver, 607 
Hodgkin's disease, 286 

blood changes in, 288 
bronzing of skin in, 289 
definition of, 286 
diagnosis of, 289 

from true leukemia, 289 
from tuberculous, lymph glands, 
289 



Hodgkin's disease, dyspnea in, 288 

etiology of, corynebacterium granulo- 
matis maligni in, 287 
hodgkini in, 287 
history of, 286 
morbid anatomy of, 287 
edema in, 288 
pathology of, 287 
prognosis in, 289 
symptoms of, 288 
treatment of, 289 
Hoffman's sign of tetany, 692 
Hookworm disease, 338 
Horseshoe kidney, 638 

Hour-glass stomach, 555. See Stomach, hour- 
glass. 
Human trypanosomiasis, 333 
Hungarian itch, 69 
Hunger typhus, 55 
Huntington's disease, 893 
Hutchinson's pupil in apoplexy, 792 

teeth in syphilis, 312 
Hyaline degeneration of heart, 449 
Hybrid scarlet fever, 98 
Hydatid cysts of liver, 351 

of mediastinum, 431 
of pancreas, 636 
of peritoneum, 599 
of spleen, 703 
Hydrocephalus, 927 
Hydronephrosis, 665 
acquired, 665 
congenital, 665 
definition of, 665 
diagnosis of, 666 
etiology of, 665 
pathology of, 665 
prognosis of, 666 
in tuberculosis of kidney, 284 
symptoms of, 666 
treatment of, 666 
Hydropericardium, 442 
prognosis of, 443 
symptoms of, 443 
treatment of, 443 
Hydrophobia, 222 
definition of, 222 
diagnosis of, 225 

from pseudohydrophobia, 225 
from tetanus, 225 
distribution of, 222 
etiology of, 223 
frequency of, 223 
history of, 222 
incubation of, 223 
morbid anatomy of, 223 
Negri bodies in, 223 
pathology of, 223 
prevention of, 223 
prognosis of, 225 
symptoms of, in animals, 224 

in man, 225 
treatment of, 225 

antirabic vaccine in, 226 
by serum, 226 
Hydropneumothorax, 429 
coin sound in, 431 
in croupous pneumonia, 140 
metallic tinkling in, 431 
physical signs of, 431 
Skodaic resonance in, 431 
Hydrotherapy in typhoid fever, 47 
Hydrothorax, 428 
Hymenolipsis nana, 350 



INDEX 



943 



Hyperemia of kidney, acute, 640 
chronic, 640 

of liver, 612 
Hyperesthesia of stomach, 558 
Hyperleukocytosis in scarlet fever, 84 
Hypernephromata of kidney, 668 
Hyperperistalsis, gastric, 557 
Hyperplastic goitre, 681 

tuberculosis, chronic, 243 
Hypertrophic cirrhosis of liver, 610 

emphysema, 400 

pulmonary osteo-arthropathy, 765 

rhinitis, 361 

stenosis of pylorus, 552 

tonsillitis, chronic, 521 
Hypertrophy, pseudomuscular, 884 
Hypodermoclysis in cholera infantum, 570 
Hypoglossal nerve, disease of, 883 
Hypostatic pneumonia, 410 
Hysteria, 894 

anesthesia, 896 

aphonia in, 896 

convulsion in, 895 

in chorea minor, 892 

definition of, 894 

diagnosis of, 897 

from organic nervous disease, 897 

disturbances of special sense in, 896 

etiology of, 894 

globus in, 897 

hemianesthesia in, 896 

major, 895 

merycismus in, 897 

ovarian tenderness in, 896 

paralysis of motion in, 896 

pathology of, 895 

prognosis in, 898 

pseudo-angina in, 897 

symptoms of, 895 
sensory, 896 

tachycardia in, 897 

treatment of, 898 
Hysteroepilepsy, 897 



Ice, infection by, in typhoid fever, 18 
"Iced liver,;' 440 
Ichthyosis lingualis, 513 
Ichthyotoxismus, 782 
Icterus neonatorum, 630 
Idiocy, acquired, 798 

amaurotic family, 798 
Idiopathic dilatation of colon, 592 

muscular spasm, 691 
Ileocecal intussusception of bowel, 580 
Ileocolic intussusception of bowel, 580 
Ileocolitis of childhood, 566 

definition of, 566 

diagnosis of, 569 

from typhoid fever, 569 

etiology of, 566 

morbid anatomy of, 567 

pathology of, 567 

prognosis in, 569 

symptoms of, 568 

treatment of, 569 
Ileotyphus, 55 
Immunity, natural, to diphtheria, Schick 

for, 161 
Impetigo, 69 
Incarcerated kidney, 638 
Inclusion bodies in scarlet fever, 89 



test 



Inco-ordination in Friedreich's ataxia, 832 

in locomotor ataxia, 825 
"India-rubber bottle stomach," 546 
Indicanuria, 679 

test for, 679 
Indurative mediastinopericarditis, 440 

parotitis, chronic, 514 
Infantile cerebral paralysis, 795 

eclampsia, 909. See Eclampsia, infantile. 

palsy, acute, 111 

spinal paralysis, 111 

scurvy, 760 
Infantilism, 702 
Infarct of spleen, 702 

in septicemia, 172 
Infarction of lung in typhoid fever, 39 
Infection, diseases due to specific, 17 

gonorrheal, 165 

of larvae of diptera, 357 

latent malarial, 328 
Infectious jaundice, 296 
Inflammation of bile-ducts, suppurative, 619 

of liver, 602 

of salivary glands, 514 
Influenza, 106 

bacillus of Pfeiffer in, 106, 107 

bronchitis in, 107 

chill in, 107 

complications of, 109 
cardiac, 108, 109 

definition of, 106 

diagnosis of, 109 

diarrhea in, 108 

endemic-epidemic, 106 

etiology of, 106 

fever in, 107 

history of, 106 

incubation in, 107 

jaundice in, 108 

kidneys in, 109 

meningitis, 108 

mental disturbances in, 108 

nervous manifestations of, 108 

pleurisy in, 108 

pneumonia in, 108 

prophylaxis of, 111 

pulmonary congestion in, 108 

sequelae of, 109 

symptoms of, 107 

toxic neuritis in, 109 

treatment of, 110 

vera, 107 

vomiting in, 108 
Infusoria, parasitic," 357 
Ingravescent apoplexy, 792 
Inoculation preventive in plague, 197 
Insolation, 920 
Insomnia in croupous pneumonia, 138 

in typhoid fever, 26 
treatment of, 52 

in uremia, 660 
Insular sclerosis, 820 
Intermittent fever, diagnosis of, 323 
from septicemia, 323 
from tuberculosis, 323 
from ulcerative endocarditis, 323 
prognosis of, 323 
treatment of, 323 

hepatic fever of Charcot, 624 

malarial fever, 316 
Interstitial emphysema, 400, 405 

myocarditis, acute, 450 
chronic, 450 

nephritis, chronic, 644 



944 



INDEX 



Interstitial neuritis, 857 

parotitis, suppurative, 514 
Interventricular septum, perforated, 494 
Intestinal amebiasis, 201 

antisepsis in typhoid fever, 50 
changes in yellow fever, 191 
hemorrhage in typhoid fever, 34 

treatment of, 51 
perforation in typhoid fever, 34 

treatment of, 52 
myiasis, 358 
obstruction, 579 
acute, 579 
causes of, 579 
chronic, 579 

by congenital malformations, 579 
diagnosis of, 579 
prognosis of, 579 
symptoms of, 579 
treatment of, 579 
definition of, 579 
by foreign bodies, 579, 582 
by internal strangulation, 579, 581 

symptoms of, 581 
by intestinal paralysis, 579 
by intussusception, 579 
etiology of, 580 
frequency of, 580 
pathology of, 580 
prognosis in, 581 
symptoms of, 580 
treatment of, 581 
by volvulus, 581 

prognosis in, 582 
symptoms of, 581 
treatment of, 582 
ulcers in paratyphoid fever, 53 
Intestines, diseases of, 561 
tuberculosis of, 278 

chronic hyperplastic, 279 
Intoxications, 771 

Intubation in edematous laryngitis, 367 
Intussusception, 579 
acute, 579 
enteric, 580 
etiology of, 580 
frequency of, 580 
ileocecal, 580 
ileocolic, 580 
pathology of, 580 
prognosis in, 581 
retrograde, 580 
subacute, 579 
symptoms of, 580 
treatment of, 581 
ultra-acute, 579 
Iritis in acute rheumatic fever, 178 

syphilitic, 309 
Italian itch, 69 
Itch, Dhobie, 69 



JACKSONIAN epilepsy, 909 

Japanese measles, 69 

Jaundice in acute pancreatitis, 632 
in cancer of gall-bladder, 628 
catarrhal, 617 
in cholelithiasis, 623 
in croupous pneumonia, 138 
infect ious, 296 
in influenza, L08 
in new born, 630, 720 
in relapsing lever, 330 



Jaundice in typhoid fever, 37 

in yellow fever, 191 
Jaw, lumpy, 233 

Joint complications in typhoid fever, 40 
Joints in gonorrheal infection, 165 

in gout, changes in, 743 

inflammation of, in acute rheumatic fever, 
176 

in verruga, 301 

K 

Kakke, 861 
Kala-azar, 335 

definition of, 335 
etiology of, 335 
morbid anatomy of, 335 
mortality of, 335 
pathology of, 335 
symptoms of, 335 
treatment of, 336 
Kangaroo itch, 69 
Keratitis in measles, 96 

syphilitic, 312 
Kernig's sign in meningococcic meningitis, 123 
Kidney, adenoma of, 668 
alveolar, 668 
papillary, 668 
amyloid disease of, 657 

definition of, 657 
etiology of, 657 
pathology of, 657 
prognosis in, 658 
symptoms of, 657 
treatment of, 658 
urine in, 657 
angiomata of, 668 
cancer of, 668 
chronic contracted, 650 
"cinder-sifting," 638 
circulatory disturbances in, 640 
cirrhosis of, 650 
contracted, 650 
in croupous pneumonia, 133 
cystic disease of, 667 
cysts of, congenital, 667 
echinococcus, 668 
multiple, 667 
in diabetes mellitus, changes in, 727 
diseases of, 638 
endothelioma of, 668 
fibromata of, 668 
floating, 638 
granular, 650 
horseshoe, 638 
hyperemia of, acute, 640 
treatment of, 640 
chronic, 640 

albuminuria in, 640 
diagnosis of, 641 
symptoms of, 640 
treatment of, 641 
hypcrnephromata of, 668 
incarcerated, 638 
in influenza, 109 
large white, 646 
lesions in diphtheria, 156 
lipomata of, 668 

in malarial fever, changes in, 320, 321 
malformations of, 638 
movable, 638 

definition of, 638 
diagnosis of, 638 
Dietl's crises in, 639 



INDEX 



945 



Kidney, etiology of, 638 

hematuria in, 639 
symptoms of, 639 
treatment of, 640 

papilloma of, 668 

sarcoma of, 668 

in scarlet fever, 84, 87 

sclerotic, 650 

small white, 646 

stone in, 669 

suppuration of, in septicemia, 172 

tuberculosis of, 283 

tumors of, 668 

malignant, hematuria in, 669 
symptoms of, 669 

in typhoid fever, changes in, 25 

in typhus fever, 57 
Klebs-Loeffler bacillus of diphtheria, 152 
Knee-jerks in locomotor ataxia, 826 
Knife-grinders' rot, 399 
Kopf-tetanus, 231 
Koplik's spots in measles, 94 
Korsakoff's disease, 862 
Kreotoxismus, 782 
Kussmaul's coma in diabetes mellitus, 730 



La Grippe, 106. See Influenza. 
Landouzy-Dejerine type of muscular dystrophy, 

885 
Landry's paralysis, 854 
Lane's kink, 579 
Large-lunged emphysema, 400 
Larval plague, symptoms of, 199 
Laryngeal diphtheria, 157 
tuberculosis, 259 
ulceration in typhoid fever, 38 
Laryngitis, catarrhal, acute, 364 
definition of, 364 
diagnosis of, 365 
etiology of, 364 
intubation in, 367 
pathology of, 364 
prognosis of, 365 
symptoms of, 365 
treatment of, 365 
chronic, 366 
diagnosis of, 366 
pathology of, 366 
symptoms of, 366 
treatment of, 366 
edematous, 366 

cyanosis in, 367 
definition of, 366 
diagnosis of, 367 

from foreign body, 367 
from laryngeal crises in locomotor 
ataxia, 367 
etiology of, 366 
intubation in, 367 
pathology of, 367 
prognosis in, 367 
symptoms of, 367 
tracheotomy in, 367 
treatment of, 367 
in smallpox, 70 
spasmodic, 368 

definition of, 368 
etiology of, 368 
treatment of, 368 
syphilitic, 370 

60 



Laryngitis, syphilitic, diagnosis of, 370 

from tuberculous ulceration, 
370 
etiology of, 370 
prognosis of, 370 
symptoms of, 370 
treatment of, 370 
tuberculous, 368 
aphonia in, 369 
cough in, 369 
definition of, 368 
diagnosis of, 369 

from carcinoma of larynx, 369 
from syphilitic laryngitis, 369 
dysphagia in, 369 
etiology of, 368 
lesion in, 369 
pathology of, 368 
prognosis of, 369 
symptoms of, 369 
treatment of, 369 
Larynx, diseases of, 364 
Latah, 911 
Lateral sclerosis, 836 

amyotrophic, 838 
Lavage in chronic gastritis, 530 
Lead poisoning, 778 
acute, 778 
chronic, 778 

anemia in, 780 
blue line on gums in, 779 
colic in, 780 
convulsions in, 779 
• diagnosis of, 780 

from acute poliomyelitis, 780 
from chronic poliomyelitis, 

780 
from epilepsy palsy, 780 
from pressure palsy, 780 
etiology of, 778 
gouty lesions in, 779 
morbid anatomy of, 779 
neuritis in, 779 
optic neuritis in, 779 
pathology of, 779 
prevention of, 778 
prognosis in, 780 
squint in, 779 
symptoms of, 779 
treatment of, 780 
wrist-drop in, 779 
Leathery stomach, 546 
Leontiasis, 293 
ossea, 765 
Leprosy, 289 

anesthetic, 293 
bacillus of, 290 
clinical forms of, 292 
definition of, 289 
diagnosis of, 294 
distribution of, 290 
epistaxis in, 292 
eruptions in, 293 
etiology of, 290 
history of, 289 
incubation period in, 292 
leontiasis in, 293 
leprous chancre in, 292 
manner of infection in, 290 
mixed, 293 

morbid anatomy of, 292 
nodular, 293 
prognosis in, 294 
prophylaxis of, 295 



946 



INDEX 



Leprosy, symptoms of, 292 
treatment of, 294 
tubercular, 293 
Leprous chancre, 292 
Leptomeningitis, 814 
diagnosis of, 815 
morbid anatomy of, 815 
pathology of, 815 
symptoms of, 815 
treatment of, 816 
Lethargy, African, 331, 333 
Leukemia, 714 

definition of, 714 
diagnosis of, 717 
etiology of, 714 
history of, 714 
lymphatic, 714, 716 

symptoms of, 716 
morbid anatomy of, 715 
myelogenous, 714 
pathology of, 715 
prognosis in, 717 
splenomedullary, 714, 715 
blood changes in, 715 
spleen in, 716 
symptoms of, 716 
treatment of, 717 
Leukocythemia, 714 
Leukocytosis in typhoid fever, 31 

in whooping-cough, 103 
Leukoplakia buccalis, 513 
Lingual goitre, 681 
Lipomata of kidney, 668 
Lithiasis, 398 
Lithuria, 680 
Little's disease, 799 
Liver, abscess of, 602 

diagnosis of, 605 
in dysentery, 205 
etiology of, 602 
multiple, 603 
pathology of, 603 
prognosis of, 606 
pyemic, 602 
single large, 603 
symptoms of, 605 
traumatic, 602 
treatment of, 606 
tropical, 602 
amyloid, 614 

symptoms of, 614 
treatment of, 614 
angiomata, cavernous of, 615 
carcinoma of, 614 

secondary, 615 
changes in, in typhoid fever, 25, 37 
in cholera, 183 
cirrhosis of, 606 
atrophic, 607 

etiology of, 607 
hepatic coma in, 609 
morbid anatomy of, 607 
pathology of, 607 
physical signs of, 609 
prognosis in, 609 
symptoms of, 609 
treatment of, 610 
capsular, 612 
definition of, 606 
hypertrophic, 606, 610 
definition of, 610 
diagnosis of, 611 
etiology of, 610 
llanot's type, 611 



Liver, cirrhosis of, hypertrophic, morbid 
- anatomy of, 610 
pathology of, 610 
prognosis in, 611 
symptoms of, 611 
treatment of, 611 
syphilitic, 611 

treatment of, 612 
congestion of, 612 

nutmeg appearance in, 613 
symptoms of, 613 
treatment of, 613 
cystic disease of, 615 
diseases of, 602 
distomatosis of, 356 
hyperemia of, 612 
fatty, 614 
flukes, 356 

varieties of, 356 
hydatid cysts of, 351 
;'"iced," 440 
inflammation of, 602 
in malarial fever, changes in, 320 
pericarditic pseudocirrhosis of, 440 
red atrophy of, 613 
sarcoma of, 615 
syphilis of, 307 
tuberculosis of, 281 
tumors of, 614 

diagnosis of, 615 

from echinococcus cyst, 615 
from gumma, 615 
from hypertrophic cirrhosis, 615 
prognosis in, 615 
symptoms of, 615 
treatment of, 616 
in typhoid fever, changes in, 25 
yellow atrophy of, acute, 616 
definition of, 616 
diagnosis of, 616 
etiology of, 616 
morbid anatomy of, 616 
pathology of, 616 
prognosis in, 616 
symptoms of, 616 
treatment of, 616 
Lobar pneumonia, 128 
Lobular pneumonia, 386 
Localized epilepsy, 909 

peritonitis, 594 
" Lock-jaw" in tetanus, 228 
Locomotor ataxia, 823 

allochiria in, 827 

Argyll-Robertson pupil in, 827 

Charcot joint in, 828 

crises in, 826 

cystitis in, 828 

definition of, 823 

diagnosis of, 828 

from caries of vertebrae, 828 

from cerebellar tumor, 828 

from general paralysis of insane, 

828 
from paraplegia, 828 
from peripheral neuritis, 828 
diplopia in, 827 
etiology of, 823 
gait in, 825 

girdle sensations in, 826 
history of, 823 
inco-ordination in, 825 
knee-jerk in, 826 
lightning pains in, 826 
morbid anatomy of, 823 



INDEX 



947 



Locomotor ataxia, ocular symptoms of, 827 
optic atrophy in, 827 
pathology of, 823 
perforating ulcer of foot in, 828 
prognosis in, 828 
Romberg's symptom in, 826 
symptoms of, 825 
treatment of, 829 
baths in, 830 
electrical, 830 
Westphal's symptom in, 826 
Loculated peritonitis, 594 
Lombardian leprosy, 782 
Lucilia macellaria, 357 
Ludwig's angina, 520 

symptoms of, 520 
treatment of, 521 
Lues, 302 

venerea, 302 
Lumbar puncture as aid to diagnosis of cerebro- 
spinal fever, 125 
"Lumpy jaw," 233 
Lung, abscess of, 407 

in croupous pneumonia, 132, 140 
congestion of, 409 
diseases of, 386 
distomatosis of, 353, 355 
edema of, in cholera, 185 
emphysema of, 400 
fever, 128 
flukes, 355 
gangrene of, 405 

in croupous pneumonia, 132, 140, 144 
hemorrhage from, 560 

hypostatic congestion of, in typhoid fever, 
38 
in typhus fever, 57 
infarction of, in typhoid fever, 39 
syphilis of, 307 
tumors in, 412 
Lungs, diseases of, 386 
Lymph nodes, syphilitic, 308 
scrotum in filariasis, 346 
Lymphadenoma of mediastinum, 431 
Lymphatic areas of stomach, 546 
constitution, 694 
glands, tuberculosis of, 245 
involvement in diphtheria, 157 
leukemia, 714, 716 
system, diseases of, 681 
Lymphocytosis in whooping-cough, 103 
Lymphoma of mediastinum, 431 
Lyssa, 222 

M 

McBurney's point, 575 
Macular syphilide, 309 
Madura foot, 234 
Mai de sole, 782 
Malarial fever, 316 

estivo-autumnal, diagnosis of, 327 
parasite of, 319 
symptoms of, 324 
treatment of, 327 
ague cake in, 321, 326 
blood changes in, 320 

examination in, 320 
bone-marrow in, 320 
chill in, 321 
chronic, 316 

changes in, 320 
complications of, 325 
nervous, 326 



Malarial fever, definition of, 316 
distribution of, 317 
etiology of, 317 

mosquito as, 317 
hemiplegia, 326 
hepatic changes in, 320 
history of, 316 
intermittent, 316 
morbid anatomy of, 320 
nephritic changes in, 320, 321 
pathology of, 320 
pernicious, 316, 325 
algid form of, 325 
comatose form of, 325 
symptoms of, 325 
Plasmodium, 316 
prevention of, 319 
quartan, parasite of, 318 

symptoms of, 321 
relapse in, 328 
remittent, 316 

symptoms of, 324 
retinal hemorrhages in, 326 
sequelae of, 325 
splenic changes in, 320, 321 

enlargement in, 322, 326 
symptoms of, 321 
tertian, parasite of, 318 
symptoms of, 321 
infection, latent, 328 
Malformations, congenital, of bowel, 579 

of kidney, 638 
Malignant anthrax edema, 220 
goitre, 681 

growths of gallbladder and biliary ducts, 
627 
of spleen, 703 
of vertebrae, 850 
Mali-mali, 911 
Malta fever, 215 

complications of, 218 
definition of, 215 
diagnosis of, 217 
distribution of, 215 
duration of, 217 
etiology of, 215 
fever in, 216 
history of, 215 
incubation of, 216 
micrococcus melitensis in, 215 
pathology of, 216 
prognosis of, 217 
spleen in, 216 
symptoms of, 216 
treatment of, 218 
Mania in uremia, 660 
Manila itch, 69 

scab, 69 
Marie's cerebellar hereditary ataxia, 833 

disease, 699 
Measles, 92 

bacteriology of, 92 
"black," 95 
bronchitis in, 93, 95 
bronchopneumonia in, 93, 96 
chill in, 94 
complications of, 96 

nervous, 96 
conjunctivitis in, 96 
coryza in, 94 
diagnosis of, 97 
diarrhea in, 96 
diphtheria in, 96 
distribution of, 92 



948 



INDEX 



Measles, eruption of, 94, 95 
etiology of, 93 
fever in, 94 
frequency of, 93 
German, 98. See Rubella, 
hemorrhagic, 95 
incubation of, 93 
keratitis in, 96 
"Koplik's spots" in, 94 
leukocytosis in, 96 
leukopenia in, 95 
meningitis in, 96 
morbid anatomy of, 93 
noma in, 96 
pathology of, 93 
prevention of, 93 
prognosis in, 97 
respiratory form of, 95 
sequelae of, 96 
stomatitis in, 96 
symptoms of, 94 
transmission of, mode of, 93 
treatment of, 98 
tuberculosis after, 96 
ulcerations in, 96 
variations of, 95 
vomiting in, 95, 96 
whooping-cough in, 96 
Mediastinal glands, tuberculosis of, 246 
Mediastinopericarditis, indurative, 440 
Mediastinum, abscess of, 431, 433 
carcinoma of, 431 
dermoid cyst of, 431 
diseases of, 431 
fibroma of, 431 
hydatid cyst of, 431 
lymphadenoma of, 431 
lymphoma of, 431 
sarcoma of, 431 
teratoma of, 431 
tumors of, 431 

abdominal effusion in, 432 

dropsy in, 432 

dyspnea in, 432 

pain in, 433 

symptoms of, 432 
Medina worm, 346 
Mediterranean fever, 215 
Melanuria, 680 
Membranous esophagitis, 522 

pericolitis, 592 
Meniere's disease, 879 

treatment of, 879 
Meningeal tuberculosis, acute, 247 
Meningitis in acute rheumatic fever, 178 
basilar, 248 
cerebral, 813 

definition of, 813 

etiology of, 813 
cerebrospinal, 120 
in croupous pneumonia, 133, 142 
granular, 247 
in influenza, 108 
in measles, 96 
meningococcic, 120 

arthritis in, 123 

blood in, 123 

Brudzinski's contralateral reflex in, 123 

complications in, 124 

croupous pneumonia in, 124 

deafness from 124 

definition of, 120 

delirium in, 123 

diagnosis of, 124 



Meningitis, meningococcic, diagnosis of, from 
acute poliomyelitis, 125 
from croupous pneumonia, 125 
from influenza, 125 
lumbar puncture as aid to, 125 
from tuberculous meningitis, 125 
from typhoid fever, 124 
diplococcus of Weichselbaum in, 120 
eruption in, 123 
etiology of, 120 
fever in, 122 
forms of, 123 
chronic, 123 
intermittent, 123 
malignant, 123 
moderate, 123 
typhoid, 123 
frequency of, 121 
headache in, 122 
herpes in, 123 
history of, 120 
incubation of, 122 
Kernig's sign in, 123 
morbid anatomy of, 122 
nervous complications, 124 
otitis media in, 124 
pathology of, 122 
prevention of, 121 
prognosis of, 127 
respiration in, 123 

Cheyne-Stokes, 123 
sequelae of, 124 
symptoms of, 123 
treatment of, 127 
serum in, 127 
vaccine in, 121 
in mumps, 101 
spinal, 851 

chronic, 853 

diagnosis of, 853 
etiology of, 853 
symptoms of, 853 
treatment of, 854 
definition of, 851 
diagnosis of, 852 
etiology of, 851 
morbid anatomy of, 852 
pathology of, 852 
prognosis in, 853 
symptoms of, 852 
treatment of, 853 
in typhoid fever, 39, 40 
Meningoencephalitis, 816 
Mental disturbances in influenza, 108 

state in chorea minor, 892 
Merycismus, 557 

in hysteria, 897 
Mesenteric artery, superior, aneurysm of, 507 
glands, tuberculosis of, 247 
nodes in typhoid fever, 24 
Mesentery, cysts of, 599 
Metallic tinkling in hydropneumothorax, 431 

in pulmonary tuberculosis, 264 
Metastatic pneumonia, 396 
Micrococcus catarrhalis in acute coryza, 359 
lanceolatus in pneumonia, 128, 131 
melitensis in Malta fever, 215 
rheumaticus in acute rheumatic fever, 175 
Migraine, 918 

definition of, 918 
fulgurating, 919 
fulminant, 919 
symptoms of, 918 
treatment of, 919 



INDEX 



949 



Mikulicz's disease, 514 
Miliary fever, 299 

definition of, 299 
eruption in, 300 
etiology of, 299 
history of, 299 
prognosis in, 300 
symptoms of, 300 
treatment of, 300 
tubercle, 242 
tuberculosis, acute, 243 
Milk, infection by, in typhoid fever, 18 
sickness, 295 

bacillus lactamorbi in, 296 
definition of, 295 
mortality in, 296 
symptoms of, 296 
treatment of, 296 
Miners' anemia, 338 
cachexia, 338 
disease, 338 
phthisis, 399 
Minor epilepsy, 909 
Mitral regurgitation, 464 

blood-spitting in, 467 
club-shaped fingers in, 467 
cyanosis in, 467 
diagnosis of, 468 
dyspnea in, 467 
edema in, 467 
pathology of, 465 
physical signs of, 467, 468 
prognosis in, 468 
symptoms of, 467 
objective, 467 
subjective, 467 
stenosis, 469 

definition of, 469 
diagnosis of, 472 

from adhesive pericarditis, 473 
from "Flint's murmur, 473 
from tricuspid stenosis, 473 
etiology of, 469 
pathology of, 469 
physical signs of, 470 
prognosis in, 473 
symptoms of, 470 
Mobius' sign in exophthalmic goitre, 685 
Monoplegia in croupous pneumonia, 142 

in uremia, 660 
Morbilli, 92. See Measles. 
Morbus maculosus neonatorum, 720 
Moro test in acute meningeal tuberculosis, 249 
Morphinism, 775 
chronic, 775 

symptoms of, 775 
treatment of, 775 
Morvan's disease, 845 
Motor neuritis, 861 
Mountain fever, 297 

Mouth breathing in chronic hypertrophic ton- 
sillitis, 521 
diseases of, 509 
dry, 514 

lesions in sprue, 589 
putrid sore, 510 
Movable kidney, 638 

spleen, 703 
Movements in chorea minor, 891 

in paralysis agitans, 889 
Mucomembranous enteritis, 586 
Mucous colitis, 586 
patches, 513 

in syphilis, 309 



Muguet, 511 
Multiple neuritis, 860 
endemic, 784 
myoclonus, 887 
sclerosis, 820 
serositis, 440 
Mumps, 99 

arthritis in, 101 
complications of, 100 
convulsions in, 101 
definition of, 99 
etiology of, 100 
fever in, 100 
incubation of, 100 
meningitis in, 101 
orchitis in, 100 
pancreatitis in, 101 
pathology of, 100 
sequelae of, 100 
symptoms of, 100 
treatment of, 101 
Mural endocarditis, 454 
Muscle changes in croupous pneumonia, 133 
Muscles, diseases of, 884 
Muscular atrophy, peroneal type of, 886 
definition of, 886 
etiology of, 886 
morbid anatomy of, 886 
pathology of, 886 
prognosis in, 886 
symptoms of, 886 
treatment of, 886 
in apoplexy, 792 
progressive, 833, 886 

Char cot-Marie-Tooth form of, 886 
neural, of Hoffman, 886 
contractions in paramyoclonus multiplex, 

887 
dystrophies, 884 

definition of, 884 
Erb's juvenile, 885 
etiology of, 884 

Landouzy-Dejerine type of, 885 
morbid anatomy of, 884 
pathology of, 884 
treatment of, 886 
rheumatism, 754 
rigidity in paralysis agitans, 889 

in tetanus, 228 
spasm, idiopathic, 691 
tremors in typhoid fever, 26 
Mycetoma, 234 

treatment of, 235 
Mycotic aneurysm, 500 

gastritis, 528 
Myelitis, 840 
acute, 840 

etiology of, 840 
morbid anatomy of, 840 
paraplegia in, 841 
pathology of, 840 
prognosis in, 842 
symptoms of, 841 
treatment of, 842 
ascending, 840 
central, 840 
chronic, 842 

definition of, 842 
diagnosis of, 843 
etiology of, 842 
morbid anatomy of, 843 
pathology of, 843 
prognosis in, 843 
symptoms of, 843 



950 



INDEX 



Myelitis, chronic, treatment of, 843 

definition of, 840 

descending, 840 

disseminated, 840 

subacute, 840 

transverse, 840 
Myelogenous leukemia, 714 
Myelomalacia, 844 
Myelopathic albumosuria, 680 
Myiasis, 358 

intestinal, 358 
Myocarditis, 450 

acute, 450 

chronic, 450 

definition of, 450 

interstitial, acute, 450 
chronic, 450 

Nauheim baths in, 452 

physical signs of, 451 

prognosis in, 451 

in rheumatic fever, acute, 178 

in smallpox, 70 

symptoms of, 451 

treatment of, 451 

in typhoid fever, 32 

in typhus fever, 57 
Myocardium, degeneration of, 448 
amyloid, 449 
calcareous, 449 
fatty, 448 
hyaline, 449 
parenchymatous, 448 
prognosis of, 449 
symptoms of, 449 

disease of, 448 

tuberculosis of, 285 
Myoclonus, 887. See Paramyoclonus multiplex. 

epilepticus, 887 

multiple, 887 
Myomalacia cordis in syphilis, 306 
Myositis, acute, in diphtheria, 155 

in typhoid fever, 40 
Myotonia congenita, 886 
definition of, 886 
symptoms of, 887 
Myriachit, 911 
Mytilotoxismus, 781 

treatment of, 782 
Myxedema, 688 

congenital, 688 

definition of, 688 

etiology of, 688 

frequency of, 688 

morbid anatomy of, 688 

pathology of, 688 

prognosis in, 688 

treatment of, 688 

thyroid gland in, 689 



N 



Nasal catarrh, atrophic, 361 
chronic, 361 

diphtheria, 157 
Nauheim baths in myocarditis, 452 
Neapolitan fever, 215 
Negri bodies in hydrophobia, 223 
Nematodes, 336 
Neoplastic goitre, 681 
Nephritic changes in yellow fever, 190 
Nephritis, acute, 641 

in glandular fever, 296 

caseative, 663 



Nephritis in cholera, 185 

desquamative, chronic, 645 
diffuse, acute, 641 

definition of, 641 
diagnosis of, 643 
etiology of, 641 
morbid anatomy of, 641 
edema in, 642 
pathology of, 641 
prognosis of, 643 
symptoms of, 642 
treatment of, 643 
urine in, 642 
chronic, 645 
in diphtheria, 156 
exudative, 642 
glomerular, 641 
hemorrhagic, 642 
interstitial, chronic, 644, 650 

hemorrhagic glaucoma in, 653 
Hirschberg's vessels in, 653 
pathology of, 650 
prognosis in, 655 
retinal detachment in, 653 

lesions in, 653 
symptoms of, 652 
cerebral, 653 
circulatory, 652 
respiratory, 653 
treatment of, 655 
climatic, 657 
dietetic, 656 
medicinal, 656 
urine in, 652 
parenchymatous, chronic, 643, 644, 645 
coma, 646 
definition of, 643 
diagnosis of, 647 
dropsy in, 646 
etiology of, 644 
frequency of, 644 
morbid anatomy of, 645 
pathology of, 645 
prognosis in, 647 
retinitis in, 646 
symptoms of, 646 
treatment of, 648 
dietetic, 648 
urine in, 646 
in scarlet fever, 84, 87 
syphilitic, 306 
tubular, chronic, 645 
in typhoid fever, 28, 38 
in varicella, 78 
Nephrolithiasis, 669 
colic in, 671 
definition of, 669 
diagnosis of, 671 

from acute appendicitis, 671 
from gallstone colic, 671 
from hydronephrosis, 671 
from neuralgia, 671 
from twist of ureter, 671 
etiology of, 669 
frequency of, 670 
pathology of, 669 
prognosis in, 670 
symptoms of, 671 
treatment of, 671 
urine in, 671 
Nerve, abducens, paralysis of, 873 
auditory, diseases of, 878 
facial, diseases of, 875 
glossopharyngeal, paralysis of, 880 



INDEX 



951 



Nerve, hypoglossal, diseases of, 883 
oculomotor, diseases of, 870 
olfactory, diseases of, 865 
optic, diseases of, 865 

paralysis of, 867 
pathetic, paralysis of, 871 
trifacial, paralysis of, 871 
vagus, diseases of, 880 
Nerves, cranial, diseases of, 865 
diseases of, 857 
inflammation of, 857 
Nervous complications of acute rheumatic fever, 
178 

of malarial fever, 326 

of scarlet fever, 88 

of typhoid fever, 39 
diseases, functional, 886 
disorders of gastric secretion, 558 
eructation, 558 
exhaustion, 899 
manifestations in diphtheria, 156, 157 

in influenza, 108 
system in diabetes mellitus, changes in, 727 

diseases of, 785 

syphilis of, 308, 310 
Neuralgia, gastric, 558 
Neurasthenia, 899 
definition of, 899 
diagnosis of, 900 
etiology of, 899 
prognosis of, 900 
symptoms of, 899 
treatment of, 900 
Neuritis, 857 

cervicobrachial, 859 

prognosis in, 860 

treatment of, 860 
in croupous pneumonia, 143 
definition of, 857 
diagnosis of, 858 
in diphtheria, 156 
endemic multiple, 780 
etiology of, 857 
interstitial, 857 
morbid anatomy of, 857 
motor, 861 
multiple, 860 

definition of, 860 

diagnosis of, 863 

etiology of, 860 

prognosis in, 863 

symptoms of, 861 

treatment of, 864 
obstetrical, 860 
optic, 865 

in brain tumor, 802 

in chronic lead poisoning, 779 

symptoms of, 865 

treatment of, 866 
parenchymatous, 857 
pathology of, 857 
periaxial, of Gombault in lead poisoning, 

779 
peripheral, 860 

in chronic arsenical poisoning, 862 
lead poisoning, 779, 862 
prognosis in, 858 
retrobulbar, 866 
sciatic, 860 
symptoms of, 857 
toxic, in influenza, 109 
treatment of, 858 
in typhoid fever, 40 
Neuroma of brain, 801 



Neuroretinitis, albuminuric, 653 

in syphilis, 310 
Neuroses, gastric, 556 
of heart, 487, 490 
occupation, 914 
traumatic, 912 

definition of, 912 
etiology of, 913 
paralyses in, 913 
symptoms of, 913 
treatment of, 914 
Neurotic atrophy, 886 
Newborn, hemorrhagic affections of, 720 

jaundice in, 630, 720 
Nitric acid test for albumin in urine, 676 
Nodding spasm, 883 
Nodular colitis, 587 
Nodules, leprous, 293 
Noma, 511 

in measles, 96 
Nose, diseases of, 359 
Nummular sputum in tuberculosis, 261 
Nutrition, diseases of, 723 
Nystagmus in disseminated sclerosis, 821 



Obesity, 762 

definition of, 762 
etiology of, 762 
symptoms of, 762 
treatment of, 762 
dietetic, 763 
Obliterative appendicitis, 573 
Obstetrical neuritis, 860 
Obstruction, intestinal, 579 
Occupation neuroses, 914 
Ochronosis, 766 

Ocular complications of diabetes mellitus, 730 
muscles, disturbances of motility of, 873 
symptoms in apoplexy, 790 

in disseminated sclerosis, 821 
in locomotor ataxia, 827 
Oculomotor nerve, diseases of, 870 
paralysis of, 870 

diagnosis of, 871 
prognosis in, 871 
symptoms of, 870 
Ogo, 302 

Oidium albicans in thrush, 511 
Olfactory nerve, diseases of, 865 
Ophthalmoplegia, 874 
etiology of, 874 
externa, 874 
interna, 874 
pathology of, 874 
symptoms of, 875 
treatment of, 875 
Opisthotonos in tetanus, 229 
Oppler-Boas bacillus in gastric cancer, 551 
Optic atrophy, 866 

in diabetes mellitus, 730 
diagnosis of, 867 
etiology of, 866 
in locomotor ataxia, 827 
pathology of, 866 
prognosis in, 867 
symptoms of, 866 
treatment of, 867 
nerve, inflammation of, 865 
neuritis in brain tumor, 802 

in chronic lead poisoning, 779 
Orchitis in malarial fever, 326 



952 



INDEX 



Orchitis in mumps, 100 
in typhoid fever, 38 
Oriental sore, 335, 336 
Oroya fever, 300, 301 
Orthostatic albuminuria, 676 
Osteitis deformans, 765 
Osteo-arthritis, 749 

Osteo-arthropathy, pulmonary, in bronchiectasis, 
378 

hypertrophic, 765 

in pulmonary tuberculosis, 262 
Osteoma in lung, 412 
Osteomyelitis in typhoid fever, 40 
Otitis media, acute, in typhoid fever, 40 

in croupous pneumonia, 144 

in scarlet fever, 84, 87 
Ovaries, tuberculosis of, 285 
Ox-heart in aortic regurgitation, 478 
Oxaluria, 679 
Oxyuris vermicularis, 337 
Oysters, infection by, in tvphoid fever, 18 
Ozena, 361, 362 



Pachymeningitis, 813 

cervical, hypertrophic, 851 
diganosis of, 814 
externa, 813 
interna, 813, 814 

morbid anatomy of, 814 

pathology of, 814 

symptoms of, 814 
morbid anatomy of, 813 
pathology of, 813 
prognosis in, 814 
symptoms of, 813 
treatment of, 814 
Paget's disease, 765 
Painters' colic, 780 
Palpitation of heart, 487 
Palsy, acute infantile, 111 
birth, 860 
hammerers', 914 
scriveners', 914 

shaking, 888. See Paralysis agitans. 
Pancreas, adenoma, 637 
carcinoma of, 637 
cystadenoma, 636 
cystic epithelioma of, 636 
cysts of, 636 

hemorrhagic, 636 

hydatid, 636 

proliferation, 636 

pseudo-, 636 

retention, 636 
diseases of, 630 
gumma of, 637 
hemorrhages into, 637 
sarcoma of, 637 
tumors of, 637 
Pancreatic calculus, 636 

symptoms of, 636 

treatment of, 636 
cysts, 636 

diagnosis of, 637 

prognosis in, 637 

symptoms of, 637 

treatment of, 637 
tumors, 637 
Pancreatitis, 630 
acute, 630 

constipation in, 632 

diagnosis of, 632 



Pancreatitis, acute, diagnosis of, from fulmina- 
ting appendicitis, 633 
from intestinal obstruction, 632 
from perforation of duodenum, 632 

of gastric ulcer, 632 
from rupture of gallbladder, 633 
from suppurative cholecystitis, 633 
etiology of, 630 
fat-necrosis in, 631 
history of, 630 
jaundice in, 632 
morbid anatomy of, 631 
pathology of, 631 
prognosis in, 633 
symptoms of, 632 
treatment of, 633 
chronic, 630, 634 

diagnosis of, 634 

from cancer of head of pancreas, 

634, 635 
from gallstones in common duct, 

634, 635 
from subphrenic abscess, 634 
interacinar, 634 
interlobular, 634 
interstitial, 634 
intralobular, 634 
prognosis in, 635 
symptoms of, 634 
treatment of, 635 
definition of, 630 
gangrenous, 632 
hemorrhagic, acute, 637 
in mumps, 101 
subacute, 632 

symptoms of, 632 
treatment of, 634 
suppurative, 632 
Papillary endocarditis, 455 
Papillitis, 865 

albuminuric, 653 
Papilloma of kidney, 668 
Paracentesis abdominis in ascites, 602 

thoracic in pleurisy with effusion, 421, 422 
Paracholecystitis, 620 
Paragonimus westermanni in distomatosis of 

lung, 355 
Paralysis of abducens nerve, 873 
agitans, 888 

definition of, 888 
diagnosis of, 889 

from multiple sclerosis, 889 
from senile tremor, 890 
etiology of, 888 
movements in, 889 
muscular rigidity in, 889 
pathology of, 889 
prognosis in, 890 
symptoms of, 889 
treatment of, 890 
tremor in, 889 
ascending, acute, 854 

definition of, 854 
diagnosis of, 855 
etiology of, 854 
morbid anatomy of, 854 
pathology of, 854 
prognosis in, 855 
symptoms of, 854 
treatment of, 855 
atrophic, acute, 111 
of bowel, 591 
in brain tumor, 803 
bulbar, 835 



INDEX 



953 



Paralysis, bulbar, apoplectiform, 785 
diagnosis of, 836 
etiology of, 835 
morbid anatomy of, 835 
pathology of, 835 
prognosis in, 836 
symptoms of, 835 
treatment of, 836 
cerebral, infantile, 795 

convulsions in, 796 
definition of, 795 
deformities in, 796, 797, 798 
diagnosis of, 798 

from amaurotic family idiocy, 

798 
from hereditary spastic spinal 
paralysis, 798 
etiology of, 796 
lesions in, 796 
morbid anatomy of, 796 
paralysis in, 797 
pathology of, 796 
prognosis in, 798 
symptoms of, 796 
in diphtheria, 156, 158, 159 
of facial nerve, 875 
gastro-intestinal, 535 
general, of insane, 816 
glosso-labio-laryngeal, 835 
glossopharyngeal nerve, 880 
of internal and external muscles of eyeball, 

874 
Landry's, 854 

monoplegic, in croupous pneumonia, 142 
of oculomotor nerve, 870 
of pathetic nerve, 871 
periodical, 923 

of spinal accessory nerve, 883 
atrophic, chronic, 833 
infantile, 111 
spastic, syphilitic, 838 
of trifacial nerve, 871 
in whooping-cough, 104 
Paralytic chorea, 892 

dilatation of stomach, 535 
Paramyoclonus multiplex, 887 
definition of, 887 
diagnosis of, 888 

from chorea, 888 

from electrical chorea, 888 

from hysterical spasm, 888 

from "maladie des tics convulsifs," 



etiology of, 887 
muscular contractions in, 887 
prognosis in, 888 
treatment of, 888 
Paraphasia, 800 

Paraplegia in acute myelitis, 841 
ataxic, hereditary, 830 
senile, 844 

symptoms of, 844 
treatment of, 844 
spastic, 836 
Parasites, animal, diseases due to, 316 
Parasitic hemoptysis, 353, 355 
infusoria, 357 
stomatitis, 511 
strumitis, 681 
Parasyphilitic affections, 308 
Parathyroid gland, diseases of, 691 
Paratyphoid fever, 53 
bacillus, 21 
bacteriology of, 53 



Paratyphoid fever, complications of, 54 
diagnosis of, 54 
intestinal ulcers in, 53 
pathology of, 53 
prevention of, 53 
prognosis of, 54 
splenic enlargement in, 53 
symptoms of, 54 
treatment of, 54 
Parenchymatous degeneration of heart, 448 
goitre, 681 

nephritis, acute, 643, 644 
neuritis, 857 
Paresis, 816 

Parkinson's disease, 888. See Paralysis agitans. 
Parotid abscess, 514 

bubo, 514 
Parotitis, epidemic, 99. See Mumps. 
in cholera, 185 
chronic indurative, 514 
in croupous pneumonia, 144 
in scarlet fever, 88 
suppurative interstitial, 514 
in typhoid fever, 33 
Parry's disease, 683 
Pathetic nerve, paralysis of, 871 
symptoms of, 871 
Pectoriloquy, 264 
"Peg" teeth in syphilis, 312 
Peliomata in typhoid fever, 30 
Peliosis rheumatica, 719 
Pellagra, 782 

blood in, 784 
diarrhea in, 783, 784 
eruption in, 783 
etiology of, 783 
history of, 782 
prognosis of, 784 
symptoms of, 783 
nervous, 783 
synonyms of, 782 
treatment of, 784 
Pemphigus neonatorum in syphilis, 312 
Peptic ulcer, 536 

Perforation of bowel in typhoid fever, 34, 35 
in duodenal ulcer, 563 

symptoms of, 563 
in empyema, 426 
of gallbladder, 624 
in gastric ulcer, 539 
Perforative appendicitis, 573 
Pericardial effusion in croupous pneumonia, 137 
diagnosis of, 438 

from aortic aneurysm, 439 
from cardiac dilatation, 439 

hypertrophy, 439 
from pleural effusion, 439 
physical signs of, 438 
tuberculosis, 250 
" Pericarditic pseudocirrhosis of liver," 440 
Pericarditis, acute, 435 

definition of, 435 
diagnosis of, 438 

from phthisis, 438 
etiology of, 435 
forms of, 436 
frequency of, 435 
pathology of, 436 
physical signs of, 437 
prognosis in, 439 
saddle-leather sound in, 438 
symptoms of, 437 
treatment of, 439 
chronic, 440 



954 



INDEX 



Pericarditis, chronic adhesive, 440 
definition of, 440 
diagnosis of, 442 
pathology of, 440 
physical signs of, 442 
prognosis in, 442 
pulsus paradoxus in, 442 
symptoms of, 441 
treatment of, 442 
in croupous pneumonia, 133, 141 
in erysipelas, 170 
externa et interna, 440 
in rheumatic fever, acute, 177, 178 
serofibrinous, acute, 436 

symptoms of, 438 
in smallpox, 70 
in typhoid fever, 32 
Pericardium, diseases of, 435 

tuberculosis of, 251 
Pericholecystitis, 620 
Pericolitis, membranous, 592 
Perihepatitis, 612 
Perinephritic abscess, 672 
Perineuritis, 857 

Period of steep curves in typhoid fever, 28 
Periodic rhinitis, 362 
Periodical paralysis, 923 
Peripheral neuritis, 860 
Peristaltic unrest, 557 
Peritoneal abscess, 594 

tuberculosis, 251 
Peritoneum, cancer of, 599 
cystic adenoma of, 599 
diseases of, 592 
hydatid cyst of, 599 
morbid growth of, 599 
sarcoma of, 599 
tuberculosis of, 251 
Peritonitis, acute, 592 

complications of, 595 
definition of, 592 
diagnosis of, 596 

from acute hemorrhagic pancreati- 
tis, 596 
from gallstone colic, 596 
from hysteria, 596 
from intestinal obstruction, 596 
from perforation of stomach, 596 
from typhoid fever, 596 
etiology of, 592 
Hippocratic facies in, 595 
micro-organisms in, 593 
morbid anatomy of, 594 
pathology of, 594 
prognosis in, 596 
sequelae of, 595 
symptoms of, 594 
treatment of, 596 

counter-irritation in, 597 
tympany in, 595 
adhesive, sclerotic, chronic, 598 
in amebic dysentery, 207 
chronic, 598 
chronic forms of, 598 
circumscribed, -594 
hemorrhagic, 594 
localized, 594 
loculated, 594 
putrid, 594 
in scarlet fever, 88 
septic, 594 
tuberculous, 251 
in typhoid fever, 35 

diagnosis of, 35 



Pernicious anemia, 710 

malarial fever, 316, 325 
Pertussis, 101. See Whooping-cough. 
Pestis minor, 199 
Petechise in relapsing fever, 330 
in smallpox, 67 
in typhoid fever, 30 
in typhus fever, 56, 57 
Petechial fever, 120 
Petit mal, 909 

Peyer's patches in typhoid fever, 23 
Pharyngitis, acute, 515 

definition of, 515 
etiology of, 515 
pathology of, 515 
prognosis in, 516 
symptoms of, 515 
treatment of, 516 
local, 516 
chronic, 517 

etiology of, 517 
pathology of, 517 
symptoms of, 517 
treatment of, 517 
croupous, 517 

etiology of, 517 
treatment of, 517 
follicular, 517 

etiology of, 517 
treatment of, 518 
phlegmonous, 516 
in typhoid fever, 33 
ulcerative, 516 

etiology of, 516 
symptoms of, 516 
treatment of, 516 
Pharynx, diseases of, 515 
tuberculosis of, 278 
Phlebitis in typhoid fever, 32 
Phlebosclerosis, 598 
Phlebotomous fever, 218 
Phlegmonous gastritis, 526 

pharyngitis, 516 
"Phosphatic diabetes," 679 
Phosphaturia, 679 
Phthisis, syphilitic, 308 

ventriculi, 529 
Pianists' cramp, 914 
Pigeon-breast, 382 

in chronic hypertrophic tonsillitis, 521 
Pin-worm, 337 

Pistol-shot sound in aortic regurgitation, 480 
Pituitary body, diseases of, 699 
Plagiomonas urinaria, 357 
Plague, 194 

bacillus of, 195 
bubonic, 194, 197 
buboes in, 198 
fever in, 197, 198 
glandular enlargements in, 198 
symptoms of, 198 
vomiting in, 198 
definition of, 194 
diagnosis of, 199 
distribution of, 194 
etiology of, 195 
frequency of, 196 
history of, 194 
larval, symptoms of, 199 
mode of transmission of, 195 
pathological anatomy of, 197 
pneumonic, albuminuria in, 198 
blood changes in, 198 
hemorrhage in, 198 



INDEX 



955 



Plague, pneumonic, relapses in, 199 
sputum in, 198 
symptoms of, 198 
prognosis in, 199 
prophylaxis of, 196 
protective inoculation in, 197 
septicemic, symptoms of, 198 
symptoms of, 197 
treatment of, 199 
Plasmodium falciparum, 319 
malarise, 316, 318 
of malarial fever, 316 
vivax, 318 
Pleura, diseases of, 413 
Pleural effusion, 417 
bloody, 429 
purulent, 423 
Pleurisy, 413 
chronic, 427 

definition of, 427 
primitive dry, 428 
in croupous pneumonia, 133, 139 
definition of, 413 
dry, 413, 414 

cough in, 416 
diagnosis of, 416 

from intercostal neuralgia, 416 
from muscular rheumatism, 416 
soreness, 416 
fever in, 415, 416 
friction sound in, 415 

pleuropericardial, 415 
pain in, 415 
physical signs of, 415 
prognosis in, 416 
symptoms of, 415 
treatment of, 416 
etiology of, 413 
fibrinous, 413 
forms of, 413 
frequency of, 414 
influenza, 108 
purulent, 413 

in erysipelas, 170 
serofibrinous, 413 
in smallpox, 70 
tuberculous, 250, 413 
in typhoid fever, 39 
with effusion, 417 

cytoscopy in, 421 
diagnosis of, 420 

from hydatid cyst of liver, 420 
from hypostatic congestion, 

420 
from new growths in lung, 420 
from pleurisy with thickening, 

420 
from pneumonia, 420 
from pneumothorax, 421 
from pulmonary edema, 420 
from subphrenic abscess, 421 
from tubercular consolida- 
tion, 420 
duration of, 420 
dyspnea in, 418 

paracentesis thoracis in, 421, 422 
physical signs of, 418 
posture in, 418 
prognosis in, 421 
symptoms of, 418 
treatment of, 421 
blisters in, 423 
diaphoretics in, 422 
diuretics in, 422 



Pleurisy with effusion, treatment of, purges in, 
422 
tapping in, 422 
Pleuritis, 413. See Pleurisy. 
Plumbism, 774. See Lead poisoning. 
Pneumogastric nerve, disease of, 880 
symptoms of, 881 
treatment of, 881 
Pneumonia, aspiration, 387 
catarrhal, 386 
croupous, 128 

abscess in, 132, 140 

aphasia, transitory, in, 142 

arthritis in, 143 

blood in diagnosis of, 145 

brain softening in, 143 

bronchiectasis in, 141 

bronchitis in, 133 

cardiac changes in, 133 

in cerebrospinal fever, 125 

chill in, 134 

complications of, 139 

congestion of lung in, 131 

convulsions in, 138 

cough in, 135 

crisis in, 139 

protracted, 139 

cyanosis in, 136 

definition of, 128 

delirium in, 134, 136, 138 

diagnosis of, 144 

from acute pulmonary tubercu- 
losis, 145 
from appendicitis, 145 
from catarrhal pneumonia, 145 
from hypostatic congestion of 

lung, 145 
leukocytosis in, 145 
from pleurisy with effusion, 145 
from pulmonary infarction, 145 

distribution of, 130 

dyspnea in, 136 

embolism in, 143 

empyema in, 139 

endocarditis in, 133, 141 

engorgement of lung in, 131 

etiology of, 129 

fever in, 134 

frequency of, 140 

gangrene in, 132, 140, 144 

gray hepatization in, 132 

headache in, 134 

hemiplegia in, 142 

hemiplegie pneumonique, 142 

hemoglobinuria in, 138 

hepatic changes in, 133 

hepatization in, gray, 132 
red, 131 

herpes in, 136 

hydropneumothorax in, 140 

incubation of, 134 

insomnia in, 138 

jaundice in, 138 

meningitis in, 133, 142 

micrococcus lanceolatus in, 128, 
131 

monoplegia in, 142 

morbid anatomy of, 131 

muscle changes in, 133 

nephritic changes in, 133 

nervous symptoms of, 138 

neuritis in, 143 

otitis media in, 144 

pain in, 134 



956 



INDEX 



Pneumonia, croupous, paralysis in, monoplegic, 
142 

parotitis in, 144 

pathology of, 131 

pericardial effusion in, 137 

pericarditis in, 133, 141 

physical signs of, in first stage, 135 

in well-developed stage, 136 

pleurisy in, 133, 139 

pneumococcus of Fraenkel, 128 

prevention of, 131 

prognosis in, 145 

ratio of blood-pressure to pulse 
rate in, 147 

pseudocrisis in, 139 

pulse in, 134, 135, 136 

rales redux in, 139 

red hepatization in, 131 

relapse in, 144 

renal changes in, 133 

respirations in, 134, 135 

skin in, 138 

sputum in, 135 

sweating in, 138 

symptoms of, 134 

in developed stage, 135 
in stage of onset, 134 
of resolution, 139 

temperature in, 134 

tongue in, 138 

treatment of, 147 

tympanites in, 138 

unusual changes in lung in, 132 

urine in, 137, 145 

varieties of, 144 

venous thrombosis in, 143 
fibrinous, 128 
hypostatic, 410 
in influenza, 108 
lobar, 128 
lobular, 386 
metastatic, 396 

abscess in, 397 

definition of, 396 

embolism in, 397 

etiology of, 396 

pathology of, 396 

prognosis in, 398 

sputum in, 397 

symptoms of, 397 

treatment of, 398 
pyemic, 397 
in typhoid fever, 28, 38 
Pneumonic plague, symptoms of, 198 
Pneumonitis, 128 
Pneumonoconiosis, 398 
definition of, 398 
etiology of, 398 
pathology of, 399 
prognosis in, 399 
symptoms of, 399 
treatment of, 399 
Pneumopericardium, 443 

baccillus aerogenes capsulatus in, 443 
prognosis of, 444 
symptoms of, 443 
treatment of, 444 
Pneumothorax, 429 
definition of, 429 
diagnosis of, 430 

from diaphragmatic hernia, 430 

from emphysema, 430 

from pyopneumothorax subphrenicus, 
430 



Pneumothorax, dyspnea in, 430 
etiology of, 429 
history of, 429 
physical signs of, 430 
prognosis in, 430 
in pulmonary tuberculosis, 262 
symptoms of, 429 
syncope in, 430 
treatment of, 430 
in whooping-cough, 104 
Podagra, 740 
Poisoning, alcoholic, 767 
acute, 767 
chronic, 768 
arsenical, 777 
by cheese, 782 
by ergot, .781 
by fermented maize, 783 
by fish, 782 
food, 781 

by impure milk, 782 
lead, acute, 778 

chronic, 778 
by meat, 782 
morphine, chronic, 775 
by mussels, 781 
Poker back, 752 

Polioencephalitis superior of Wernicke, 812 
Poliomyelitis, 840 

anterior, acute, 111 

convulsions in, 115 
definition of, 111 
diagnosis of, 115, 116 
in diphtheria, 156 
etiology of, 111 
morbid anatomy of, 113 
paralysis in, 114 
pathology of, 113 
prognosis in, 116 
symptoms of, 114 
treatment of, 116 
chronic, 833 

Aran-Duchenne type of, 834 
claw-hand in, 834 
definition of, 833 
diagnosis of, 834 

from amyotrophic lateral scle- 
rosis, 834 
from muscular dystrophy, 834 
from neuritis, 835 
from syringomyelia, 835 
drop-foot in, 834 
etiology of, 833 
morbid anatomy of, 833 
pathology of, 833 
prognosis in, 835 
symptoms of, 834 
treatment of, 835 
Poliomyeloencephalitis, acute, 111 
definition of, 111 
diagnosis of, 115, 116 
etiology of, 111 
morbid anatomy of, 113 
pathology of, 113 
prevention of, 113 
prognosis of, 116 
symptoms of, 114 
treatment of, 116 
Polycythemia, splenomegalic, chronic, 713 
definition of, 713 
etiology of, 713 
morbid anatomy of, 713 
pathology of, 713 
symptoms of, 714 



INDEX 



957 



Polycythemia, splenomegalic, chronic, treat- 
ment of, 714 
Polyneuritis, 860 
Polyuria in typhoid fever, 38 
Porencephaly, 796 
Pork- worm, 350 
Portal vein, thrombosis of, 613 
Porto Rican anemia, 338 
Porto Rico itch, 69 

scratches, 69 
Posture in pleurisy with effusion, 418 
Potassium ferrocyanide test for albumin in 

urine, 676 
Potters' rot, 398 
Pox, 302 • 
Pregnancy, smallpox complicating, 71 

typhoid fever complicating, 41 
Prevention of smallpox, 62 

of tetanus, 228 
Primitive dry pleurisy, 428 
Proctitis, epidemic gangrenous, 213 
Progressive muscular atrophy, 833 
Proliferation cysts of pancreas, 636 
Prophylaxis of acute poliomyeloencephalitis, 113 
against diphtheria, 161 
influenza, 111 
plague, 196 
scarlet fever, 83 
smallpox, 72 
tetanus, 228 
yellow fever, 189 
Pseudoangina in hysteria, 897 
Pseudocrisis in croupous pneumonia, 139 
Pseudocysts of pancreas, 636 
Pseudohydrophobia, 225 
Pseudoleukemia, 286 
Pseudolyssaphobia, 225 
Pseudomembranous colitis, 588 

pyelonephritis, 664 
Pseudomuscular hypertrophy, 884 

prognosis in, 885 
Pseudotabes arsenical, 777 
Psilosis, 588 
Psoriasis, buccal, 513 
Psorospermiasis, 331 
Psychoneurosis maidica, 782 
Ptyalism, 513 
Puerperal eclampsia, 910 
"Puking fever," 295 
Pulex penetrans, 357 
Pulmonary abscess, 407 
diagnosis of, 409 
etiology of, 407 
multiple, 408 
prognosis in, 409 
in septicemia, 172 
symptoms of, 409 
treatment of, 409 
in typhoid fever, 39 
complications of rheumatic fever, acute, 

178 
congestion, 409 

in influenza, 108 
emphysema, 400 
gangrene, 405 

in bronchiectasis, 378 
edema in cholera, 185 
osteo-arthropathy in bronchiectasis, 378 
hypertrophic, 765 
in pulmonary tuberculosis, 262 
regurgitation, 483 
stenosis, 483 
tuberculosis, 255 
valves of heart, diseases of, 482 



Pulsus paradoxus in chronic adhesive pericardi- 
tis, 442 
Purpura, 719 

causes of, 719 
fulminating, 720 
hematemesis in, 559 
hemorrhagica, 720 
Henoch's, 720 
micro-organisms in, 719 
in rheumatic fever, acute, 178 
rheumatica, 719 
treatment of, 720 
Purulent pericarditis, 436 
pleural effusion, 423 
pleurisy, 413 
Pus in urine, 678 
Putrid fever, 55 
peritonitis, 594 
sore mouth, 510 
Pyelitis, 662 
Pyelonephritis, 662 
catarrhal, 664 
definition of, 662 
diagnosis of, 664 

from aneurysm, 665 
from malarial fever, 664 
from perinephritis abscess, 664 
from suppurative cystitis, 664 
from typhoid fever, 664 
etiology of, 663 
gangrenous, 664 
micro-organisms in, 663 
morbid anatomy of, 664 
pathology of, 664 
prognosis in, 665 
pseudomembranous, 664 
suppurative, 663, 664 
symptoms of, 664 
treatment of, 665 
Pyemia, 171. See Septicemia. 

gonorrheal, 165 
Pyemic abscess of liver, 602 

pneumonia, 397 
Pylephlebitis, suppurative, 613 
Pylorospasm, 557 

Pylorus, stenosis of, congenital, 553, 554 
hypertrophic, 552 

definition of, 552 
diagnosis of, 553 

from cicatricial contraction, 

553 
from gastric cancer, 553 
etiology of, 552 
morbid anatomy of, 552 
prognosis of, 554 
symptoms of, 553 
treatment of, 554 
Pym's fever, 218 
Pyonephritis, 663 
Pyonephrosis, 663 

in tuberculosis of kidney, 284 
Pyopericardium, 438 
Pyopneumothorax, 429 
Pyuria, 678 

treatment of, 678 
in typhoid fever, 38 



Quartan parasite of malarial fever, 318 
Quincke's pulse in aortic regurgitation, 

478 



958 



INDEX 



R 



Rabies, 222 

dumb, 224 
Rachitic rosary, 757 
Rachitis, 755 
Ragweed fever, 362 

Rales redux in croupous pneumonia, 139 
Rashes, initial, in smallpox, 67 
Ray fungus in actinomycosis, 233 
Raynaud's disease, 916 

definition of, 916 

etiology of, 916 

gangrene in, 916 

treatment of, 916 
Recrudescence in typhoid fever, 29 
Rectal crises in locomotor ataxia, 826 
Rectum, tuberculosis of, 279 
Red-light treatment of smallpox, 74 
Redundancy of colon, 592 
Reflexes in apoplexy, 790 
Regurgitation, aortic, 476 
mitral, 464 
pulmonary, 483 
tricuspid, 480 
Relapse in croupous pneumonia, 144 
Relapsing fever, 329 

chill in, 330 

crisis in, 331 

definition of, 329 

delirium in, 331 

distribution of, 329 

etiology of, 329 

fever in, 330 

history of, 329 

incubation in, 330 

jaundice in, 330 

morbid anatomy of, 330 

pathology of, 330 

petechias in, 330 

prognosis of, 331 

relapse in, 331 

spirillum in, 329 

spirocheta novyi in, 329 
recurrentis in, 329 

spleen in, 330 

symptoms of, 330 

treatment of, 331 

vomiting in, 330 
Remittent fever, bilious, 324 

complications of, 325 

diagnosis of, 327 

hemoglobinuria in, 325 

prognosis of, 327 

sequelae of, 325 

symptoms of, 324 

treatment of, 327 
Renal artery, aneurysm of, 508 
asthma, 382 
calculus, 669 

changes in croupous pneumonia, 133 
colic, 671 
disease, acute, in typhoid fever, 28 

in diphtheria, 159 
tuberculosis, 283 
Respiratory lesions in typhoid fever, 25 

system, diseases of, 359 
Retention cyst of pancreas, 636 
Retinal hemorrhages in malarial fever, 326 

lesions in chronic interstitial nephritis, 653 
Retinitis, albuminuric, in chronic parenchyma- 
tous nephritis, 646 

degenerative, 653 

hemorrhagic, 653 



Retinitis, albuminuric, in puerperal eclampsia 
910 
typical, 653 
diabetic, 730 
Retrobulbar neuritis, 866 
Retrocedent gout, 747 
Retrograde intussusception of bowel, 580 
Retroperitoneal glands, tuberculosis of, 247 
Rheumatic fever, acute, 174 
arthritis in, 176 
bacteriology of, 175 
chorea in, 178 
complications of, 177 
definition of, 174 
delirium in, 178 
diagnosis of, 179 

from arthritis, acute, 179 

septic, 179 
from gonorrheal rheumatism, 

179 
from mono-articular inflam- 
mation, 179 
from osteomyelitis, acute, 179 
distribution of, 174 
duration of, 177 
endocarditis in, 177, 178 
erythema in, 178 
etiology of, 175 
iritis in, 178 
joints in, 176 
meningitis in, 178 
micrococcus rheumaticus, 175 
morbid anatomy of, 176 
myocarditis in, 178 
nervous complications in, 178 
pericarditis in, 177, 178 
prognosis of, 179 
pulmonary complications in, 178 
purpura rheumatica in, 178 
rheumatic nodules in, 178 
sweating in, 176 
symptoms of, 176 
tongue in, 176 
treatment of, 179 
urine in, 177 
urticaria in, 178 
Rheumatism, acute articular, 174. See Rheu- 
matic fever, acute, 
chronic, 753 

definition of, 753 
etiology of, 753 
morbid anatomy of, 753 
symptoms of, 753 
treatment of, 753 
gonorrheal, 167 
• muscular, 754 

treatment of, 754 
Rheumatoid arthritis, 749 

in bronchiectasis, 378 
Rhinitis, atrophic, 361 
hypertrophic, 361 
periodic, 362 
syphilitic, 312 
Rhinopharyngitis mutilans, 302 
Rice-water stools in Asiatic cholera, 183 
Rickets, 755 

bossy frontals in, 757 
chicken-breast in, 757 
definition of, 755 
dentition in, 757 
diagnosis of, 758 
etiology of, 755 
Harrison's groove in, 757 
morbid anatomy of, 756 



INDEX 



959 



Rickets, prognosis in, 758 

symptoms of, 757 

treatment of, 758 
Risus sardonicus in epilepsy, 903 

in tetanus, 228 
Rock fever, 215 

Rocky mountain spotted fever, 297 
Romberg's symptom in locomotor ataxia, 826 
Rose cold, 362 

rash in rubella, 99 

spots in typhoid fever, 27 
Roseola, epidemic, 98 

in syphilis, 309 
Rotch's sign of pericardial effusion, 438 
Rotheln, 98. See Rubella. 
Round-worm, 336 
Rubella, 98 

definition of, 98 

diagnosis of, 99 

from measles, 99 
from scarlet fever, 99 

eruption in, 99 

etiology of, 99 

Forchheimer's spots in, 99 

glandular enlargements in, 99 

incubation of, 99 

prognosis in, 99 

"rose rash" of, 99 

symptoms of, 99 

treatment of, 99 
Rubeola notha, 98 

Rumpel-Leede test for scarlet fever, 89 
Running amok, 911 
Rupture of spleen, 326, 703 
Russian tapeworm, 350 



Saccharomyces albicans in thrush, 511 
Sacculated aneurysm, 500 
Saddle-leather sound in acute pericarditis, 438 
Salivary glands, diseases of, 513 

functional disorders of, 513 
inflammation of, 514 
swelling, bilateral, 514 
Salivation, 513 
Sand flea, 357 
Sanduhrmagen, 555 

Sansom's sign of pericardial effusion, 438 
Sarcoma of brain, 801 
of kidney, 668 
of liver, 615 
in lung, 412 
of mediastinum, 431 
of pancreas, 637 
of peritoneum, 599 
of thyroid gland, 683 . 
Saturnine epilepsy, 779 
Scarlatina, 79 
Scarlet fever, 79 

anaphylactic manifestations in, 84 
bacillus diphtherise in, 87 
bacteriology of, 82 
bronchopneumonia in, 88 
"collar of brawn" in, 84 
complications of, 87 
definition of, 79 
desquamation in, 85, 89, 92 
diagnosis of, 88 

from erythema scarlatiniform, 89 
from German measles, 88 
from nephritic eruption, 89 
from rash of sepsis, 89 



Scarlet fever, diagnosis of, from rose rash of 
indigestion, 88 
from syphilitic rash, 88 
dislocation of hip-joint in, 87 
distribution of, 79 
eruption in, 85 

peculiarities of, 85 
etiology of, 79 
fever in, 85 
fulminant form of, 86 
glandular enlargements in, 84, 88 
history of, 79 
hybrid, 98 

hyperleukocytosis in, 84 
"inclusion bodies" in, 89 
incubation period of, 84 
kidneys in, 84, 87 
malignant, 86 
morbid anatomy of, 83 
mortality of, 90 
nephritis in, 84, 87 
nervous complications in, 88 
otitis in, 84, 87 
parotitis in, 88 
pathology of, 83 
peritonitis in, 88 
prognosis of, 90 
prophylaxis of, 83 
Rumpel-Leede test for, 89 
septic arthritis in, 87 
infections in, 84 
sequelae of, 87 
sore throat in, 84, 85, 86 
"strawberry tongue" in, 89 
streptococcus conglomerans in, 82 
suppression of urine in, 86 
surgical, 86 
symptoms of, 84 
temperature in, 85 
treatment of, 90 

antiscarlatinal serum in, 92 
hygienic, 90 
valvular disease of heart in, 88 
vomiting in, 85 
Schick test of natural immunity against diph- 
theria, 161 
Schistosoma hematobium in bilharzia disease, 

353 
" Schluck-pneumonie, " 387 
Schonlein's disease, 719 
Sciatica, 860 

treatment of, 860 
Scleroderma, 765 

treatment of, 766 
Sclerosis, disseminated, 820 

Argyll-Robertson pupil in, 821 
definition of, 820 
diagnosis of, 822 

from general paralysis of insane, 

822 
from hysteria, 822 
from locomotor ataxia, 822 
from paralysis agitans, 822 
from spastic paraplegia, 822 
etiology of, 820 
morbid anatomy of, 820 
nystagmus in, 821 
pathology of, 820 
prognosis in, 822 
symptoms of, 821 
treatment of, 822 
insular, 820 
lateral, 836 

amyotrophic, 838 



960 



INDEX 



Sclerosis, lateral, amyotrophic, Babinski reflex 
in, 839 
definition of, 838 
diagnosis of, 839 

from bulbar paralysis, 839 
from syringomyelia, 839 
etiology of, 838 
pathology of, 838 
prognosis in, 840 
symptoms of, 839 
treatment of, 840 
ankle clonus in, 837 
Babinski reflex in, 837 
definition of, 836 
diagnosis of, 837 
etiology of, 836 
history of, 836 
morbid anatomy of, 836 
pathology of, 836 
prognosis in, 837 
Strumpell's family type of, 836 
symptoms of, 836 
treatment of, 837 
multiple, 820 
spinal, posterior, 823 
Sclerotic kidney, 650 

peritonitis, chronic adhesive, 598 
Scorbutus, 759 
Screw-worm, 357 

treatment of infection by, 358 
Scriveners' palsy, 914 
Scrofula, 245 
Scurvy, 759 

definition of, 759 
diagnosis of, 761 
etiology of, 759 
infantile, 760 
morbid anatomy of, 759 
pathology of, 759 
symptoms of, 760 
treatment of, 761 
Seat-worm, 337 
Secondary anemia, 707 
Secretion, gastric, nervous disorders of, 558 

treatment of, 558 
Segmentation of heart muscle, 449 
Senile emphysema, 400 

paraplegia, 844 
Sepsis in empyema, 426 
Septic arthritis in scarlet fever, 87 
in smallpox, 71 
diarrhea in pulmonary gangrene, 407 
peritonitis, 594 
pneumonia, 397 
Septicemia, 171 
anemia in, 172 
blood in, 172 
chill in, 172 
chronic, 173 
definition of, 171 
diagnosis of, 173 
empyema in, 172 
etiology of, 171 
infarction of spleen in, 172 
morbid anatomy of, 171 
pathology of, 171 
pulmonary abscess in, 172 
subacute, 173 

suppuration of kidney in, 172 
sweating in, 172 
symptoms of, 172 
treat ment of, 173 

antistreptococcic serum in, 173 
Septicemic plague, symptoms of, L98 



Septum, interventricular, perforated, 494 
Serofibrinous pericarditis, acute, 436, 438 

pleurisy, 413 
Serositis, multiple, 440 
Serous diarrhea, 565 

membranes, tuberculosis of, 247 
Serum antidiphtheritic, 162, 163 
antigonococcic, 167 
antimeningococcic, 127 
antirabic, 226 
antiscarlatinal, 92 
antistreptococcic, in erysipelas, 171 

in septicemia, 173 
antitetanic, 229 
antitubercle, 275 
treatment of dysentery, 210 
of exophthalmic goitre, 687 
. of pulmonary tuberculosis, 275 
of ulcerative endocarditis, 460 
Seven days' fever, 329 
Sewing spasm, 914 

Shaking palsy, 888. See Paralysis agitans. 
Shiga's bacillus in dysentery, 201 
Ship fever, 55 
Siderosis, 398 
Simla diarrhea, 214 
Sitotoxismus, 781 
Skin changes in typhoid fever, 30 
in verruga, 301 
eruptions, syphilitic, 308, 309 
gangrene of, in smallpox, 70 
in Hodgkin's disease, 289 
in leprosy, 293 

pigmentation of, in Addison's disease, 697 
Skodaic resonance in hydropneumothorax, 431 
Sleeping sickness, 331, 333 
diagnosis of, 334 
etiology of, 333 
pathology of, 334 
prognosis in, 334 
symptoms of, 334 
treatment of, 334 
"Slows" in cattle, 295 
Smallpox, 60 

aberrant manifestations of, 69 

abscesses in, 70 

aphonia in, 70 

backache in, 65 

bed-sores in, 70 

black, 68 

bronchitis in, 70 

bronchopneumonia in, 70 

complications of, 70 

confluent, 68 

cytoryctes vaccinae in, 61 

definition of, 60 

delirium in, 67 

diagnosis of, 71 

from chicken-pox, 71 
from measles, 71 
from scarlet fever, 71 
from syphilides, 71 
distribution of, 61 
earache in, 70 
endocarditis in, 70 
eruption in, 64, 65 

development of, 65 
forms of, 65 

on mucous membrane, 67 
stages of, 65 
variations in, 67 
erysipelas in, 70 
etiology of, 61 
fever in, 65, 67 K 



INDEX 



961 



Smallpox, forms of, 69 
frequency of, 64 
gangrene of skin in, 70 
hematemesis in, 559 
headache in, 65 
hemorrhagic, 68 
history of, 60 
incubation of, 61 
laryngitis in, 70 

mode of spreading contagion, 61 
morbid anatomy of, 64 
myocarditis in, 70 
pathology of, 64 
pericarditis in, 70 
pleurisy in, 70 
in pregnancy, 71 
prevention of, 62 
prognosis of, 72 
pulse in, 65 
rashes in, 67 
septic arthritis in, 71 
sequelae of, 70 
symptoms of, 65 
temperature in, 65, 67 
treatment of, 73 
red-light, 74 
urine in, 65 

vaccination as a preventive, 62, 74 
varioloid, 69 
Smokers' tongue, 513 
"Snuffles," 304 
Soor, 511 

Sore mouth, putrid, 510 
throat, 515 

auctioneer's, 517 
clergymen's, 517 
in diphtheria, 156 
epidemic, 518 

definition of, 518 
etiology of, 518 
symptoms of, 518 
treatment of, 518 
in scarlet fever, 84, 85, 86 
ulcerated, 516 
Spanish measles, 69 
Spasm of diaphragm in tetanus, 228 
facial, 878 

of glottis in tetanus, 229 
muscular, idiopathic, 691 
nodding, 883 
of esophagus, 524 
sewing, 914 
Spasmodic croup, 368 
laryngitis, 368 
wryneck, 882 
Spasmus nutans, 883 
Spastic diplegia, 795, 797 
hemiplegia, 795 
paraplegia, 836 
Speech in Friedreich's ataxia, 832 
Spinal accessory nerve, disease of, 882 
symptoms of, 882 
paralysis of, 883 
cord, compression of, 848 
by aneurysm, 850 
definition of, 848 
by disease of vertebras, 848 
diagnosis of, 849 
prognosis in, 849 
symptoms of, 849 
treatment of, 850 
etiology of, 848 

by hypertrophic cervical pachy- 
meningitis, 851 
61 



Spinal cord, compression of, by hypertrophic 

cervical pachy- 
meningitis, symp- 
toms of, 851 
treatment of, 851 
by malignant growths, 850 
hemorrhage into, 846 
definition of, 846 
diagnosis of, 847 
prognosis in, 847 
symptoms of, 846 
treatment of, 847 
inflammation of, 840 
syphilis of, 308, 310 
tuberculosis of, 286 
epilepsy, 887. See Paramyoclonus multi- 
plex, 
membranes, hemorrhage into, 847 
definition of, 847 
etiology of, 847 
extrameningeal, 847 
intrameningeal, 847 
prognosis in, 848 
symptoms of, 848 
treatment of, 848 
meningitis, 851 

chronic, 853 
paralysis, atrophic, chronic, 833 
infantile, 111 
spastic, syphilitic, 838 
sclerosis, posterior, 823 
syphilis, 308, 310 
Spine typhoid, 40 
Spirillum cholerse asiaticae, 181 

of relapsing fever, 329 
Splanchnoptosis, 582 
Spleen, abscess of, 703 
diseases of, 702 
in diphtheria, 156 

enlargement of, in paratyphoid fever, 53 
epithelioma of, primary, 705 
in hepatic cirrhosis, 608 
hydatid cyst of, 703 
infarct of, 702 

in septicemia, 172 
in malarial fever, 326 

changes in, 320, 321 
malignant growths of, 703 
in Malta fever, 216 
movable, 703 
in relapsing fever, 330 
rupture of, 326, 703 
in splenic anemia, 704 
in splenomedullary leukemia, 705, 716 
in typhoid fever, 24, 26, 28, 702 
in typhus fever, 57 
wandering, 703 

treatment of, 703 
Splenic anemia, 704 

artery, aneurysm of, 507 
Splenization of lung, 410 
Splenomedullary leukemia, 714, 715 
Splenomegalic polycythemia, chronic, 713 
Splenomegaly, hemolytic, 706 
large-celled, 705 
primary, 705 
tropical, 335 
Spondylitis deformans, 752 

rhizomelique, 752 
Spotted fever, 55, 120, 297 
Sprue, 588 

anemia in, 590 
definition of, 588 
diagnosis of, 590 



962 



INDEX 



Sprue, diarrhea in, 590 
etiology of, 589 
flatulence in, 590 
mouth lesions of, 589 
pathology of, 589 
predisposing causes of, 588 
prognosis in, 590 
symptoms of, 589 
tongue in, 589 
treatment of, 590 
Sputum in bronchial asthma, 382 
in bronchiectasis, 377 
in croupous pneumonia, 135 
in distomatosis of lung, 356 
in metastatic pneumonia, 397 
in pneumonic plague, 198 
in pulmonary gangrene, 406 

tuberculosis, 261 

microscopic examination of, 265 
Squint in chronic lead poisoning, 779 
St. Anthony's fire, 168 
St. Gothard's tunnel disease, 338 
St. Vitus' dance, 890. See Chorea minor. 
Status epilepticus, 904 

thymolymphaticus, 694 

definition of, 694 

etiology of, 694 

morbid anatomy of, 694 

pathology of, 694 

symptoms of, 695 

tetany of, 695 

treatment of, 695 
Stel wag's sign in exophthalmic goitre, 685 
Stenosis, aortic, 474 
mitral, 469 
pulmonary, 483 

congenital, 494 
of pylorus, congenital, 552, 553 

hypertrophic, 552 
of right conus arteriosus, 494 
tricuspid, 482 
Still's disease, 752 
Stokes-Adams syndrome, 450 
Stomach, bilocular, 555 
cancer of, 545 
dilatation of, 531. See Gastric dilatation. 

paralytic, 535 
diseases of, 525 
hemorrhage from, 559 
hour-glass, 555 

definition of, 555 

etiology of, 555 

morbid anatomy of, 556 

pathology of, 556 

symptoms of, 556 

treatment of, 556 
hyperesthesia of, 558 

symptoms of, 558 
lymphatic areas of, 546 
neuroses of, 556 
tuberculosis of, 278 
ulcer of, 536. See Gastric ulcer. 
Stomatitis, 509 
aphthous, 509 
catarrhal, 509. 

prognosis of, 509 

symptoms of, 509 
definition of, 509 
fetid, 510 
follicular, 509 
gangrenous, 51 1 

symptoms of, 512 

treatment of, 512 
in measles, 96 



Stomatitis, parasitic, 511 

endomyces albicans in, 511 
oidium albicans in, 511 
prognosis in, 511 
saccharomyces albicans in, 511 
symptoms of, 511 
treatment of, 511 
ulcerative, 510 

treatment of, 510 
vesicular, 509 
Stone in kidney, 669 
Stools in cholera, 183 
in dysentery, 206 
in typhoid fever, 33 
Strangulation, internal, of bowel, 579, 581 
" Strawberry tongue" in scarlet fever, 89 
Streptococcus conglomerans in scarlet fever, 82 

erysipelatus, 168 
Streptothrix actinomyces, 233 
madurse, 234 
mycetomse, 234 
Stricture of bowel, 579 

of esophagus, organic, 523 
Strongyloides intestinalis, 348 
classification of, 348 
definition of, 348 
diarrhea in, 348 
distribution of, 348 
emaciation in, 348 
treatment of, 348 
Struma, 681 

colloid, 681 
Strumitis, echinococcic, 681 
parasitic, 681 
syphilitic, 681 
traumatic, 681 
tuberculous, 681 
Strumpell's family type of lateral sclerosis, 836 
Sudamina in miliary fever, 300 

in typhoid fever, 30 
Suffocative catarrh, acute, 389, 391 
Sunstroke, 920 

definition of, 920 
diagnosis of, 921 
etiology of, 920 
morbid anatomy of, 921 
pathology of, 921 
prognosis in, 921 
symptoms of, 921 
treatment of, 921 

hydrotherapeutic, 921 
venesection in, 922 
Suppression of urine, 672 
Suppuration of kidney in septicemia, 172 
Suppurative hematitis, 714 

inflammation of bile-ducts, 619 
interstitial parotitis, 514 
pancreatitis, 632 
pyelonephritis, 663, 664 
pylephlebitis, 613 
Suprarenal glands, diseases of, 695 
Surgical emphysema, 400 
kidney, 665 
scarlet fever, 86 
Sweat, stage of, in malarial fever, 321 
Sweating sickness, 299 
Swelling of thyroid, 682 
Swine-pox, 69 

Sydenham's chorea, 890. See Chorea minor. 
Symmetrical stricture of esophagus, 523 
Syncope in pneumothorax, 430 
Syphilis, 302 

acquired, 302 
anemia in, 309 



INDEX 



963 



Syphilis, arteritis in, 306 
of bones, 312 

of brain and spinal cord, 308, 310 
chancre of, 302, 306, 308 
condylomata in, 309 
definition of, 302 
diagnosis of, 310 

luetin test in, 311 

Wassermann test in, 311 
distribution of, 302 
etiology of, 302 
frequency of, 305 
gummata in, 306, 309 
headache in, 310 
heart changes in, 306 
hereditary, 302, 304, 312 

epiphysitis in, 312 

eruptions in, 312 

Hutchinson teeth in, 312 

mucous patches in, 312 

rhinitis in, 312 

symptoms of, 312 
iritis, 309 
of larynx, 370 
lesions of, primary, 306 

secondary, 306 

tertiary, 306 
of liver, 307 
of lungs, 307 
lymph nodes, 308 
macular syphilide in, 309 
morbid anatomy of, 306 
mucous patches in, 309 
myomalacia cordis in, 306 
nephritis in, 306 
of nervous system, 308, 310 
neuroretinitis in, 310 
paralysis in, 310 
pathology of, 306 
prevention of, 304 
prognosis of, 311 
roseola in, 309 
skin eruptions in, 308, 309 
spirocheta pallida in, 302 
stages of, 302, 306 
symptoms of, 308 
transmission of, 303, 304 
treatment of, 312 

neosalvarsan in, 314 

salvarsan in, 313 

contra-indications to, 314 
Herxheimer reaction after, 314 
treponema pallidum in, 302 
Syphilitic alopecia, 309 
arteritis, 306 
cirrhosis of liver, 611 
condylomata, 309 
dactylitis, 3 12 
epiphysitis, 312 
eruptions, 308, 309 
gummata, 306, 309 
infantilism, 312 
iritis, 309 
keratitis, 312 
laryngitis, 370 
lymph nodes, 308 
marasmus, 312 
nephritis, 306 
phthisis, 308 
rhinitis, 312 

spastic spinal paralysis, 838 
strumitis, 681 
Syringomyelia, 844 
definition of, 844 



Syringomyelia, diagnosis of, 846 
etiology of, 844 
hands in, 845 
history of, 844 
morbid anatomy of, 844 
pathology of, 844 
prognosis in, 846 
symptoms of, 845 
treatment of, 846 



Tabes of brain, 817 

dorsalis, 823 

mesenterica, 247 
Tache blenatre in typhoid fever, 30 

cerebrale in typhoid fever, 30 
Tachycardia, 487 

in exophthalmic goitre, 685 

in hysteria, 897 
Tapeworm, 350 

dog, double-pored, 350 

dwarf, 350 

Russian, 350 

symptoms of, 352 

treatment of, 352 

varieties of, 350 
Tapping in pleurisy with effusion, 422 
Teeth in syphilis, 312 
Telegraphers' cramp, 914 
Tenia confusa, 350 

cucumerina, 352 

echinococcus, 350, 351 

mediocanellata, 350 

nana, 350 

saginata, 350 

solium, 350, 351 
Teratoma of mediastinum, 431 
Tertian parasite of malarial fever, 318 
Testicle, tuberculosis of, 281 
Test, Rumpel-Leede, for scarlet fever, 89 

Widal, in typhoid fever, 43 
Test-meal in gastric cancer, 549 
Tests for albumin in urine, 676 

blood, in diabetes mellitus, 731 

for sugar in urine, 732 
Tetanilla, 691 
Tetanus, 227 

baccilus of, 227 

definition of, 227 

diagnosis of, 229 

from hysteria, 229 

from strychnine poisoning, 229 

from tetany, 229 

distribution of, 227 

emprosthotonos in, 229 

etiology of, 227 

frequency of, 227 

head, 231 

history of, 227 

incubation of, 228 

kopf-, 231 

"lock- jaw" in, 228 

morbid anatomy of, 228 

muscular rigidity in, 228 

opisthotonos in, 229 

pain in, 229 

pathology of, 228 

prevention of, 228 

prognosis of, 229 

risus sardonicus in, 228 

spasm of diaphragm in, 228 
of glottis in, 229 



964 



INDEX 



Tetanus, symptoms of, 228 
treatment of, 229 
antitoxin, 229 
Tetany, 691 

Chvostek's sign of, 692 
diagnosis of, 692 

from Jacksonian epilepsy, 692 
from hysteria, 692 
Erb's sign of, 692 
etiology of, 691 
gastric, 533 

Chvostek's sign in, 534 
Erb's sign in, 534 
Trousseau's sign in, 534 
Hoffmann's sign of, 692 
morbid anatomy of, 691 
pathology of, 691 
prognosis in, 692 
in status lymphaticus, 695 
symptoms of, 691 
treatment of, 692 
Trousseau's sign of, 692 
symptoms of, 692 
Thermic fever, 920 
Thomsen's disease, 886 
Thread-worm, 337 
Three-day fever, 218 
Thrombosis, cerebral, 785 

in croupous pneumonia, 144 
of portal vein, 613 
in typhoid fever, 32 
venous, in croupous pneumonia, 143 
sinuses, 812 

etiology of, 812 
morbid anatomy of, 812 
pathology of, 812 
prognosis of, 813 
symptoms of, 813 
treatment of, 813 
Thrush, 511. See Stomatitis, parasitic. 
Thymus, enlarged, 694 

gland, diseases of, 693 
Thyreocele, 681 

Thyroid gla,nd, adenoma of, 683 
carcinoma of, 683 
carcinosarcoma of, 683 
diseases of, 681 
endothelioma of, 683 
sarcoma of, 683 
swelling of, 682 
tuberculosis of, 286 
tumors of, 683 
Tic convulsif, 878 
Tick fever, 297 

albuminuria in, 298 
definition of, 297 
diagnosis of, 298 
epistaxis in, 298 
etiology of, 298 
fever in, 298 
gangrene in, 298 
morbid anatomy of, 298 
prognosis of, 299 
prophylaxis in, 299 
pulse in, 298 
rash in, 298 
symptoms of, 298 
treatment of, 299 
Tinnitus, 878 

Tongue in croupous pneumonia, 138 
eczema of, 512 

treatment of, 513 
geographical, 512 
smokers', 513 



Tongue in sprue, 589 

strawberry, in scarlet fever, 89 
wooden, 233 
Tonsillitis, acute, 518 

definition of, 518 
diffuse, 518 
endocarditis in, 519 
etiology of, 518 
follicular, 518 
forms of, 518 
morbid anatomy of, 519 
pathology of, 519 
symptoms of, 519 
treatment of, 520 
hypertrophic, chronic, 521 

barrel-shaped chest in, 521 
definition of, 521 
funnel chest in, 521 
mouth breathing in, 521 
pigeon-breast in, 521 
symptoms of, 521 
treatment of, 522 
Tonsils, diseases of, 518 
tuberculosis of, 278 
Torticollis, 882 
Toxic gastrectasis, 535 

gastritis, acute, 525 
Tracheotomy in edematous laryngitis, 367 
Transverse myelitis, 840 
Traumatic abscess of liver, 602 
neuroses, 912 
strumitis, 681 
Trematodes, 353 

definition of, 353 
" Trembles" in cattle, 295 
Tremor in exophthalmic goitre, 686 

in paralysis agitans, 889 
Trichina spiralis, 337 
Trichiniasis, 337 

diagnosis of, 338 
etiology of, 337 
morbid anatomy of, 338 
pathology of, 338 
prognosis in, 338 
symptoms of, 338 
treatment of, 338 
Trichocephalus dispar, 349 
Trichomonas hominis, 357 

vaginalis, 357 
Tricuspid regurgitation, 480 
definition of, 480 
diagnosis of, 482 
etiology of, 481 
pathology of, 481 
physical signs of, 481 
prognosis in, 482 
symptoms of, 481 
stenosis, 482 

diagnosis of, 482 
Trifacial nerve, paralysis of, 871 
symptoms of, 871 
Trilocular heart, 494 

Trip-hammer pulse in aortic regurgitation, 479 
Trommer's test for sugar in urine, 732 
Tropical abscess of liver, 602 
adenitis, 200 
bubo, 200 
chlorosis, 338 
sore, 336 

splenomegaly, 335 
Trousseau's sign in gastric tetany, 534 

of tetany, 692 
Trypanosoma fever, 333 

treatment of, 333 



INDEX 



965 



Trypanosomata, varieties of, 332 
Trypanosomiasis, 331 
definition of, 331 
human, 333 
prevention of, 332 
transmission of, 332 
tsetse fly in, 332 
Tubercle, 242 
of brain, 801 
miliary, 242 
Tuberculin treatment of tuberculosis, 275 
Tuberculosis, 237 

in Addison's disease, 698 
of alimentary canal, 278 
bacillus of, 237 
of bladder, 282 

diagnosis of, 283 
symptoms of, 283 
treatment of, 283 
bovine, 237 
of brain, 286 
of cecum, 279 
of cervical glands, 246 
chronic hyperplastic, 243 
definition of, 237 
of esophagus, 278 
etiology of, 237 
of Fallopian tubes, 285 
frequency of, 240 
of geni to-urinary system,. 281 
glandular, 245 
signs of, 246 
treatment of, 247 
of heart, 285 
of intestine, 278 

chronic hyperplastic, 279 
prognosis in, 280 
symptoms of, 279 
treatment of, 281 
of kidneys, 283 
acute, 284 
chronic, 284 
hydronephrosis in, 284 
pyonephrosis in, 284 
symptoms of, 284 
of liver, 281 

of mediastinal glands, 246 
meningeal, acute, 247 

diagnosis of, 249 

from acute meningitis, 249 
from cerebrospinal meningi- 
tis, 249 
diagnosis of, Moro test in, 249 
in children, types of, 249 
prognosis of, 249 

symptoms of, 248 
of mesenteric glands, 247 
miliary, acute, 243 

bacillus in, 243 
diagnosis of, 245 
prognosis of, 245 
symptoms of, 244 
treatment of, 245 
mode of infection in, 237 
morbid anatomy of, 242 
mortality of, 241 
of myocardium, 285 
of ovaries, 285 
pathology of, 242 
of pericardium, 250 

symptoms of, 251 
of peritoneum, 251 
acute miliary, 251 
caseous type of, 252 



Tuberculosis of peritoneum, chronic fibroid, 
253 
symptoms of, 253 
treatment of, 254 
of pharynx, 278 
of pleura, 250 

lesions in, 250 
pneumonic, acute, diagnosis of, 263 

.physical signs of, 263 
predisposing causes of, 239 
prevention of, 240 
pulmonary, 255 

amphoric breathing in, 264 
bacillus of, method of staining, 265 
caseation in, 256 
cavities in, 256 
complications of, 261 
"cracked-pot sound" in, 263 
diagnosis of, 263 

nuoroscope in, 266 

microscopic, 265 

ophthalmotuberculin test in, 
267 

von Pirquet test in, 267 

tuberculin in, 266 
hemoptysis in, 261 

prognosis of, 269 

treatment of, 276 
hemorrhage in, 261 
infiltration of Laennec in, 256 
lesions in, 255 
metallic tinkling in, 264 
mode of infection in, 255 
.pectoriloquy in, 264 
physical signs of, 263 
pneumothorax in, 262 
prognosis in, 268 

pulmonary osteo-arthropathy, 262 
reparation in, 257 
symptoms of, 259 

cough, 261 

dyspnea, 261 

fever, 260 

laryngeal, 259 

loss of weight, 260 

sputum, 261 

sweating, 260 
treatment of, 269 

antistreptococcic serum in, 275 

artificial pneumothorax in, 277 

bronchitis, 274 

climatic, 270 

cough, 274 

diet in, 269 

drugs in, 273 

exercise in, 270 

fever, 274 

hemoptysis in, 276 

laryngeal, 276 

medicinal, 273 

night-sweats, 273 

out-door life in, 270 

serum, 275 

special symptoms, 273 

tuberculin in, 275 
types of, 255 

caseating, 256 

chronic, 255 

fibroid, 255, 258 

miliary, 255 

ulcerative, 255 
vascular changes in, 255 
vomiting in, treatment of, 276 
of rectum, 279 



966 



INDEX 



Tuberculosis of retroperitoneal glands, 247 
of serous membranes, 247 
acute, 247 
chronic, 247 
treatment of, 254 
of spinal cord, 286 
of stomach, 278 
of testicle, 281 

diagnosis of, 282 
symptoms of, 282 
treatment of, 282 
of thyroid gland, 286 
of tonsils, 278 
of uterus; 285 
Tuberculous laryngitis, 368 
leprosy, 293 
pleurisy, 250, 413 
strumitis, 681 

vegetative endocarditis, 285 
Tubular nephritis, chronic, 645 
Tumbu-fly disease, 358 

Tumors of bowel as cause of obstruction, 579 
of brain and its membranes, 801 
of kidney, 668 
of liver, 614 
in lungs, 412 
of mediastinum, 431 
of pancreas, 637 
of thyroid gland, 683 
Tungau, 357 
Tunnel anemia, 338 
disease, 338 

St. Gothard's, 338 
Tympanites, 591 

in croupous pneumonia, 138 
in typhoid fever, 27, 36 
treatment of, 51 
Tympany in acute peritonitis, 595 

in typhoid fever, 27 
Typhoid fever, 17 

albuminuria in, 38 
anemia in, 30 
antisepsis in, 50 
appendicitis in, 28, 36 
arthritis in, 40 
atypical forms of, 28 
bacillus of, 17 

in blood, 24 
bathing in, 48 
bed-sores in, 30 

treatment of, 52 
blood in, 30 

bloodvessels, lesions of, in, 32 
boils in, 30 

bone complications in, 40 
bone-marrow changes in, 25 
Brand bath in, 48 

contra-indications to, 48 
cardiac failure in, 32 
carrier, 18 
in children, 28 
chills in, 28, 30 
cholecystitis in, 37 
cholelithiasis in, 37 
circulatory complications in, 32 
cold in, 47 
coma vigil in, 39 
complicating pregnancy, 41 
complications of, 32, 33 
constipation in, 26 

treatment of, 50 
convulsions in, 40 
cystitis in, 38 
definition of, 17 



Typhoid fever, delirium in, 27, 28 
delusions in, 39 
diagnosis of, 41 
diarrhea in, 26, 27, 28, 33 

treatment of, 51 
diazo-reaction of urine in, 45 
diet in, 48 
differentiation of, from other fevers, 42, 

43 
disinfection of discharges in, 18 
dislocation of hip in, spontaneous, 40 
distribution of, 17 
Ehrlich's reaction in, 45 
embolism in, 32 
embryocardia in, 32 
empyema in, 39 
endarteritis in, 25 
epididymitis in, 38 
erysipelas in, 30 

migrans in, 30 
esophagitis in, 33 
esophagus in ulceration of, 33 
etiology of, 17 
facial expression in, 26 
frequency of, 21 
gallbladder in, 37 
gangrene in, 30 
gastric ulcer in, 33 
genito-urinary complications in, 38 
headache. in, 26, 27 
heart clot, 32 

muscle in, changes in, 25 

sounds in, 32 
hemiplegia in, 40 
hemorrhage in, 29, 33 

diagnosis of, 34 

symptoms of, 34 

treatment of, 51 
hepatic complications in, 37 
herpes in, 30 
history of, 17 
hydrotherapy in, 47 
hypostatic congestion of lung in, 38 
incubation of, 25 
infarction of lung in, 39 
insomnia in, 26 

treatment of, 52 
jaundice in, 37 
joint complications in, 40 
kidneys in, 25 
laryngeal ulceration in, 38 
leukocytosis in, 31 
liver in, 25, 37 
medicines in, 49 
meningitis in, 39, 40 
mesenteric nodes in, 24 
mixed infection in, 32 
mode of infection in, 18 
morbid anatomy of, 21 
mortality of, 21 
muscle, complications in, 40 
muscular tremors in, 28 
myocarditis in, 32 
myositis in, 40 
nephritis in, 38 
nervous complications of, 39 
neuritis in, 40 
nose-bleed in, 26 
orchitis in, 38 
osteomyelitis in, 40 
otitis media, acute, in, 40 
parotitis in, 33 
pathology of, 21 
peliomata in, 30 



INDEX 



967 



Typhoid fever, pericarditis in, 32 
perforation in, 34 

diagnosis of, 35 

signs of, 34 

treatment of, 52 
period of steep curves in, 28 
peritonitis in, 35 

diagnosis of, 35 
petechia? in, 30 
pharyngitis in, 33 
phlebitis in, 32 
pleurisy in, 39 
pneumonia in, 28, 38 
polyuria in, 38 . 
prevention of, 18 
preventive inoculation in, 20 
prognosis of, 46 
pulmonary abscess in, 39 
pulse in, 27 
pyuria in, 38 
recrudescence in, 29 
renal disease, acute, in, 28 
respiratory complications in, 38 

lesions in, 25 
rose spots in, 27 
sequelae in, 32 
skin changes in, 30 
splenic enlargement in, 24, 26, 28 
stimulants in, 49 
stools in, 33 
stupor in, 27 
sudamina in, 30 
symptoms of, 26 
tache blenatre in, 30 

cerebrale in, 30 
temperature in, 26, 29 
tests in, 43 
thirst in, 20 
thrombosis in, 32 
tongue in, 26 
treatment of, 47 

during convalescence, 53 

medicinal, 49 
special symptoms, 50 
tympanites in, 27, 36 

treatment of, 51 
typhoid spine in, 40 
ulcer in, 23 

vaccination against, 20 
vaccine in, 50 
vomiting in, 33 

treatment of, 51 
Widal's test, 43 
Typhomania, in typhus fever, 57 
Typhus fever, 54 

chill in, 57 
complications of, 58 
definition of, 54 
delirium in, 57 
diagnosis of, 58 
distribution of, 55 
eruption in, 56, 57 
etiology of, 55 
fever in, 57 
hepatic changes in, 57 
history of, 55 

hypostatic congestion of lungs in, 57 
intestinal lesions in, 57 
kidneys in, 57 
morbid anatomy of, 56 
myocarditis in, 57 
pathology of, 56 
. petechia? in, 57 
prevention of, 56 



Typhus fever, prognosis of, 59 

pulse in, 57 

pupils in, 58 

relapses in, 58 

retention of urine in, 60 

spleen in, 57 

termination of, 58 

treatment of, 60 
siderans, 57 
Tyrotoxicon, 782 
Tyrotoxismus, 782 



U 



Ulcer, duodenal, 561 

diagnosis of, 563 

from acute fat-necrosis, 564 
from gallstone colic, 564 
from gastric ulcer, 563 
from intestinal obstruction, 564 
rc-rays in, 564 
etiology of, 561 
hemorrhage in, 563 
morbid anatomy of, 562 
pathology of, 562 
perforation in, 563 

symptoms of, 563 
prognosis in, 564 
symptoms of, 563 
treatment of, 564 
gastric, 536. See Gastric ulcer, 
intestinal, in paratyphoid fever, 53 

in typhoid fever, 34 
peptic, 536 

perforating, of foot, in locomotor ataxia, 828 
of stomach, 536 
Ulceration of esophagus in typhoid fever, 33 
laryngeal, in typhoid fever, 38 
Peyer's patch in typhoid fever, 23 
Ulcerative appendicitis, 573, 574 
endocarditis, 458 
pharyngitis, 516 
stomatitis, 510 
Ulcus ventriculi, 536 
Uncinaria Americana, 340 

duodenale, 338 
Uncinariasis, 338 
anemia in, 341 

Charcot-Leyden crystals in, 340 
definition of, 338 
diagnosis of, 341 
etiology of, 339 
frequency of, 338 
morbid anatomy of, 339 
pathology of, 339 
prophylaxis of, 339 
symptoms of, 340 
treatment of, 343 
Undulant fever, 215 
Uremia, 658 

amaurosis in, 660 
convulsive type of, 659 
definition of, 658 
diagnosis of, 660 

from heatstroke, 661 
from opium poisoning, 661 
etiology of, 658 
hemiplegia in, 660 
insomnia in, 660 
latent, 660 
mania in, 660 
monoplegia in, 660 
odor in, 660 
paralytic form of, 660 



968 



INDEX 



Uremia, pathology of, 658 

prognosis in, 661 

symptoms of, 659 

treatment of, hot pack in, 667 
Uremic apoplexy, 793 
Uric acid diathesis, 680 
Urinary secretion, disorders of, 672 
Urine acetone in, tests for, 732 

in acute diffuse nephritis, 642 

albumin in, 675 
tests for, 676 

albumose in, 680 

in beriberi, 783 

blood in, 673 

in cholelithiasis, 623 

in chronic interstitial nephritis, 652 
parenchymatous nephritis, 646 

chyle in, 678 

in croupous pneumonia, 137, 145 

in diabetes insipidus, 740 
mellitus, 729 

hemoglobin in, 674 

indican in, 679 

melanin in, 680 

oxalates in, 679 

phosphates in, 679 

pus in, 678 . 

in renal calculus, 669 

in rheumatic fever, acute, 177 

in smallpox, 65 

sugar in, tests for, 732 

suppression of, 672 

in scarlet fever, 86 

uric acid in, 680 

in yellow fever, 191 
Urticaria in acute rheumatic fever, 178 
Uterus, tuberculosis of, 285 



Vaccination, 74 

antityphoid, 20 

history of, 74 

method of, 75 

in smallpox, 62, 74 
Vaccine, anticholera, 182 

antirabic, 226 

lymph, glycerinated, 75 

meningococcic, in meningococcic meningi- 
titis, 121 

treatment of whooping-cough, 105 
Vaccinia, 74 

in man, primary, 76 
secondary, 76 
Vagus nerve, disease of, 880 
Valvular anomalies, congenital, 494 

endocarditis, 454 
Varicella, 77 

definition of, 77 

diagnosis of, 78 

from smallpox, 71, 78 

eruption in, 78 

erysipelas in, 78 

etiology of, 77 - 

incubation in, 77 

nephritis in, 78 

prognosis in, 79 

symptoms of, 78 

treatment of, 79 
Varicose aneurysm, 500 

groin glands in filiariasis, 346 
Variola, 60. See Smallpox. 

fulminans, 69 



Variola pustulosa hemorrhagica, 69 

sine eruptione, 70 
Varioloid, 69 
Vascular goitre, 681 

Venesection in pulmonary emphysema, 404 
Venous sinuses, thrombosis of, 812 

thrombosis in croupous pneumonia, 143 
Verrucous endocarditis, 456 
Verruga, 300 

definition of, 300 

distribution of, 300 

eruption in, 301 

etiology of, 300 

incubation of, 301 

joints in, 301 

Peruviana, 300 

prognosis in, 301 

skin in, 301 

symptoms of, 301 

treatment of, 301 
Vertebrae, disease of, 849 
diagnosis of, 849 
prognosis in, 849 
symptoms of, 849 
treatment of, 850 

malignant growths of, 850 
Vertigo, 878 

in brain tumor, 802 
Vesical crises in locomotor ataxia, 826 

tuberculosis, 282 
Vesicular stomatitis, 509 
Vincent's angina, 521 
Violinists' cramp, 914 
Visceral lesions in diphtheria, 155 
Visceroptosis, 582 
Visual tract, 868 
Volvulus, 581 

prognosis of, 582 

symptoms of, 581 

treatment of, 582 
Vomiting, cyclic, 560 
Von Graefe's sign in exophthalmic goitre, 685 



W 



Water-hammer pulse in aortic regurgitation, 
479 

infection by, in typhoid fever, 18 
Weber's syndrome in brain tumor, 803 
Weil's disease, 296 
Weisses blut, 714 
Westphal's symptom in locomotor ataxia, 

826 
Wet brain, 770 
Whipworm, 349 
White flux, 588 
Whooping-cough, 101 

amblyopia in, 104 

bacillus pertussis, 102 

bronchopneumonia in, 103 

cardiac changes in, 104 

conjunctival hemorrhages in, 104 

complications of, 103 

definition of, 101 

diagnosis of, 104 

distribution of, 101 

duration of, 105 

emphysema in, 103 

etiology of, 102 

frequency of, 101 

glandular enlargement in, 104 

history of, 101 



INDEX 



969 



Whooping-cough, incubation in, 102 

in measles, 96 

leukocytosis in, 103 

lymphocytosis in, 103 

morbid anatomy of, 101 

mortality in, 104 

paralysis in, 104 

paroxysm of, 102 

pathology of, 101 

physical signs in, 103 

pneumothorax in, 104 

prognosis in, 104 

symptoms of, 101 

treatment of, 105 

bronchitis tent in, 105 
vaccine, 105 

vomiting in, 104 
Widal test in typhoid fever, 43 
WinckePs disease, 720 
"Wooden tongue," 233 
Wool-sorters' disease, 219 
Word-blindness, 800 

deafness, 800 
Worm, beef-, 350 

guinea-, 346 

hook-, 338 

Medina, 346 

pin-, 337 

pork-, 337, 350 

round-, 336 

screw-, 357 

seat-, 337 

tape, 350 

thread-, 337 

whip-, 349 
Wounds of heart, 454 
Wrist-drop in lead poisoning, 779 
Writers' cramp, 914 
Wryneck, 882 

congenital, 882 

spasmodic, 882 

spurious, 883 



Xerostomia, 514 

treatment of, 514 



Yaws, 235 

Yellow atrophy of liver, acute, 616 
fever, 187 

albuminuria in, 191, 192 

apoplectiform type of, 191 

blood in, 190 

cardiac changes in, 190 

convulsions in, 190 

definition of, 187 

diagnosis of, 192 

from dengue, 192 

from malarial hemoglobinuric 

fever, 192 
from pernicious malarial fever, 192 

etiology of, 187 

gastric changes in, 190 

hematemesis in, 191, 559 

headache in, 190 

history of, 187 

intermittent changes in, 191 

jaundice in, 191 

morbid anatomy of, 190 

mortality of, 192 

nephritic changes in, 190 

pain in, 190 

pathology of, 190 

prevention of, 187 

prognosis of, 192 

prophylaxis of, 189 

remission in, 191 

respiration in, 191 

symptoms of, 190 

temperature in, 190 

tongue in, 191 

treatment of, 192 

urine in, 191 

vomiting in, 191 



H 13? eJ «« 




















































o • » 









iP-ai 




• ■ 



• » 1 • .^ 








^••^r.- A o 







vv 







** . 

















A V- ^ : 





















.7* A 




<* *<.* 



^k <^ o*/^ MPti^ *^ gfc 



^ * . * • 














iV 



°c 



•■-*- c*\-^% y % -afe.v ***£&%* a 




Si? *£ 







\A<5" 








*?% : -^K-* /\ -.-r,-, - . -T^S*^ „ .--. 




^ FEB 83 ^ ^ \J 

„_» N.MANCHESTER, I j» 

^^ INDIANA 46962 J X> <X 






